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  </channel><item rdf:about="https://www.niddk.nih.gov/about-niddk/strategic-plans-reports/diabetes-in-america-3rd-edition">
    <title>Diabetes in America, 3rd Edition - NIDDK</title>
    <dc:date>2023-06-21T06:49:32+00:00</dc:date>
    <link>https://www.niddk.nih.gov/about-niddk/strategic-plans-reports/diabetes-in-america-3rd-edition</link>
    <dc:creator>Michael.Massing</dc:creator><dc:subject>insulin type 2 diabetes T2D treatment exogenous medication</dc:subject>
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    <title>FAQs | Wearable Insulin Device | CeQur Simplicity Patch</title>
    <dc:date>2023-05-10T21:08:26+00:00</dc:date>
    <link>https://myceqursimplicity.com/faqs/</link>
    <dc:creator>Michael.Massing</dc:creator><description><![CDATA[Patients can augment adhesion if needed by using medical grade adhesive bandages or tapes such as Hy-Tape® or Micropore™ Surgical Tape over the patch’s adhesion.]]></description>
<dc:subject>insulin delivery patch CGM supplemental adhesion</dc:subject>
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    <title>Scientific Frontline: Adipose tissue as a culprit: How obesity leads to diabetes</title>
    <dc:date>2023-03-28T21:50:07+00:00</dc:date>
    <link>https://www.sflorg.com/2023/03/bio03282302.html</link>
    <dc:creator>Michael.Massing</dc:creator><dc:subject>type 2 diabetes T2D insulin resistance fat dietary adipose tissue pathophysiology risk factor etiology diet behavior behavioral environment environmental obesity endocrine body</dc:subject>
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<item rdf:about="https://www.rush.edu/news/understanding-link-between-covid-19-and-diabetes">
    <title>Understanding the Link Between COVID-19 and Diabetes | Rush System</title>
    <dc:date>2023-01-10T17:15:30+00:00</dc:date>
    <link>https://www.rush.edu/news/understanding-link-between-covid-19-and-diabetes</link>
    <dc:creator>Michael.Massing</dc:creator><description><![CDATA[Scientists already know that for some people, it’s not just a faulty immune system that triggers type 1 diabetes or insulin resistance that leads to type 2 diabetes. The National Institute of Diabetes, Digestive and Kidney Diseases recognizes more than 50 different ways that a person can develop diabetes, from defects in a single gene to other health issues like liver disease.

“Ideally, we would like to investigate each and every one of those 50 causes,” Kazlauskaite says. “And we are finding that some people have several diabetes causes at the same time. In other words, a patient may not just have the purely insulin-resistant type of diabetes, what’s typically defined as type 2, but they might also be affected by steroids or autoimmune diabetes at the same time.” Doctors may call this “hybrid diabetes,” suggesting that the etiology, or cause, of diabetes may be much more complex than originally believed.

Could COVID-19 be a new cause of diabetes?
It’s possible, Kazlauskaite says. A study recently published in the medical journal Lancet found that people who survived COVID have a 40% higher risk for developing diabetes. She believes many of the new cases of type 2 diabetes are occurring in people with pre-diabetes who don’t know it.

“People might have pre-diabetes with chronic, subclinical inflammation before they get COVID-19. So, when they do get infected with the virus, they could develop hyperinflammation that causes metabolic stress and more insulin resistance. As a result, they manifest overt diabetes,” she says.

Another theory is that COVID-19 disrupts the immune system. “We know hyperinflammation can cause autoimmune disease. When this happens, the immune system gets ‘confused’ and starts attacking its own tissues, including insulin-producing cells in the pancreas,” she says. This is the process that causes type 1 diabetes, which primarily develops in childhood but may also affect adults.

A third theory is that steroids given during COVID-19 treatment could cause diabetes because they often raise blood glucose, Kazlauskaite says. For some patients, glucose levels return to normal after the steroids have been discontinued, but for others, the effects are lasting.

A fourth reported hypothesis is that COVID-19 can cause severe inflammation of the pancreas (known as pancreatitis), where the body’s insulin-producing cells reside. This can trigger diabetes, although it is relatively rare]]></description>
<dc:subject>diabetes etiology cause risk factors type 1 2 T1D T2D autoimmune hyperinflammation prediabetes inflammation subclinical overview resarch long COVID post-acute sequelae liver hybrid insulin resistance immune system steroids pancreatitis pancreas metabolic stress</dc:subject>
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<item rdf:about="https://diatribe.org/is-your-pancreas-responsible-for-your-diabetes">
    <title>Is Your Pancreas Responsible for Your Diabetes?</title>
    <dc:date>2022-08-11T19:09:00+00:00</dc:date>
    <link>https://diatribe.org/is-your-pancreas-responsible-for-your-diabetes</link>
    <dc:creator>Michael.Massing</dc:creator><description><![CDATA[For people with type 1 diabetes, the body’s immune system attacks the cells in the islets of Langerhans, including beta cells. This means that the body is no longer able to produce insulin or regulate glucose levels.

The problem for individuals with type 1 diabetes is that excessive hunger and thirst causes blood glucose levels to increase. There are no hormones being secreted to tell the body to begin using this glucose for energy or storage. 

Even without a properly functioning endocrine pancreas, the exocrine pancreas can still function as it is supposed to. The exocrine pancreas will help the stomach break down food into components to be absorbed into the blood. But without insulin, this results in high blood glucose levels, which can damage other organs like the kidneys, nerves, eyes, and heart. 

In those with type 2 diabetes, the issue is slightly different. The pancreas still secretes some, but not enough, insulin. In addition, the body’s cells cannot properly use the insulin being made. This is called insulin resistance. This also leads to blood glucose levels that are higher than they should be. 

However, many medications and other interventions can help people manage their type 2 diabetes and lower glucose levels into a healthy range. These interventions include insulin (the medication), other diabetes medications like metformin, SGLT-2 inhibitors, and GLP-1 receptor agonists, and lifestyle modifications that focus on eating less and exercising more.]]></description>
<dc:subject>diabetes type 1 2 T1D T2D insulin production resistance pancreas sufficiency function</dc:subject>
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<item rdf:about="https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(21)02188-7/fulltext">
    <title>Tirzepatide versus insulin glargine in type 2 diabetes and increased cardiovascular risk (SURPASS-4): a randomised, open-label, parallel-group, multicentre, phase 3 trial - The Lancet</title>
    <dc:date>2021-10-25T01:20:04+00:00</dc:date>
    <link>https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(21)02188-7/fulltext</link>
    <dc:creator>Michael.Massing</dc:creator><description><![CDATA[[Lilly assesses] efficacy and [especially cardiovascular] safety of the novel dual GIP and GLP-1 receptor agonist tirzepatide vs insulin glargine in adult [type 2 diabetics with high CV] risk inadequately controlled on oral glucose-lowering medications.
]]></description>
<dc:subject>insulin glargine GIP GLP-1 receptor A1c Hb hemoglobin benefit risk cardiovascular peer-reviewed research clinical trial human in vivo</dc:subject>
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<item rdf:about="https://www.mdpi.com/2072-6643/13/10/3299/htm#B94-nutrients-13-03299">
    <title>Nutrients | Free Full-Text | Alternative Dietary Patterns for Americans: Low-Carbohydrate Diets | HTML</title>
    <dc:date>2021-10-06T03:12:26+00:00</dc:date>
    <link>https://www.mdpi.com/2072-6643/13/10/3299/htm#B94-nutrients-13-03299</link>
    <dc:creator>Michael.Massing</dc:creator><description><![CDATA[Data Availability Statement
No original data were generated for this manuscript.

Conflicts of Interest
JSV receives royalties for low-carbohydrate nutrition books, is co-founder and has equity in Virta Health Corp, and is a scientific advisor to Simply Good Foods; SDP receives royalties for low-carbohydrate nutrition books and is co-founder and has equity in Virta Health Corp; RMK is on the scientific advisory boards of Virta Health Corp, Seraphina Therapeutics, and Day Two, and has licensed patents for lipoprotein particle analysis; RJJ has received honoraria from Horizon Pharma and Danone, has stocks with XORTX Therapeutics, and has equity with Colorado Partners LLC (CRP); LRS is a consultant with Sentinel Management; WSY is a consultant for Guideline Central and dietdoctor.com; NT receives book royalties and honoraria for speeches via the Harry Walker Agency.

The decades-long dietary experiment embodied in the Dietary Guidelines for Americans (DGA) focused on limiting fat, especially saturated fat, and higher carbohydrate intake has coincided with rapidly escalating epidemics of obesity and type 2 diabetes (T2D) that are contributing to the progression of cardiovascular disease (CVD) and other diet-related chronic diseases. Moreover, the lack of flexibility in the DGA as it pertains to low carbohydrate approaches does not align with the contemporary trend toward precision nutrition. We argue that personalizing the level of dietary carbohydrate should be a high priority based on evidence that Americans have a wide spectrum of metabolic variability in their tolerance to high carbohydrate loads. Obesity, metabolic syndrome, and T2D are conditions strongly associated with insulin resistance, a condition exacerbated by increased dietary carbohydrate and improved by restricting carbohydrate. Low-carbohydrate diets are grounded across the time-span of human evolution, have well-established biochemical principles, and are now supported by multiple clinical trials in humans that demonstrate consistent improvements in multiple established risk factors associated with insulin resistance and cardiovascular disease. The American Diabetes Association (ADA) recently recognized a low carbohydrate eating pattern as an effective approach for patients with diabetes. Despite this evidence base, low-carbohydrate diets are not reflected in the DGA. As the DGA Dietary Patterns have not been demonstrated to be universally effective in addressing the needs of many Americans and recognizing the lack of widely available treatments for obesity, metabolic syndrome, and T2D that are safe, effective, and sustainable, the argument for an alternative, low-carbohydrate Dietary Pattern is all the more compelling....
Recently, the American Diabetes Association (ADA) has updated its nutrition recommendations to allow for more flexibility. Starting with their 2019 standards of care for patients with diabetes, the ADA stated that “Low-carbohydrate eating patterns, especially very low-carbohydrate (VLC) eating patterns, have been shown to reduce A1C and the need for antihyperglycemic medications. These eating patterns are among the most studied eating patterns for type 2 diabetes.”]]></description>
<dc:subject>low carbohydrate diet carb dietary guidelines for Americans DGA insulin resistance metabolic syndrome risk benefit peer-reviewed research</dc:subject>
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<item rdf:about="https://www.endocrinologyadvisor.com/home/topics/diabetes/increased-risk-for-major-adverse-cardiovascular-events-with-insulin-in-patients-with-diabetes-and-acs/?NID=-1&amp;cpn&amp;email_hash=983917dd1eba78eb44e393fea65df5ca&amp;hmEmail=Jw_YJjhVyI84iX-Oepu7iw7YiNSIB0EK31LP7LVx8w01&amp;hmSubId=YY-zPItNrOw1&amp;mpweb=1323-153862-7624403">
    <title>Insulin Use Linked to Risk for MACE Among Individuals With Stable Diabetes and Acute Coronary Syndrome - Endocrinology Advisor</title>
    <dc:date>2021-09-21T02:51:49+00:00</dc:date>
    <link>https://www.endocrinologyadvisor.com/home/topics/diabetes/increased-risk-for-major-adverse-cardiovascular-events-with-insulin-in-patients-with-diabetes-and-acs/?NID=-1&amp;cpn&amp;email_hash=983917dd1eba78eb44e393fea65df5ca&amp;hmEmail=Jw_YJjhVyI84iX-Oepu7iw7YiNSIB0EK31LP7LVx8w01&amp;hmSubId=YY-zPItNrOw1&amp;mpweb=1323-153862-7624403</link>
    <dc:creator>Michael.Massing</dc:creator><dc:subject>treatment risk benefit insulin cardiovascular heart ACS acute coronary syndome peer-reviewed research in vivo human clinical trial</dc:subject>
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<item rdf:about="https://diabeteswise.org/check-up/#/">
    <title>Checkup Tool — DiabetesWise</title>
    <dc:date>2021-06-12T03:26:19+00:00</dc:date>
    <link>https://diabeteswise.org/check-up/#/</link>
    <dc:creator>Michael.Massing</dc:creator><dc:subject>diabetes supplies tech meter pump comparison CGM sensors insulin injections MDI</dc:subject>
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<item rdf:about="https://www.mayoclinic.org/diseases-conditions/type-2-diabetes/expert-answers/blood-sugar/faq-20057941#:~:text=The%20average%20U.S.%20adult%20drinks,day%20appears%20to%20be%20safe.">
    <title>Caffeine: Does it affect blood sugar? - Mayo Clinic</title>
    <dc:date>2021-05-06T00:36:48+00:00</dc:date>
    <link>https://www.mayoclinic.org/diseases-conditions/type-2-diabetes/expert-answers/blood-sugar/faq-20057941#:~:text=The%20average%20U.S.%20adult%20drinks,day%20appears%20to%20be%20safe.</link>
    <dc:creator>Michael.Massing</dc:creator><description><![CDATA[The average U.S. adult drinks about two 8-ounce (240-milliliter) cups of coffee a day, which can contain around 280 milligrams of caffeine. For most young, healthy adults, caffeine doesn't appear to noticeably affect blood sugar (glucose) levels, and having up to 400 milligrams a day appears to be safe.

Some studies suggest that drinking coffee — whether caffeinated and decaffeinated — may actually reduce your risk of developing type 2 diabetes.

If you already have diabetes, however, the impact of caffeine on insulin action may be associated with higher or lower blood sugar levels. For some people with diabetes, about 200 milligrams of caffeine — or the equivalent of one to two 8-ounce (240-milliliter) cups of plain, brewed coffee — may cause this effect.

Caffeine affects every person differently. If you have diabetes or you're struggling to control your blood sugar levels, limiting the amount of caffeine in your diet may provide a benefit.]]></description>
<dc:subject>coffee caffeine blood sugar glucose fluctuation correlation variability sensitivity insulin overview risk benefit human research in vivo</dc:subject>
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<item rdf:about="https://www.webmd.com/diabetes/diabetes-and-caffeine">
    <title>Type 2 Diabetes and Caffeine: The Truth about Blood Sugar</title>
    <dc:date>2021-05-06T00:33:53+00:00</dc:date>
    <link>https://www.webmd.com/diabetes/diabetes-and-caffeine</link>
    <dc:creator>Michael.Massing</dc:creator><description><![CDATA[A growing body of research suggests people with type 2 diabetes react to caffeine differently. It can raise blood sugar and insulin levels for those with the disease.

One study looked at people with type 2 diabetes who took a 250-milligram caffeine pill at breakfast and another at lunchtime. That’s about the same amount as drinking two cups of coffee with each meal. The result: Their blood sugar was 8% higher than on days when they didn’t have caffeine. Their reading also jumped by more after each meal.

That’s because caffeine can affect how your body responds to insulin, the hormone that allows sugar to enter your cells and get changed into energy.


Caffeine may lower your insulin sensitivity. That means your cells don’t react to the hormone by as much as they once did. They don’t absorb as much sugar from your blood after you eat or drink. This causes your body to make more insulin, so you have higher levels after meals.]]></description>
<dc:subject>coffee caffeine blood sugar glucose fluctuation correlation variability sensitivity insulin peer-reviewed research human in vivo randomized controlled trial RCT crossover risk benefit</dc:subject>
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<item rdf:about="https://care.diabetesjournals.org/content/27/12/2990">
    <title>Effects of Coffee Consumption on Fasting Blood Glucose and Insulin Concentrations | Diabetes Care</title>
    <dc:date>2021-05-06T00:32:33+00:00</dc:date>
    <link>https://care.diabetesjournals.org/content/27/12/2990</link>
    <dc:creator>Michael.Massing</dc:creator><description><![CDATA[Higher habitual coffee consumption was associated with higher insulin sensitivity (1) and a lower risk for type 2 diabetes (2–6) in diverse populations. In contrast, short-term metabolic studies showed that caffeine intake can acutely lower insulin sensitivity (7–9) and increase glucose concentrations (10–15). ]]></description>
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<item rdf:about="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6544578/">
    <title>Effects of coffee consumption on glucose metabolism: A systematic review of clinical trials</title>
    <dc:date>2021-05-01T01:23:31+00:00</dc:date>
    <link>https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6544578/</link>
    <dc:creator>Michael.Massing</dc:creator><dc:subject>coffee glucose metabolism risk benefit systematic review in vivo clinical trials human peer-reviewed research caffeine insulin resistance sensitivity</dc:subject>
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</item>
<item rdf:about="https://twitter.com/fallabel/status/1271546651031658496?s=12">
    <title>twitter.com</title>
    <dc:date>2020-06-13T13:32:41+00:00</dc:date>
    <link>https://twitter.com/fallabel/status/1271546651031658496?s=12</link>
    <dc:creator>Michael.Massing</dc:creator><dc:subject>T2D 2 infusion 1 self sensor care diabetes INSULIN T1D irritation skin typ pump site rash</dc:subject>
<dc:identifier>https://pinboard.in/u:Michael.Massing/b:0c807a14cba2/</dc:identifier>
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	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:INSULIN"/>
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</item>
<item rdf:about="https://www.nature.com/articles/ejcn201539/">
    <title>Metabolic and physiologic effects from consuming a hunter-gatherer (Paleolithic)-type diet in type 2 diabetes | European Journal of Clinical Nutrition</title>
    <dc:date>2019-12-30T03:27:53+00:00</dc:date>
    <link>https://www.nature.com/articles/ejcn201539/</link>
    <dc:creator>Michael.Massing</dc:creator><description><![CDATA[Both groups had improvements in metabolic measures, but the Paleo diet group had greater benefits on glucose control and lipid profiles. Also, on the Paleo diet, the most insulin-resistant subjects had a significant improvement in insulin sensitivity (r=0.40, P=0.02), but no such effect was seen in the most insulin-resistant subjects on the ADA diet (r= 0.39, P=0.3).

Conclusions:
Even short-term consumption of a Paleolithic-type diet improved glucose control and lipid profiles in people with type 2 diabetes compared with a conventional diet containing moderate salt intake, low-fat dairy, whole grains and legumes.]]></description>
<dc:subject>Paleo diet grain legumes dairy RCT random controlled trial human in vivo situ clinical research lipids hyperlipidemia management blood glucose insulin resistance sensitivity ADA diabetes type 2 T2D</dc:subject>
<dc:source>https://pinboard.in/</dc:source>
<dc:identifier>https://pinboard.in/u:Michael.Massing/b:14f5a3ef80a5/</dc:identifier>
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	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:diabetes"/>
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</item>
<item rdf:about="https://www.sciencedaily.com/releases/2010/07/100712103453.htm">
    <title>Early predictors of metabolic syndrome in healthy 7-9 year-olds identified -- ScienceDaily</title>
    <dc:date>2019-08-12T01:42:02+00:00</dc:date>
    <link>https://www.sciencedaily.com/releases/2010/07/100712103453.htm</link>
    <dc:creator>Michael.Massing</dc:creator><description><![CDATA[Markers that may precede the metabolic syndrome and mechanisms that explain these relationships have yet to be identified. These mechanisms may originate in the intrauterine environment, be exacerbated in susceptible populations, such as African Americans and, be further promoted by a genetic predisposition, particularly among African American children. These abnormalities may work synergistically to create a childhood metabolic syndrome phenotype and may originate earlier in youth than previously proposed.

The purpose of the study was to explore potential correlates of insulin sensitivity, fasting insulin, and insulin resistance, and to determine the best model to predict them in young children. The study of more than 100 healthy children, ages 7-9, found that fat in the liver, abdominal fat, and fat oxidation predicted insulin resistance and appear to be early markers for the metabolic syndrome via a mechanism of impaired lipid metabolism and fat oxidation. Impaired metabolic function may be due, in part, to pre-and post natal factors that are modified by current physical activity. Therefore, race, low or high pregnancy weight and/or birth weight, and low physical activity collectively create a phenotype for poor metabolic function leading to increased risk for insulin resistance in young children.

"Although some of the risk factors cannot be changed, pregnancy weight, birth weight, and physical activity can all be modified and are targets for early intervention to prevent or delay insulin resistance and reduce the risk for metabolic syndrome," noted Dr. Sothern, who is the study's principal investigator.]]></description>
<dc:subject>low birth weight risk metabolic syndrome lipids fats blood cholesterol skeletal fat fatty liver epigenetic insulin resistance child development children youth health disparities diabetes teen diet body disorder etiology T2D research correlation type 2 factor public genetics genetic biomarkers prognosis diagnosis screening in vivo human clinical trial prognostic leg prenatal perinatal breast feeding childhood cause factors chicken-and-egg</dc:subject>
<dc:source>https://pinboard.in/</dc:source>
<dc:identifier>https://pinboard.in/u:Michael.Massing/b:e1148767b47d/</dc:identifier>
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</item>
<item rdf:about="https://www.lsuhsc.edu/news/MELINDAFULL.html">
    <title>LSUHSC RESEARCHERS 1ST TO DOCUMENT EARLY SIGNS FOR DIABETES IN KIDS AS YOUNG AS 7</title>
    <dc:date>2019-08-11T04:13:29+00:00</dc:date>
    <link>https://www.lsuhsc.edu/news/MELINDAFULL.html</link>
    <dc:creator>Michael.Massing</dc:creator><description><![CDATA[Insulin resistance/poor insulin sensitivity is closely associated with increased total body fat and may precede development of the metabolic syndrome and type 2 diabetes. Indicators of impaired insulin sensitivity have yet to be clearly identified in children prior to puberty.

The LSUHSC researchers found that the child’s current fat weight is the strongest predictor for poor insulin sensitivity which is a risk factor for type 2 diabetes. LDL (bad cholesterol) was also strongly associated with insulin sensitivity in the prediction model. Previously unidentified Metabolic Syndrome markers discovered by Dr. Sothern’s team include:

• Fat in the liver cells and fat in the skeletal (leg) muscle cells also predict poor insulin sensitivity and high insulin resistance (pre-diabetes) along with an impaired fat burning ability in the muscles.

• These relationships were only found after the researchers considered the child's current fat weight, so the strongest predictor is whether or not these young children are currently overweight or obese.

• The fat in the skeletal muscle became less important after Dr. Sothern’s team considered the mother’s weight prior to and during pregnancy, whether the child was breast-fed, and the current physical activity level of these young children.

“This means that if the mother has a healthy weight gain during pregnancy and the child is breast-fed and physically active, the fat may not accumulate in the skeletal muscle and/or liver and the child may not experience an impaired fat burning ability in the muscle. All of these factors are significantly associated with poor insulin sensitivity that may eventually lead to type 2 diabetes in adolescence or young adulthood. We hope to conduct future prospective studies in this cohort of healthy children to confirm this finding,” notes Dr. Melinda Sothern, LSU Health Sciences Center New Orleans Professor of Public Health and study leader.

Collectively, fat oxidation (how well the body is able to utilize fat as a fuel), blood pressure, and lipids (HDL and LDL) were identified as the best physiologic predictors of insulin sensitivity.

Arlette Soros, MD, an LSUHSC Pediatrics fellow who is a member of Dr. Sothern’s research team, is presenting results of the first study to examine why some children become hypoglycemic (low blood sugar) during insulin sensitivity testing. She will report that children who are lean and have less fat in their skeletal muscle are more likely to get hypoglycemia. Also those with the best insulin sensitivity were the most likely to get low blood sugar.

“We are not sure why this is but think they may be more fit and less prone to diabetes,” concludes Dr. Sothern.
----------
American Diabetes Association 2009 Annual Scientific Session Meeting in New Orleans. Dr. Sothern’s group is the first to document previously unknown markers for obesity, heart disease and diabetes, collectively called the Metabolic Syndrome, in children [ages 7–9]. Posters will be presented on Saturday, June 6, 2009, and Brian Bennett, a Research Associate in Dr. Melinda Sothern’s laboratory will make the oral presentation, Early Markers for the Metabolic Syndrome in Youth, on Monday, June 8, 2009.]]></description>
<dc:subject>risk metabolic syndrome fat fatty liver insulin resistance child development children youth health disparities diabetes teen diet body disorder etiology T2D research correlation type 2 factor public genetics genetic biomarkers prognosis diagnosis screening in vivo human clinical trial prognostic low birth weight skeletal leg prenatal perinatal breast feeding epigenetic lipids fats blood cholesterol cause factors chicken-and-egg</dc:subject>
<dc:source>https://pinboard.in/</dc:source>
<dc:identifier>https://pinboard.in/u:Michael.Massing/b:2930aa243327/</dc:identifier>
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</item>
<item rdf:about="https://www.diabetesselfmanagement.com/blog/how-do-you-do-fiber/">
    <title>How Do You Do Fiber? - Diabetes Self-Management</title>
    <dc:date>2019-07-21T00:30:12+00:00</dc:date>
    <link>https://www.diabetesselfmanagement.com/blog/how-do-you-do-fiber/</link>
    <dc:creator>Michael.Massing</dc:creator><dc:subject>fiber carbohydrates management blood glucose insulin</dc:subject>
<dc:source>https://pinboard.in/</dc:source>
<dc:identifier>https://pinboard.in/u:Michael.Massing/b:dbf5a77ad130/</dc:identifier>
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</item>
<item rdf:about="https://glucosezone.com/#/article/w6u-wreaacuarumf">
    <title>GlucoseZone</title>
    <dc:date>2019-04-26T20:36:50+00:00</dc:date>
    <link>https://glucosezone.com/#/article/w6u-wreaacuarumf</link>
    <dc:creator>Michael.Massing</dc:creator><description><![CDATA[How protein affects glucose levels]]></description>
<dc:subject>protein insulin dosage metabolism amino acids dosing diet glucose management monitoring self care blood</dc:subject>
<dc:source>https://pinboard.in/</dc:source>
<dc:identifier>https://pinboard.in/u:Michael.Massing/b:e7271b84c450/</dc:identifier>
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	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:management"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:monitoring"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:self"/>
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<item rdf:about="https://academic.oup.com/edrv/article/39/4/489/4982126?__s=dyb5besisjpaqonnmfuj">
    <title>Metabolic Flexibility as an Adaptation to Energy Resources and Requirements in Health and Disease | Endocrine Reviews | Oxford Academic</title>
    <dc:date>2018-08-30T15:00:19+00:00</dc:date>
    <link>https://academic.oup.com/edrv/article/39/4/489/4982126?__s=dyb5besisjpaqonnmfuj</link>
    <dc:creator>Michael.Massing</dc:creator><description><![CDATA[metabolic flexibility can be placed in the broad context of health and disease and a deeper understanding of its intricacies will significantly affect health care. As a final note, the situation portrayed here does not necessarily reflect that of each individual. Because of the genetic and epigenetic disparity of humans and the enormous varieties in lifestyle, it is not unthinkable that each person fashions a unique way to maintain energy homeostasis. In light of the rapid developments in the field of nutrigenomics and personalized medicine, future research will likely focus on the union between metabolic flexibility and personalized medicine.]]></description>
<dc:subject>metabolic metabolism flexibility evolution genetics epigenetics individual variation endocrine neurotransmitter hormone insulin peer-reviewed research pathophysiology risk genetic factor energy homeostasis</dc:subject>
<dc:source>https://pinboard.in/</dc:source>
<dc:identifier>https://pinboard.in/u:Michael.Massing/b:f4ad2aff8985/</dc:identifier>
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<item rdf:about="https://twitter.com/mattbc/status/1028727980397391873">
    <title>Twitter</title>
    <dc:date>2018-08-12T19:44:35+00:00</dc:date>
    <link>https://twitter.com/mattbc/status/1028727980397391873</link>
    <dc:creator>Michael.Massing</dc:creator><description><![CDATA[People on #insulin have known that Azar was a terrible person for a very long time. #insulin4all ]]></description>
<dc:subject>insulin4all insulin</dc:subject>
<dc:source>https://twitter.com/</dc:source>
<dc:identifier>https://pinboard.in/u:Michael.Massing/b:165656cd12ef/</dc:identifier>
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	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:insulin"/>
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<item rdf:about="http://www.physiology.org/doi/pdf/10.1152/jappl.1998.84.4.1311">
    <title>Diet-induced insulin resistance precedes other aspects of the metabolic syndrome</title>
    <dc:date>2018-01-11T01:44:44+00:00</dc:date>
    <link>http://www.physiology.org/doi/pdf/10.1152/jappl.1998.84.4.1311</link>
    <dc:creator>Michael.Massing</dc:creator><description><![CDATA[full text]]></description>
<dc:subject>insulin resistance metabolic syndrome factor risk etiology diabetes in vivo animal peer-reviewed research diet high fat sugar complex carbohydrate low symptoms cause chicken-and-egg</dc:subject>
<dc:source>https://pinboard.in/</dc:source>
<dc:identifier>https://pinboard.in/u:Michael.Massing/b:58e1556445f6/</dc:identifier>
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<item rdf:about="https://www.google.com/search?newwindow=1&amp;rlz=1C5CHFA_enUS637US637&amp;ei=XsBWWo-oH4jPjwSB9ZrIAw&amp;q=DeFronzo+Ferrannini+insulin+resistance+syndrome&amp;oq=DeFronzo+Ferrannini+insulin+resistance+syndrome&amp;gs_l=psy-ab.3...33546.71840.0.75663.29.28.1.0.0.0.258.3035.5j19j1.25.0....0...1c.1.64.psy-ab..3.4.599...0i7i30k1j0i8i7i30k1j0i13k1.0.5hJrVhQYCKA">
    <title>DeFronzo Ferrannini insulin resistance syndrome - Google Search</title>
    <dc:date>2018-01-11T01:42:20+00:00</dc:date>
    <link>https://www.google.com/search?newwindow=1&amp;rlz=1C5CHFA_enUS637US637&amp;ei=XsBWWo-oH4jPjwSB9ZrIAw&amp;q=DeFronzo+Ferrannini+insulin+resistance+syndrome&amp;oq=DeFronzo+Ferrannini+insulin+resistance+syndrome&amp;gs_l=psy-ab.3...33546.71840.0.75663.29.28.1.0.0.0.258.3035.5j19j1.25.0....0...1c.1.64.psy-ab..3.4.599...0i7i30k1j0i8i7i30k1j0i13k1.0.5hJrVhQYCKA</link>
    <dc:creator>Michael.Massing</dc:creator><dc:subject>insulin resistance metabolic syndrome factor risk etiology diabetes peer-reviewed research diet environment genetics human in vivo genetic symptoms cause factors</dc:subject>
<dc:source>https://pinboard.in/</dc:source>
<dc:identifier>https://pinboard.in/u:Michael.Massing/b:19e1dbed863b/</dc:identifier>
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<item rdf:about="https://www.google.com/search?q=Haffner+insulin+resistance+syndrome&amp;rlz=1C5CHFA_enUS637US637&amp;oq=Haffner+insulin+resistance+syndrome&amp;aqs=chrome..69i57.7732j0j7&amp;sourceid=chrome&amp;ie=UTF-8">
    <title>Haffner insulin resistance syndrome - Google Search</title>
    <dc:date>2018-01-11T01:39:42+00:00</dc:date>
    <link>https://www.google.com/search?q=Haffner+insulin+resistance+syndrome&amp;rlz=1C5CHFA_enUS637US637&amp;oq=Haffner+insulin+resistance+syndrome&amp;aqs=chrome..69i57.7732j0j7&amp;sourceid=chrome&amp;ie=UTF-8</link>
    <dc:creator>Michael.Massing</dc:creator><dc:subject>insulin resistance metabolic syndrome factor risk etiology diabetes peer-reviewed research diet environment genetics human in vivo genetic symptoms cause factors</dc:subject>
<dc:source>https://pinboard.in/</dc:source>
<dc:identifier>https://pinboard.in/u:Michael.Massing/b:36c839dbf611/</dc:identifier>
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<item rdf:about="https://www.ncbi.nlm.nih.gov/m/pubmed/9516198/">
    <title>Diet-induced insulin resistance precedes other aspects of the metabolic syndrome. - PubMed - NCBI</title>
    <dc:date>2018-01-11T01:33:02+00:00</dc:date>
    <link>https://www.ncbi.nlm.nih.gov/m/pubmed/9516198/</link>
    <dc:creator>Michael.Massing</dc:creator><description><![CDATA[This study was designed to examine the effects of a high-fat refined-sugar (HFS) or a low-fat complex-carbohydrate (LFCC) diet on insulin-stimulated skeletal muscle glucose transport, plasma insulin, blood pressure, plasma triglycerides, plasma glycerol, body weight, and body fat in female Fischer rats. Insulin-stimulated glucose transport was significantly reduced in the HFS group at 2 wk, 2 mo, and 2 yr, whereas serum insulin was significantly elevated at all time points. Blood pressure was not significantly elevated in the HFS group until 12 mo, and all HFS animals were hypertensive by 18 mo. Glycerol, triglycerides, and abdominal fat cell size were not significantly different at 2 wk but were significantly elevated in the HFS rats at 2 and 6 mo. Body weight was similar in both groups until 20 wk on the diet, when the HFS rats started to gain more weight. These results demonstrate that insulin resistance and hyperinsulinemia occur before the other manifestations of the metabolic syndrome and that diet, not obesity, is the underlying cause.]]></description>
<dc:subject>insulin resistance metabolic factor risk etiology diabetes in vivo animal peer-reviewed research diet high fat complex carbohydrate low syndrome sugar symptoms cause chicken-and-egg</dc:subject>
<dc:source>https://pinboard.in/</dc:source>
<dc:identifier>https://pinboard.in/u:Michael.Massing/b:c33772922871/</dc:identifier>
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<item rdf:about="http://www.physiology.org/doi/abs/10.1152/jappl.1998.84.4.1311">
    <title>Diet-induced insulin resistance precedes other aspects of the metabolic syndrome | Journal of Applied Physiology</title>
    <dc:date>2018-01-11T01:24:19+00:00</dc:date>
    <link>http://www.physiology.org/doi/abs/10.1152/jappl.1998.84.4.1311</link>
    <dc:creator>Michael.Massing</dc:creator><description><![CDATA[This study was designed to examine the effects of a high-fat refined-sugar (HFS) or a low-fat complex-carbohydrate (LFCC) diet on insulin-stimulated skeletal muscle glucose transport, plasma insulin, blood pressure, plasma triglycerides, plasma glycerol, body weight, and body fat in female Fischer rats. Insulin-stimulated glucose transport was significantly reduced in the HFS group at 2 wk, 2 mo, and 2 yr, whereas serum insulin was significantly elevated at all time points. Blood pressure was not significantly elevated in the HFS group until 12 mo, and all HFS animals were hypertensive by 18 mo. Glycerol, triglycerides, and abdominal fat cell size were not significantly different at 2 wk but were significantly elevated in the HFS rats at 2 and 6 mo. Body weight was similar in both groups until 20 wk on the diet, when the HFS rats started to gain more weight. These results demonstrate that insulin resistance and hyperinsulinemia occur before the other manifestations of the metabolic syndrome and that diet, not obesity, is the underlying cause.]]></description>
<dc:subject>insulin resistance metabolic factor risk etiology diabetes in vivo animal peer-reviewed research diet high fat complex carbohydrate low syndrome sugar symptoms cause chicken-and-egg</dc:subject>
<dc:source>https://pinboard.in/</dc:source>
<dc:identifier>https://pinboard.in/u:Michael.Massing/b:fd70eaa3dbe1/</dc:identifier>
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<item rdf:about="https://www.ncbi.nlm.nih.gov/pubmed/27935520">
    <title>Effect of fructose consumption on insulin sensitivity in nondiabetic subjects: a systematic review and meta-analysis of diet-intervention trials. - PubMed - NCBI</title>
    <dc:date>2017-11-11T19:40:11+00:00</dc:date>
    <link>https://www.ncbi.nlm.nih.gov/pubmed/27935520</link>
    <dc:creator>Michael.Massing</dc:creator><description><![CDATA[Twenty-nine articles that described 46 comparisons in 1005 normal-weight and overweight or obese participants met the eligibility criteria. An energy-matched (isocaloric) exchange of dietary carbohydrates by fructose promoted hepatic insulin resistance (SMD: 0.47; 95% CI: 0.03, 0.91; P = 0.04) but had no effect on fasting plasma insulin concentrations (MD: -0.79 pmol/L; 95% CI: -6.41, 4.84 pmol/L; P = 0.78), the homeostasis model assessment of insulin resistance (HOMA-IR) (MD: 0.13; 95% CI: -0.07, 0.34; P = 0.21), or glucose disposal rates under euglycemic hyperinsulinemic clamp conditions (SMD: 0.00; 95% CI: 20.41, 0.41; P = 1.00). Hypercaloric fructose (∼25% excess of energy compared with that of the weight-maintenance control diet) raised fasting plasma insulin concentrations (MD: 3.38 pmol/L; 95% CI: 0.03, 6.73 pmol/L; P < 0.05) and induced hepatic insulin resistance (SMD: 0.77; 95% CI: 0.28, 1.26; P < 0.01) without affecting the HOMA-IR (MD: 0.18; 95% CI: -0.02, 0.39; P = 0.08) or glucose disposal rates (SMD: 0.10; 95% CI: -0.21, 0.40; P = 0.54). Results may have been limited by the low quality, small sample size, and short duration (mostly <60 d) of included trials.
CONCLUSIONS:
Short-term fructose consumption, in isocaloric exchange or in hypercaloric supplementation, promotes the development of hepatic insulin resistance in nondiabetic adults without affecting peripheral or muscle insulin sensitivity. Larger and longer-term studies are needed to assess whether real-world fructose consumption has adverse effects on insulin sensitivity and long-term outcomes.]]></description>
<dc:subject>fructose normoglycemia hyperglycemia insulin resistance hepatic liver peer-reviewed research overview review in vivo human clinical trial</dc:subject>
<dc:source>https://pinboard.in/</dc:source>
<dc:identifier>https://pinboard.in/u:Michael.Massing/b:c804dd3233bb/</dc:identifier>
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	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:insulin"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:resistance"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:hepatic"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:liver"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:peer-reviewed"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:research"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:overview"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:review"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:in"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:vivo"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:human"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:clinical"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:trial"/>
</rdf:Bag></taxo:topics>
</item>
<item rdf:about="https://www.ncbi.nlm.nih.gov/pubmed/28146065">
    <title>Effect on Insulin, Glucose and Lipids in Overweight/Obese Australian Adults of 12 Months Consumption of Two Different Fibre Supplements in a Random... - PubMed - NCBI</title>
    <dc:date>2017-11-10T03:15:53+00:00</dc:date>
    <link>https://www.ncbi.nlm.nih.gov/pubmed/28146065</link>
    <dc:creator>Michael.Massing</dc:creator><description><![CDATA[Higher fibre intakes are associated with risk reduction for chronic diseases. This study investigated the effects of supplementation with PolyGlycopleX® (PGX), a complexed polysaccharide, on insulin, glucose and lipids in overweight and obese individuals. In this double-blind 12 months study, participants were randomised into three groups: control (rice flour); PGX or psyllium (PSY). Participants followed their usual lifestyle and diet but consumed 5 g of their supplement before meals. Insulin was significantly lower in the PGX and PSY groups compared to control at 3 and 6 months and in the PSY group compared to control at 12 months. Serum glucose was significantly lower in the PGX group at 3 months compared to control. Total cholesterol was significantly lower in the PGX and PSY groups compared to control at 3 and 6 months. High density lipoprotein (HDL) cholesterol was significantly increased in the PGX group compared to control at 12 months. low density lipoprotein (LDL) cholesterol was significantly lower in the PGX group at 3 and 6 months compared to control and in the PSY group at 3 months compared to control. A simple strategy of fibre supplementation may offer an effective solution to glucose, insulin and lipid management without the need for other nutrient modification.]]></description>
<dc:subject>fiber blood glucose lipids management risk diet self care peer-reviewed research supplements cholesterol harm reduction insulin psyllium in vivo human clinical trial</dc:subject>
<dc:source>https://pinboard.in/</dc:source>
<dc:identifier>https://pinboard.in/u:Michael.Massing/b:dba9f3929841/</dc:identifier>
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	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:blood"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:glucose"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:lipids"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:management"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:risk"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:diet"/>
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	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:research"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:supplements"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:cholesterol"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:harm"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:reduction"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:insulin"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:psyllium"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:in"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:vivo"/>
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	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:trial"/>
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</item>
<item rdf:about="https://www.drugs.com/npp/nutmeg.html">
    <title>Nutmeg Uses, Benefits &amp; Dosage - Drugs.com Herbal Database</title>
    <dc:date>2017-11-01T23:07:46+00:00</dc:date>
    <link>https://www.drugs.com/npp/nutmeg.html</link>
    <dc:creator>Michael.Massing</dc:creator><description><![CDATA[Diabetes
Nutmeg has shown insulin-like activity in vitro. 38 Inhibitory effects on protein tyrosine phosphate 1B, involved in insulin cellular signaling, have been demonstrated. 39

Animal data
Serum glucose and lipid profiles improved in mice when mace lignan was administered. 40 In rabbits given an ethanolic extract of nutmeg, total and low-density lipoprotein (LDL) cholesterol and triglyceride were reduced; however, high-density lipoprotein levels were not changed. 41....

Other effects
Screening and in vitro experiments in nutmeg components demonstrated ultraviolet-protectant effects and inhibition of melanin biosynthesis. 65 , 66 Anti-inflammatory and analgesic activities of nutmeg have been recorded in mice, as well as antithrombotic activity. 67 , 68 Other studies document hepatoprotective properties, 69 effects on osteoblast differentiation, 70 and reduced acidity and volume of gastric secretion. 71 , 72]]></description>
<dc:subject>nutmeg mace diabetes insulin cholesterol blood glucose lipids peer-reviewed research in vitro vivo animal triglyceride</dc:subject>
<dc:source>https://pinboard.in/</dc:source>
<dc:identifier>https://pinboard.in/u:Michael.Massing/b:549675c7f22c/</dc:identifier>
<taxo:topics><rdf:Bag>	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:nutmeg"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:mace"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:diabetes"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:insulin"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:cholesterol"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:blood"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:glucose"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:lipids"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:peer-reviewed"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:research"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:in"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:vitro"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:vivo"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:animal"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:triglyceride"/>
</rdf:Bag></taxo:topics>
</item>
<item rdf:about="https://www.ncbi.nlm.nih.gov/pubmed/17992181">
    <title>Dietary carbohydrate: relationship to cardiovascular disease and disorders of carbohydrate metabolism. - PubMed - NCBI</title>
    <dc:date>2017-09-18T00:25:41+00:00</dc:date>
    <link>https://www.ncbi.nlm.nih.gov/pubmed/17992181</link>
    <dc:creator>Michael.Massing</dc:creator><description><![CDATA[The nature of carbohydrate is of considerable importance when recommending diets intended to reduce the risk of type II diabetes and cardiovascular disease and in the treatment of patients who already have established diseases. Intact fruits, vegetables, legumes and wholegrains are the most appropriate sources of carbohydrate. Most are rich in nonstarch polysaccharides (NSPs) (dietary fibre) and other potentially cardioprotective components. Many of these foods, especially those that are high in dietary fibre, will reduce total and low-density lipoprotein cholesterol and help to improve glycaemic control in those with diabetes. There is no good long-term evidence of benefit when NSPs or other components of wholegrains, fruits, vegetables and legumes are added to functional and manufactured foods. Frequent consumption of low glycaemic index foods has been reported to confer similar benefits, but it is not clear whether such benefits are independent of the dietary fibre content of these foods or the fact that low glycaemic index foods tend to have intact plant cell walls. Furthermore, it is uncertain whether functional and manufactured foods with a low glycaemic index confer the same long-term benefits as low glycaemic index plant-based foods. A wide range of carbohydrate intake is acceptable, provided the nature of carbohydrate is appropriate. Failure to emphasize the need for carbohydrate to be derived principally from wholegrain cereals, fruits, vegetables and legumes may result in increased lipoprotein-mediated risk of cardiovascular disease, especially in overweight and obese individuals who are insulin resistant.]]></description>
<dc:subject>risk benefit industrialized processed lipids vegetables cardiovascular blood whole grain fruit carbohydrate legumes glucose peer-reviewed research response insulin fiber comparison overview correlation type 2 T2D effect diet epidemiology etiology self care management long term short soluble insoluble metabolism prevention intact integrity diabetes cause factor factors</dc:subject>
<dc:source>https://pinboard.in/</dc:source>
<dc:identifier>https://pinboard.in/u:Michael.Massing/b:617bdbd5d015/</dc:identifier>
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	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:lipids"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:vegetables"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:cardiovascular"/>
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	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:whole"/>
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	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:carbohydrate"/>
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	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:epidemiology"/>
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	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:term"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:short"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:soluble"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:insoluble"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:metabolism"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:prevention"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:intact"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:integrity"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:diabetes"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:cause"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:factor"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:factors"/>
</rdf:Bag></taxo:topics>
</item>
<item rdf:about="https://www.ncbi.nlm.nih.gov/pubmed/15162131">
    <title>Cereal grains, legumes and diabetes. - PubMed - NCBI</title>
    <dc:date>2017-09-17T18:39:06+00:00</dc:date>
    <link>https://www.ncbi.nlm.nih.gov/pubmed/15162131</link>
    <dc:creator>Michael.Massing</dc:creator><description><![CDATA[Epidemiological studies strongly support the suggestion that high intakes of whole grain foods protect against the development of type II diabetes mellitus (T2DM). People who consume approximately 3 servings per day of whole grain foods are less likely to develop T2DM than low consumers (<3 servings per week) with a risk reduction in the order of 20-30%. The role of legumes in the prevention of diabetes is less clear, possibly because of the relatively low intake of leguminous foods in the populations studied. However, legumes share several qualities with whole grains of potential benefit to glycaemic control including slow release carbohydrate and a high fibre content. A substantial increase in dietary intake of legumes as replacement food for more rapidly digested carbohydrate might therefore be expected to improve glycaemic control and thus reduce incident diabetes. This is consistent with the results of dietary intervention studies that have found improvements in glycaemic control after increasing the dietary intake of whole grain foods, legumes, vegetables and fruit. The benefit has been attributed to an increase in soluble fibre intake. However, prospective studies have found that soluble fibre intake is not associated with a lower incidence of T2DM. On the contrary, it is cereal fibre that is largely insoluble that is associated with a reduced risk of developing T2DM. Despite this, the addition of wheat bran to the diets of diabetic people has not improved indicators of glycaemic control. These apparently contradictory findings might be explained by metabolic studies that have indicated improvement in glucose handling is associated with the intact structure of food. For both grains and legumes, fine grinding disrupts cell structures and renders starch more readily accessible for digestion. The extent to which the intact structure of grains and legumes or the composition of foods in terms of dietary fibre and other constituents contribute to the beneficial effect remains to be quantified. Other mechanisms to help explain improvements in glycaemic control when consuming whole grains and legumes relate to cooking, type of starch, satiety and nutrient retention. Thus, there is strong evidence to suggest that eating a variety of whole grain foods and legumes is beneficial in the prevention and management of diabetes. This is compatible with advice from around the world that recommends consumption of a wide range of carbohydrate foods from cereals, vegetables, legumes and fruits both for the general population and for people with diabetes.]]></description>
<dc:subject>breakfast blood whole grain lsgumes glucose peer-reviewed research response insulin fiber comparison review overview correlation type 2 T2D effect diet epidemiology etiology self care management long term short soluble insoluble metabolism prevention diabetes cause factor risk factors</dc:subject>
<dc:source>https://pinboard.in/</dc:source>
<dc:identifier>https://pinboard.in/u:Michael.Massing/b:9ae2b227f972/</dc:identifier>
<taxo:topics><rdf:Bag>	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:breakfast"/>
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	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:whole"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:grain"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:lsgumes"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:glucose"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:peer-reviewed"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:research"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:response"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:insulin"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:fiber"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:comparison"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:review"/>
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	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:effect"/>
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	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:epidemiology"/>
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	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:soluble"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:insoluble"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:metabolism"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:prevention"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:diabetes"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:cause"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:factor"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:risk"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:factors"/>
</rdf:Bag></taxo:topics>
</item>
<item rdf:about="https://www.ncbi.nlm.nih.gov/pubmed/27184288">
    <title>The Effects of Breakfast Consumption and Composition on Metabolic Wellness with a Focus on Carbohydrate Metabolism. - PubMed - NCBI</title>
    <dc:date>2017-09-17T16:59:23+00:00</dc:date>
    <link>https://www.ncbi.nlm.nih.gov/pubmed/27184288</link>
    <dc:creator>Michael.Massing</dc:creator><description><![CDATA[Findings from epidemiologic studies indicate that there are associations between breakfast consumption and a lower risk of type 2 diabetes mellitus (T2DM) and metabolic syndrome, prompting interest in the influence of breakfast on carbohydrate metabolism and indicators of T2DM risk. The objective of this review was to summarize the available evidence from randomized controlled trials assessing the impact of breakfast on variables related to carbohydrate metabolism and metabolic wellness. Consuming compared with skipping breakfast appeared to improve glucose and insulin responses throughout the day. Breakfast composition may also be important. Dietary patterns high in rapidly available carbohydrate were associated with elevated T2DM risk. Therefore, partial replacement of rapidly available carbohydrate with other dietary components, such as whole grains and cereal fibers, proteins, and unsaturated fatty acids (UFAs), at breakfast may be a useful strategy for producing favorable metabolic outcomes. Consumption of fermentable and viscous dietary fibers at breakfast lowers glycemia and insulinemia. Fermentable fibers likely act through enhancing insulin sensitivity later in the day, and viscous fibers have an acute effect to slow the rate of carbohydrate absorption. Partially substituting protein for rapidly available carbohydrate enhances satiety and diet-induced thermogenesis, and also favorably affects lipoprotein lipids and blood pressure. Partially substituting UFA for carbohydrate has been associated with improved insulin sensitivity, lipoprotein lipids, and blood pressure. Overall, the available evidence suggests that consuming breakfast foods high in whole grains and cereal fiber, while limiting rapidly available carbohydrate, is a promising strategy for metabolic health promotion.]]></description>
<dc:subject>breakfast blood whole grain unsaturated fatty acids lipids UFA glucose peer-reviewed research response insulin fiber high low glycemic index correlation type 2 T2D effect diet self care management long term short viscous soluble fermentable insoluble metabolism carbohydate protein risk reduction harm prevention diabetes metabolic syndrome</dc:subject>
<dc:source>https://pinboard.in/</dc:source>
<dc:identifier>https://pinboard.in/u:Michael.Massing/b:46c7f21c663c/</dc:identifier>
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	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:response"/>
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	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:short"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:viscous"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:soluble"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:fermentable"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:insoluble"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:metabolism"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:carbohydate"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:protein"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:risk"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:reduction"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:harm"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:prevention"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:diabetes"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:metabolic"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:syndrome"/>
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</item>
<item rdf:about="https://www.ncbi.nlm.nih.gov/pubmed/28753929">
    <title>Whole Grain Intake and Glycaemic Control in Healthy Subjects: A Systematic Review and Meta-Analysis of Randomized Controlled Trials. - PubMed - NCBI</title>
    <dc:date>2017-09-17T11:34:12+00:00</dc:date>
    <link>https://www.ncbi.nlm.nih.gov/pubmed/28753929</link>
    <dc:creator>Michael.Massing</dc:creator><description><![CDATA[There is growing evidence from both observational and intervention studies that Whole Grain (WG) cereals exert beneficial effects on human health, especially on the metabolic profile. The aim of this study was to perform a meta-analysis of randomised controlled trials (RCT) to assess the acute and medium/long-term effect of WG foods on glycaemic control and insulin sensitivity in healthy individuals.
METHODS:
A search for all the published RCT on the effect of WG food intake on glycaemic and insulin response was performed up to December 2016. Effect size consisted of mean difference (MD) and 95% CI between the outcomes of intervention and the control groups using the generic inverse-variance random effects model.
RESULTS:
The meta-analysis of the 14 studies testing the acute effects of WG foods showed significant reductions of the post-prandial values of the glucose iAUC (0-120 min) by -29.71 mmol min/L (95% CI: -43.57, -15.85 mmol min/L), the insulin iAUC (0-120 min) by -2.01 nmol min/L (95% CI: -2.88, -1.14 nmol min/L), and the maximal glucose and insulin response. In 16 medium- and long-term RCTs, effects of WG foods on fasting glucose and insulin and homeostatic model assessment-insulin resistance values were not significant.
CONCLUSIONS:
The consumption of WG foods is able to improve acutely the postprandial glucose and insulin homeostasis compared to similar refined foods in healthy subjects. Further research is needed to better understand the long-term effects and the biological mechanisms.]]></description>
<dc:subject>blood whole rye glucose metabolism peer-reviewed research response insulin fiber correlation review meta-analysis diet self care management metabolic profile</dc:subject>
<dc:source>https://pinboard.in/</dc:source>
<dc:identifier>https://pinboard.in/u:Michael.Massing/b:43459fdf8959/</dc:identifier>
<taxo:topics><rdf:Bag>	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:blood"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:whole"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:rye"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:glucose"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:metabolism"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:peer-reviewed"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:research"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:response"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:insulin"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:fiber"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:correlation"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:review"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:meta-analysis"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:diet"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:self"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:care"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:management"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:metabolic"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:profile"/>
</rdf:Bag></taxo:topics>
</item>
<item rdf:about="https://www.ncbi.nlm.nih.gov/pubmed/28431559">
    <title>Effects of whole grain rye, with and without resistant starch type 2 supplementation, on glucose tolerance, gut hormones, inflammation and appetite... - PubMed - NCBI</title>
    <dc:date>2017-09-17T10:55:19+00:00</dc:date>
    <link>https://www.ncbi.nlm.nih.gov/pubmed/28431559</link>
    <dc:creator>Michael.Massing</dc:creator><description><![CDATA[Whole grain has shown potential to lower the risk of obesity, cardiovascular disease and type 2 diabetes. One possible mechanism behind the benefits of whole grain is the gut fermentation of dietary fiber (DF), e.g. non-starch polysaccharides and resistant starch (RS), in whole grain. The purpose of the study is to investigate the effect of whole grain rye-based products on glucose- and appetite regulation.
METHOD:
Twenty-one healthy subjects were provided four rye-based evening test meals in a crossover overnight study design. The test evening meals consisted of either whole grain rye flour bread (RFB) or a 1:1 ratio of whole grain rye flour and rye kernels bread (RFB/RKB), with or without added resistant starch (+RS). White wheat flour bread (WWB) was used as reference evening meal. Blood glucose, insulin, PYY, FFA, IL-6 as well as breath H2 and subjective rating of appetite were measured the following morning at fasting and repeatedly up to 3.5 h after a standardized breakfast consisting of WWB. Ad libitum energy intake was determined at lunch, 14.5 h after evening test and reference meals, respectively.
RESULTS:
The evening meal with RFB/RKB + RS decreased postprandial glucose- and insulin responses (iAUC) (P < 0.05) and increased the gut hormone PYY in plasma the following morning 0-120 min after the standardized breakfast, compared to WWB (P = 0.01). Moreover, RFB increased subjective satiety and decreased desire to eat, and both RFB and RFB/RKB decreased feeling of hunger (AUC 0-210 min). All rye-based evening meals decreased or tended to decrease fasting FFA (P < 0.05, RFB/RKB: P = 0.057) and increased breath hydrogen concentration (0-120 min, P < 0.001). No effects were noted on energy intake at lunch or inflammatory marker IL-6 (0 + 180 min) after the rye-based evening meals, compared to WWB.
CONCLUSION:
Whole grain rye bread has the potential to improve cardiometabolic variables in an 11-14.5 h perspective in healthy humans. The combination RFB/RKB + RS positively affected biomarkers of glucose- and appetite regulation in a semi-acute perspective. Meanwhile, RFB and RFB/RKB improved subjective appetite ratings. The effects probably emanate from gut fermentation events.]]></description>
<dc:subject>blood whole grain rye glucose metabolism peer-reviewed research response insulin fiber high low glycemic index correlation comparison type 2 T2D second-meal phenomenon effect diet self care management</dc:subject>
<dc:source>https://pinboard.in/</dc:source>
<dc:identifier>https://pinboard.in/u:Michael.Massing/b:f897a27ce69c/</dc:identifier>
<taxo:topics><rdf:Bag>	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:blood"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:whole"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:grain"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:rye"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:glucose"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:metabolism"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:peer-reviewed"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:research"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:response"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:insulin"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:fiber"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:high"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:low"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:glycemic"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:index"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:correlation"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:comparison"/>
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	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:2"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:T2D"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:second-meal"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:phenomenon"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:effect"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:diet"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:self"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:care"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:management"/>
</rdf:Bag></taxo:topics>
</item>
<item rdf:about="https://www.ncbi.nlm.nih.gov/pubmed/18326603">
    <title>Effect of cereal test breakfasts differing in glycemic index and content of indigestible carbohydrates on daylong glucose tolerance in healthy subj... - PubMed - NCBI</title>
    <dc:date>2017-09-17T10:49:46+00:00</dc:date>
    <link>https://www.ncbi.nlm.nih.gov/pubmed/18326603</link>
    <dc:creator>Michael.Massing</dc:creator><description><![CDATA[Frequent hyperglycemic episodes are increasingly being associated with an increased risk of type 2 diabetes and cardiovascular disease.
OBJECTIVE:
We studied the extent to which acute glycemia and glycemia after subsequent meals can be modulated by the characteristics of cereal foods, such as glycemic index (GI) and content of indigestible carbohydrates.
DESIGN:
Twelve healthy subjects consumed test meals in a random order. In series 1, the test meals were consumed at breakfast, and postprandial blood glucose incremental areas under the curve (IAUCs) were calculated after the test breakfast, standardized lunch, and standardized dinner. In series 2, the subjects consumed test evening meals and IAUCs were calculated after a subsequent standardized breakfast. Breath hydrogen was measured as an indicator of colonic fermentation.
RESULTS:
Barley or rye kernel breakfasts lowered the blood glucose IAUC (0-120 min) at breakfast, at a subsequent lunch, and the cumulative IAUCs (breakfast+lunch+dinner) when compared with white-wheat bread (P < 0.05). The lunch blood glucose IAUCs were positively correlated with breakfast IAUCs (r = 0.30, P < 0.05). Breath hydrogen excretion was negatively correlated with blood glucose IAUCs after lunch (r = -0.33, P < 0.05) and dinner (r = -0.22, P < 0.05). A barley kernel evening meal resulted in lower IAUCs (P < 0.05) and higher breath hydrogen (P < 0.001) after a subsequent breakfast compared with white-wheat bread.
CONCLUSIONS:
Glucose tolerance at subsequent meals can be notably improved during the course of a whole day or overnight by choosing specific low-GI, whole-grain cereal products. A low GI may be sufficient to achieve a second-meal effect from breakfast to lunch. A specific indigestible carbohydrate mixture appears to be required to show benefits on glucose tolerance in a longer time frame (9.5 h), most likely mediated through colonic fermentation.]]></description>
<dc:subject>breakfast blood barley rye glucose metabolism peer-reviewed research response insulin fiber high low glycemic index correlation comparison type 2 T2D second-meal phenomenon effect diet self care management</dc:subject>
<dc:source>https://pinboard.in/</dc:source>
<dc:identifier>https://pinboard.in/u:Michael.Massing/b:5d58e0052ae4/</dc:identifier>
<taxo:topics><rdf:Bag>	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:breakfast"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:blood"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:barley"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:rye"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:glucose"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:metabolism"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:peer-reviewed"/>
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	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:response"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:insulin"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:fiber"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:high"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:low"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:glycemic"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:index"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:correlation"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:comparison"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:type"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:2"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:T2D"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:second-meal"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:phenomenon"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:effect"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:diet"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:self"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:care"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:management"/>
</rdf:Bag></taxo:topics>
</item>
<item rdf:about="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5372885/">
    <title>Matching Meals to Body Clocks—Impact on Weight and Glucose Metabolism</title>
    <dc:date>2017-09-17T03:24:29+00:00</dc:date>
    <link>https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5372885/</link>
    <dc:creator>Michael.Massing</dc:creator><description><![CDATA[The prevalence of type 2 diabetes continues to rise worldwide and is reaching pandemic proportions. The notion that this is due to obesity, resulting from excessive energy consumption and reduced physical activity, is overly simplistic. Circadian de-synchrony, which occurs when physiological processes are at odds with timing imposed by internal clocks, also promotes obesity and impairs glucose tolerance in mouse models, and is a feature of modern human lifestyles. The purpose of this review is to highlight what is known about glucose metabolism in animal and human models of circadian de-synchrony and examine the evidence as to whether shifts in meal timing contribute to impairments in glucose metabolism, gut hormone secretion and the risk of type 2 diabetes. Lastly, we examine whether restricting food intake to discrete time periods, will prevent or reverse abnormalities in glucose metabolism with the view to improving metabolic health in shift workers and in those more generally at risk of chronic diseases such as type 2 diabetes and cardiovascular disease....

There is a general belief that consumption of more energy throughout the day is preferable to evening consumption. Few studies have examined this prospectively in humans, or for any length of time. Nonetheless, time restricted feeding has shown promise as a tool to mitigate the metabolic sequelae of diet induced obesity in mouse models. Good quality evidence for TRF as a dietary approach to improve glucose control in humans is lacking. Controlled trials are necessary, and must determine if there is adaptation in the approach, whilst keeping in mind the practicality of translating this approach into the community.]]></description>
<dc:subject>opblood protein glucose metabolism peer-reviewed research response insulin meal timing in vivo animal correlation comparison type 2 T2D circadian rhythms social factor environmental etiology risk shift work obesity body fat diabetes cause factors</dc:subject>
<dc:source>https://pinboard.in/</dc:source>
<dc:identifier>https://pinboard.in/u:Michael.Massing/b:654e8030dc23/</dc:identifier>
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	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:glucose"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:metabolism"/>
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	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:meal"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:timing"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:in"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:vivo"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:animal"/>
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	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:T2D"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:circadian"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:rhythms"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:social"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:factor"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:environmental"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:etiology"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:risk"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:shift"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:work"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:obesity"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:body"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:fat"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:diabetes"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:cause"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:factors"/>
</rdf:Bag></taxo:topics>
</item>
<item rdf:about="https://www.ncbi.nlm.nih.gov/pubmed/18175767">
    <title>Role of glycemic index and glycemic load in the healthy state, in prediabetes, and in diabetes. - PubMed - NCBI</title>
    <dc:date>2017-09-17T03:10:48+00:00</dc:date>
    <link>https://www.ncbi.nlm.nih.gov/pubmed/18175767</link>
    <dc:creator>Michael.Massing</dc:creator><description><![CDATA[The choice of carbohydrate-rich foods in the habitual diet should take into account not only their chemical composition but also their ability to influence postprandial glycemia (glycemic index). _Fiber-rich foods generally have a low glycemic index (GI), although not all foods with a low GI necessarily have high fiber content._ Several beneficial effects of low-GI, high-fiber diets have been shown, including lower postprandial glucose and insulin responses, an improved lipid profile, and, possibly, reduced insulin resistance. In nondiabetic persons, suggestive evidence is available from epidemiologic studies that a diet based on carbohydrate-rich foods with a low-GI, high-fiber content may protect against diabetes or cardiovascular disease. However, no intervention studies have so far evaluated the potential of low-GI, high-fiber diets to reduce the risk of diabetes, although in studies aimed at diabetes prevention by lifestyle modifications, an increase in fiber consumption was often part of the intervention. In relation to prevention of cardiovascular disease, intervention studies evaluating the effect of a low-GI diet on clinical events are not available; moreover, the results of the few available intervention studies evaluating the effects of GI on the cardiovascular disease risk factor profile are not always concordant. The best evidence of the clinical usefulness of GI is available in diabetic patients in whom low-GI foods have consistently shown beneficial effects on blood glucose control in both the short-term and the long-term. In these patients, low-GI foods are suitable as carbohydrate-rich choices, provided other attributes of the foods are appropriate.]]></description>
<dc:subject>breakfast blood protein glucose metabolism peer-reviewed research response insulin fiber high low glycemic index correlation comparison prediabetes type 2 T2D load</dc:subject>
<dc:source>https://pinboard.in/</dc:source>
<dc:identifier>https://pinboard.in/u:Michael.Massing/b:e49f8a280a69/</dc:identifier>
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	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:protein"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:glucose"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:metabolism"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:peer-reviewed"/>
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	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:insulin"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:fiber"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:high"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:low"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:glycemic"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:index"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:correlation"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:comparison"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:prediabetes"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:type"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:2"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:T2D"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:load"/>
</rdf:Bag></taxo:topics>
</item>
<item rdf:about="https://www.ncbi.nlm.nih.gov/pubmed/25833777">
    <title>A high-glycemic index, low-fiber breakfast affects the postprandial plasma glucose, insulin, and ghrelin responses of patients with type 2 diabetes... - PubMed - NCBI</title>
    <dc:date>2017-09-17T03:06:02+00:00</dc:date>
    <link>https://www.ncbi.nlm.nih.gov/pubmed/25833777</link>
    <dc:creator>Michael.Massing</dc:creator><description><![CDATA[The area under the curve (AUC) [mean (95% CI); P for LSD tests] for plasma glucose (mmol/L × min) was higher after patients consumed the HGI-LF breakfast [9.62 (8.39, 10.84)] than after the LGI-HF breakfast [8.95 (7.71, 10.18)] (P ≤ 0.05). Insulin AUC (μIU/mL × min) after patients consumed the HGI-LF meal [65.72 (38.24, 93.19)] was higher than after the HGI-HF meal [57.24 (32.44, 82.04)] (P ≤ 0.05). The other observed difference was higher insulin AUC after the consumption of the LGI-LF breakfast [61.54 (36.61, 86.48)] compared with the AUC after the LGI-HF breakfast [54.16 (31.43, 76.88)] (P ≤ 0.05). Plasma ghrelin decreased in comparison with baseline only after patients consumed the LGI-HF and LGI-LF breakfasts (P ≤ 0.05). Subjective satiety did not differ between breakfasts.
CONCLUSIONS:
Plasma glucose, insulin, and ghrelin responses were least favorable when patients with type 2 diabetes consumed a breakfast with a high GI and low fiber, which suggests that reducing the GI or increasing the fiber content or both of breakfasts may be a useful strategy to improve the postprandial metabolic profile of these patients.]]></description>
<dc:subject>breakfast blood protein glucose metabolism peer-reviewed research response insulin fiber high low glycemic index ghrelin correlation comparison</dc:subject>
<dc:source>https://pinboard.in/</dc:source>
<dc:identifier>https://pinboard.in/u:Michael.Massing/b:78fa16a0a7ac/</dc:identifier>
<taxo:topics><rdf:Bag>	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:breakfast"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:blood"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:protein"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:glucose"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:metabolism"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:peer-reviewed"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:research"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:response"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:insulin"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:fiber"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:high"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:low"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:glycemic"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:index"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:ghrelin"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:correlation"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:comparison"/>
</rdf:Bag></taxo:topics>
</item>
<item rdf:about="https://www.ncbi.nlm.nih.gov/pubmed/16670695">
    <title>Effects of breakfast meal composition on second meal metabolic responses in adults with Type 2 diabetes mellitus. - PubMed - NCBI</title>
    <dc:date>2017-09-17T02:59:42+00:00</dc:date>
    <link>https://www.ncbi.nlm.nih.gov/pubmed/16670695</link>
    <dc:creator>Michael.Massing</dc:creator><description><![CDATA[Two different breakfast meals were administered during the intervention: (A) a high glycemic load breakfast meal consisting of farina (kJ 1833; carbohydrate (CHO) 78 g and psylium soluble fiber 0 g), (B) a low-glycemic load breakfast meal consisting of a fiber-loop cereal (kJ 1515; CHO 62 g and psyllium soluble fiber 6.6 g). A standardized lunch was provided approximately 4 h after breakfast. Blood plasma concentrations and area under the curve (AUC) values for glucose, insulin and FFA were measured in response to the breakfast and mid-day lunch. Statistical analyses were performed using SAS software (8.02). Comparisons between diets were based on adjusted Bonferroni t-tests.
RESULTS:
In post-breakfast analyses, Breakfast B had significantly lower area under the curve (AUC) values for plasma glucose and insulin compared to Breakfast A (P<0.05) (95% confidence level). The AUC values for FFA were higher for Breakfast B than for Breakfast A (P<0.05) (95% confidence level). Post-lunch analyses indicated similar glucose responses for the two breakfast types. Insulin AUC values for Breakfasts B were significantly lower than Breakfast A (P<0.05) (95% confidence level). The AUC values for FFA were unaffected by breakfast type.
CONCLUSIONS:
These data indicate that ingesting a low-glycemic load meal containing psyllium soluble fiber at breakfast significantly improves the breakfast postprandial glycemic, insulinemic and FFA responses in adults with Type 2 DM. These data revealed no residual postprandial effect of the psyllium soluble fiber breakfast meal beyond the second meal consumed. Thus, there was no evidence of an improvement postprandially in the glycemic, insulinemic and FFA responses after the consumption of the lunch meal.]]></description>
<dc:subject>breakfast blood lunch protein glucose metabolism second-meal phenomenon peer-reviewed research response insulin fiber high low glycemic index</dc:subject>
<dc:source>https://pinboard.in/</dc:source>
<dc:identifier>https://pinboard.in/u:Michael.Massing/b:5727f15b31a7/</dc:identifier>
<taxo:topics><rdf:Bag>	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:breakfast"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:blood"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:lunch"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:protein"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:glucose"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:metabolism"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:second-meal"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:phenomenon"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:peer-reviewed"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:research"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:response"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:insulin"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:fiber"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:high"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:low"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:glycemic"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:index"/>
</rdf:Bag></taxo:topics>
</item>
<item rdf:about="https://www.ncbi.nlm.nih.gov/pubmed/25733459">
    <title>A high-protein breakfast induces greater insulin and glucose-dependent insulinotropic peptide responses to a subsequent lunch meal in individuals w... - PubMed - NCBI</title>
    <dc:date>2017-09-17T02:48:53+00:00</dc:date>
    <link>https://www.ncbi.nlm.nih.gov/pubmed/25733459</link>
    <dc:creator>Michael.Massing</dc:creator><description><![CDATA[BACKGROUND:
The previous meal modulates the postprandial glycemic responses to a subsequent meal; this is termed the second-meal phenomenon.
OBJECTIVE:
This study examined the effects of high-protein vs. high-carbohydrate breakfast meals on the metabolic and incretin responses after the breakfast and lunch meals.
METHODS:
Twelve type 2 diabetic men and women [age: 21-55 y; body mass index (BMI): 30-40 kg/m(2)] completed two 7-d breakfast conditions consisting of 500-kcal breakfast meals as protein (35% protein/45% carbohydrate) or carbohydrate (15% protein/65% carbohydrate). On day 7, subjects completed an 8-h testing day. After an overnight fast, the subjects consumed their respective breakfast followed by a standard 500-kcal high-carbohydrate lunch meal 4 h later. Blood samples were taken throughout the day for assessment of 4-h postbreakfast and 4-h postlunch total area under the curve (AUC) for glucose, insulin, C-peptide, glucagon, glucose-dependent insulinotropic peptide (GIP), and glucagon-like peptide 1 (GLP-1).
RESULTS:
Postbreakfast glucose and GIP AUCs were lower after the protein (17%) vs. after the carbohydrate (23%) condition (P < 0.05), whereas postbreakfast insulin, C-peptide, glucagon, and GLP-1 AUCs were not different between conditions. A protein-rich breakfast may reduce the consequences of hyperglycemia in this population. Postlunch insulin, C-peptide, and GIP AUCs were greater after the protein condition vs. after the carbohydrate condition (second-meal phenomenon; all, P < 0.05), but postlunch AUCs were not different between conditions. The overall glucose, glucagon, and GLP-1 responses (e.g., 8 h) were greater after the protein condition vs. after the carbohydrate condition (all, P < 0.05).
CONCLUSIONS:
In type 2 diabetic individuals, compared with a high-carbohydrate breakfast, the consumption of a high-protein breakfast meal attenuates the postprandial glucose response and does not magnify the response to the second meal. Insulin, C-peptide, and GIP concentrations demonstrate the second-meal phenomenon and most likely aid in keeping the glucose concentrations controlled in response to the subsequent meal.]]></description>
<dc:subject>breakfast blood lunch protein glucose metabolism second-meal phenomenon peer-reviewed research response insulin</dc:subject>
<dc:source>https://pinboard.in/</dc:source>
<dc:identifier>https://pinboard.in/u:Michael.Massing/b:402173cf2791/</dc:identifier>
<taxo:topics><rdf:Bag>	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:breakfast"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:blood"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:lunch"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:protein"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:glucose"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:metabolism"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:second-meal"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:phenomenon"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:peer-reviewed"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:research"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:response"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:insulin"/>
</rdf:Bag></taxo:topics>
</item>
<item rdf:about="https://www.ncbi.nlm.nih.gov/pubmed/28368334">
    <title>Effects of Higher Dietary Protein and Fiber Intakes at Breakfast on Postprandial Glucose, Insulin, and 24-h Interstitial Glucose in Overweight Adults. - PubMed - NCBI</title>
    <dc:date>2017-09-15T21:38:40+00:00</dc:date>
    <link>https://www.ncbi.nlm.nih.gov/pubmed/28368334</link>
    <dc:creator>Michael.Massing</dc:creator><description><![CDATA[The HPHF treatment did not affect postprandial glucose and insulin responses or 24-h glucose total area under the curve (AUC). Higher fiber intake reduced 240-min insulin AUC. Doubling the amount of protein from 12.5 g to 25 g/meal and quadrupling fiber from 2 to 8 g/meal at breakfast was not an effective strategy for modulating insulin-mediated glucose responses in these young, overweight[, nondiabetic] adults.]]></description>
<dc:subject>breakfast fiber protein glucose metabolism blood interstitial insulin response postprandial peak excursion spike peer-reviewed research</dc:subject>
<dc:source>https://pinboard.in/</dc:source>
<dc:identifier>https://pinboard.in/u:Michael.Massing/b:09f6f288202c/</dc:identifier>
<taxo:topics><rdf:Bag>	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:breakfast"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:fiber"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:protein"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:glucose"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:metabolism"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:blood"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:interstitial"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:insulin"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:response"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:postprandial"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:peak"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:excursion"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:spike"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:peer-reviewed"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:research"/>
</rdf:Bag></taxo:topics>
</item>
<item rdf:about="https://www.ncbi.nlm.nih.gov/pubmed/20226708">
    <title>Peak-time determination of post-meal glucose excursions in insulin-treated diabetic patients. - PubMed - NCBI</title>
    <dc:date>2017-09-15T02:48:34+00:00</dc:date>
    <link>https://www.ncbi.nlm.nih.gov/pubmed/20226708</link>
    <dc:creator>Michael.Massing</dc:creator><description><![CDATA[RESULTS:
The mean peak time after breakfast was 72+/-23 min, which was reached in less than 90 min in 80% of the patients. The apparent glucose rate of increase from pre-meal to the maximum postprandial value was 1.23+/-0.76 mg/dL/min, while the glucose rate of decrease was 0.82+/-0.70 mg/dL/min. Peak time correlated with the amplitude of postprandial excursions, but not with the peak glucose value. Also, peak times were similar after breakfast, lunch and dinner, and in type 1 and type 2 diabetic patients.
CONCLUSION:
To best assess peak postprandial glucose levels, the optimal time for blood glucose monitoring is about 1h and 15 min after the start of the meal, albeit with wide interpatient variability. Nevertheless, 80% of post-meal blood glucose peaks were observed at less than 90 min after the start of the meal.]]></description>
<dc:subject>hyperglycemia diabetes type 2 a T1D T2D blood glucose postprandial spike peak rhythm meal SMBG timing insulin dependent excursion peer-reviewed research</dc:subject>
<dc:source>https://pinboard.in/</dc:source>
<dc:identifier>https://pinboard.in/u:Michael.Massing/b:59f626e67e69/</dc:identifier>
<taxo:topics><rdf:Bag>	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:hyperglycemia"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:diabetes"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:type"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:2"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:a"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:T1D"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:T2D"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:blood"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:glucose"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:postprandial"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:spike"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:peak"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:rhythm"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:meal"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:SMBG"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:timing"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:insulin"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:dependent"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:excursion"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:peer-reviewed"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:research"/>
</rdf:Bag></taxo:topics>
</item>
<item rdf:about="http://jamanetwork.com/journals/jama/article-abstract/1871695">
    <title>Increasing Adiposity | Lifestyle Behaviors | JAMA | The JAMA Network</title>
    <dc:date>2017-07-18T21:30:08+00:00</dc:date>
    <link>http://jamanetwork.com/journals/jama/article-abstract/1871695</link>
    <dc:creator>Michael.Massing</dc:creator><description><![CDATA[Ninety years ago, an editorial in JAMA questioned the prevailing approach to obesity treatment: “When we read that ‘the fat woman has the remedy in her own hands—or rather between her own teeth’ . . . there is an implication that obesity is usually merely the result of unsatisfactory dietary bookkeeping. . . [Although logic suggests that body fat] may be decreased by altering the balance sheet through diminished intake, or increased output, or both . . . [t]he problem is not really so simple and uncomplicated as it is pictured.”1 Since then, billions of dollars have been spent on research into the biological factors affecting body weight, but the near-universal remedy remains virtually the same, to eat less and move more. According to an alternative view, chronic overeating represents a manifestation rather than the primary cause of increasing adiposity. Attempts to lower body weight without addressing the biological drivers of weight gain, including the quality of the diet, will inevitably fail for most individuals. This Viewpoint summarizes the evidence for this seemingly counterintuitive hypothesis, versions of which have been debated for more than a century.2]]></description>
<dc:subject>fat management control carbohydrates insulin high glycemic processed food peer-reviewed research correlation causation diet foods</dc:subject>
<dc:source>https://pinboard.in/</dc:source>
<dc:identifier>https://pinboard.in/u:Michael.Massing/b:a41404d1802d/</dc:identifier>
<taxo:topics><rdf:Bag>	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:fat"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:management"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:control"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:carbohydrates"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:insulin"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:high"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:glycemic"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:processed"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:food"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:peer-reviewed"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:research"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:correlation"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:causation"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:diet"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:foods"/>
</rdf:Bag></taxo:topics>
</item>
<item rdf:about="https://www.nytimes.com/2014/05/18/opinion/sunday/always-hungry-heres-why.html?_r=0">
    <title>Always Hungry? Here’s Why - The New York Times</title>
    <dc:date>2017-07-18T21:18:03+00:00</dc:date>
    <link>https://www.nytimes.com/2014/05/18/opinion/sunday/always-hungry-heres-why.html?_r=0</link>
    <dc:creator>Michael.Massing</dc:creator><description><![CDATA[As it turns out, many biological factors affect the storage of calories in fat cells, including genetics, levels of physical activity, sleep and stress. But one has an indisputably dominant role: the hormone insulin. We know that excess insulin treatment for diabetes causes weight gain, and insulin deficiency causes weight loss. And of everything we eat, highly refined and rapidly digestible carbohydrates produce the most insulin.]]></description>
<dc:subject>fat management control carbohydrates insulin high glycemic processed food peer-reviewed research correlation causation diet foods genetic risk genetics</dc:subject>
<dc:source>https://pinboard.in/</dc:source>
<dc:identifier>https://pinboard.in/u:Michael.Massing/b:8e34202f40cd/</dc:identifier>
<taxo:topics><rdf:Bag>	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:fat"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:management"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:control"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:carbohydrates"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:insulin"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:high"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:glycemic"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:processed"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:food"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:peer-reviewed"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:research"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:correlation"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:causation"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:diet"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:foods"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:genetic"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:risk"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:genetics"/>
</rdf:Bag></taxo:topics>
</item>
<item rdf:about="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4351933/">
    <title>Salacia reticulata (Kothala himbutu) revisited; a missed opportunity to treat diabetes and obesity?</title>
    <dc:date>2017-04-16T00:45:15+00:00</dc:date>
    <link>https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4351933/</link>
    <dc:creator>Michael.Massing</dc:creator><description><![CDATA[The evidence available from animal and human studies point towards effective reduction of plasma glucose and weight in SR treated subjects. Alpha glucosidase inhibition is the most likely mechanism for the reduction of postprandial glucose. Reduction of fasting glucose, improvement in glucose handling following glucose loading and weight is most likely explained by decreased insulin resistance mediated through increasing adiponectin, suppression of lipogenesis and increased lipolysis.

Meticulously planned studies both animal and human, addressing the unresolved issues as well as studies that involve larger number of human subjects specifically addressing long-term outcomes and safety of SR treatment needs to be performed in the future.]]></description>
<dc:subject>Salacia reticulata diabetes glucose blood insulin postprandial plasma HbA1c serum lipids peer-reviewed research in vivo vitro clinical human body fat management review overview</dc:subject>
<dc:source>https://pinboard.in/</dc:source>
<dc:identifier>https://pinboard.in/u:Michael.Massing/b:c8d61aa56a20/</dc:identifier>
<taxo:topics><rdf:Bag>	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:Salacia"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:reticulata"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:diabetes"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:glucose"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:blood"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:insulin"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:postprandial"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:plasma"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:HbA1c"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:serum"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:lipids"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:peer-reviewed"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:research"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:in"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:vivo"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:vitro"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:clinical"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:human"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:body"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:fat"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:management"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:review"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:overview"/>
</rdf:Bag></taxo:topics>
</item>
<item rdf:about="https://www.ncbi.nlm.nih.gov/pubmed/?term=Salacia+reticulata">
    <title>Salacia reticulata - PubMed - NCBI</title>
    <dc:date>2017-04-16T00:41:32+00:00</dc:date>
    <link>https://www.ncbi.nlm.nih.gov/pubmed/?term=Salacia+reticulata</link>
    <dc:creator>Michael.Massing</dc:creator><dc:subject>Salacia reticulata oblonga diabetes glucose blood insulin postprandial plasma HbA1c serum lipids peer-reviewed research in vivo vitro clinical human body fat management</dc:subject>
<dc:source>https://pinboard.in/</dc:source>
<dc:identifier>https://pinboard.in/u:Michael.Massing/b:5fcb0e7ff28f/</dc:identifier>
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	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:reticulata"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:oblonga"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:diabetes"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:glucose"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:blood"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:insulin"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:postprandial"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:plasma"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:HbA1c"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:serum"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:lipids"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:peer-reviewed"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:research"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:in"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:vivo"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:vitro"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:clinical"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:human"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:body"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:fat"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:management"/>
</rdf:Bag></taxo:topics>
</item>
<item rdf:about="https://www.ncbi.nlm.nih.gov/pubmed/26031882">
    <title>Anti-diabetic and Anti-hyperlipidemic Effects and Safety of Salacia reticulata and Related Species. - PubMed - NCBI</title>
    <dc:date>2017-04-16T00:39:49+00:00</dc:date>
    <link>https://www.ncbi.nlm.nih.gov/pubmed/26031882</link>
    <dc:creator>Michael.Massing</dc:creator><description><![CDATA[Extracts of Salacia reticulata Wight (Hypocrataceae) roots, stems, and leaves have been used in Asia for hundreds of years for the folkloric treatment of diabetes and other health problems. Constituents that have been identified as exhibiting anti-diabetic effects include salacinol, kotalanol, ponkorinol, salaprinol, and their corresponding de-0-sulfonated compounds. Mangiferin, kotalagenin 16-acetate and various proanthocyanidin oligomers have also been isolated. Studies indicate that Salacia extracts modulate multiple targets that influence carbohydrate and lipid metabolism including α-glucosidase, aldose reductase, pancreatic lipase, peroxisomal proliferator-activated receptor-α, glucose transporter-4 mediated glucose uptake, and angiotensin II type 1 receptor. Furthermore, Salacia extracts exhibit free radical scavenging, antioxidant and hepatoprotectant activities. In human studies, Salacia extracts have been shown to decrease plasma glucose and insulin levels, decrease HbA1c, and modulate serum lipid levels with no adverse effects being reported. Similar results have been demonstrated in rat and mouse models as well as in vitro systems. Safety of S. reticulata and other Salacia species as S. oblonga and S. chinensis in rats and mice indicate that extracts are exceedingly safe. No clinical studies have examined the effects of Salacia extracts on human weight loss, although weight loss and decreases in weight gain have been demonstrated in animal models. Because of the large number of pharmacologically active compounds, it is difficult to establish standards for extracts.]]></description>
<dc:subject>Salacia reticulata diabetes glucose blood insulin postprandial plasma HbA1c serum lipids peer-reviewed research in vivo vitro clinical human body fat management target range normal</dc:subject>
<dc:source>https://pinboard.in/</dc:source>
<dc:identifier>https://pinboard.in/u:Michael.Massing/b:cb589dc6dd26/</dc:identifier>
<taxo:topics><rdf:Bag>	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:Salacia"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:reticulata"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:diabetes"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:glucose"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:blood"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:insulin"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:postprandial"/>
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	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:HbA1c"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:serum"/>
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	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:peer-reviewed"/>
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	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:in"/>
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	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:vitro"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:clinical"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:human"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:body"/>
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	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:target"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:range"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:normal"/>
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</item>
<item rdf:about="http://www.npr.org/sections/thesalt/2015/01/12/376712920/minifasting-how-occasionally-skipping-meals-may-boost-health">
    <title>Minifasting: How Occasionally Skipping Meals May Boost Health : The Salt : NPR</title>
    <dc:date>2017-03-13T04:36:38+00:00</dc:date>
    <link>http://www.npr.org/sections/thesalt/2015/01/12/376712920/minifasting-how-occasionally-skipping-meals-may-boost-health</link>
    <dc:creator>Michael.Massing</dc:creator><dc:subject>fasting dietary management caloric intake restriction disease research metabolism insulin resistance peer-reviewed .AH .Plexus .week2</dc:subject>
<dc:source>https://pinboard.in/</dc:source>
<dc:identifier>https://pinboard.in/u:Michael.Massing/b:e09b65e25c14/</dc:identifier>
<taxo:topics><rdf:Bag>	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:fasting"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:dietary"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:management"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:caloric"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:intake"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:restriction"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:disease"/>
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	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:metabolism"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:insulin"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:resistance"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:peer-reviewed"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:.AH"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:.Plexus"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:.week2"/>
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</item>
<item rdf:about="https://www.ncbi.nlm.nih.gov/pubmed/20885391">
    <title>Effects of eicosapentaenoic acid (EPA) treatment on insulin sensitivity in an animal model of diabetes: improvement of the inflammatory status. - PubMed - NCBI</title>
    <dc:date>2017-03-09T04:02:23+00:00</dc:date>
    <link>https://www.ncbi.nlm.nih.gov/pubmed/20885391</link>
    <dc:creator>Michael.Massing</dc:creator><description><![CDATA[The major goal of this study was to analyze the effects of fatty acid supplementation on both insulin sensitivity and inflammatory status in an animal model of type 2 diabetes. Diabetic rats (Goto-Kakizaki model) were treated with eicosapentaenoic acid (EPA) or linoleic acid at 0.5 g/kg body weigh (bw) dose. In vivo incorporation of (14)C-triolein into adipose tissue was improved by the ω-3 administration. In vitro incubations of adipose tissue slices from EPA-treated rats showed an increase in (14)C-palmitate incorporation into the lipid fraction. These observations were linked with a decreased rate of fatty acid oxidation. EPA treatment resulted in a decreased fatty acid oxidation in incubated strips from extensor digitorum longus (EDL) muscles. The changes in lipid utilization were associated with a decrease in insulin plasma concentration, suggesting an improvement in insulin sensitivity. These changes in lipid metabolism were associated with an activation of AMP-activated protein kinase (AMPK) in white adipose tissue. In addition, EPA treatment resulted in a decreased content of peroxisome proliferator-activated receptor-α (PPARα) and PPARδ and in increased GLUT4 expression in skeletal muscle. Moreover, EPA increased 2-deoxy-D-[(14)C]glucose (2-DOG) uptake in C2C12 myotubes, suggesting an improvement in glucose metabolism. Concerning the inflammatory status, EPA treatment resulted in a decreased gene expression for both tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) both in skeletal muscle and adipose tissue. The data suggest that EPA treatment to diabetic rats clearly improves lipid metabolism although the evidences on insulin sensitization are less clear.]]></description>
<dc:subject>omega-3 fatty acids EPA DHA peer-reviewed research inflammation benefit diabetes triglycerides dyslipidemia insulin sensitivity in vivo animal</dc:subject>
<dc:source>https://pinboard.in/</dc:source>
<dc:identifier>https://pinboard.in/u:Michael.Massing/b:81c046801627/</dc:identifier>
<taxo:topics><rdf:Bag>	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:omega-3"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:fatty"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:acids"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:EPA"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:DHA"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:peer-reviewed"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:research"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:inflammation"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:benefit"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:diabetes"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:triglycerides"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:dyslipidemia"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:insulin"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:sensitivity"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:in"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:vivo"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:animal"/>
</rdf:Bag></taxo:topics>
</item>
<item rdf:about="https://www.ncbi.nlm.nih.gov/pubmed/?term=EPA+supplementation+dose+insulin">
    <title>EPA supplementation dose insulin - PubMed - NCBI</title>
    <dc:date>2017-03-02T16:25:27+00:00</dc:date>
    <link>https://www.ncbi.nlm.nih.gov/pubmed/?term=EPA+supplementation+dose+insulin</link>
    <dc:creator>Michael.Massing</dc:creator><dc:subject>EPA supplements dose insulin peer-reviewed research PubMed NCBI</dc:subject>
<dc:source>https://pinboard.in/</dc:source>
<dc:identifier>https://pinboard.in/u:Michael.Massing/b:0571196ddaa4/</dc:identifier>
<taxo:topics><rdf:Bag>	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:EPA"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:supplements"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:dose"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:insulin"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:peer-reviewed"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:research"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:PubMed"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:NCBI"/>
</rdf:Bag></taxo:topics>
</item>
<item rdf:about="https://www.ncbi.nlm.nih.gov/pubmed/20803425">
    <title>The effects of low dose n-3 fatty acids on serum lipid profiles and insulin resistance of the elderly: a randomized controlled clinical trial. - PubMed - NCBI</title>
    <dc:date>2017-03-02T06:14:39+00:00</dc:date>
    <link>https://www.ncbi.nlm.nih.gov/pubmed/20803425</link>
    <dc:creator>Michael.Massing</dc:creator><description><![CDATA[This study assessed the effects of low-dose n-3 fatty acids on serum lipid profile, lipoprotein(a), apolipoprotein B, fasting glucose, insulin, and insulin resistance in a group of elderly Iranians.
MATERIALS AND METHODS:
A 6-month randomized, double-blind placebo-controlled clinical trial was carried out in 124 elderly residents of Kahrizak Charity Foundation aged >or= 65. The intervention group was supplemented with 1 g/day fish oil capsule (with 180 mg eicosapentaenoic acid, EPA; and 120 mg docosahexaenoic acid, DHA; a total of 300 mg n-3 fatty acids as effective constituents). Fasting blood samples were collected at baseline and after 6 months of the trial.
RESULTS:
There were no significant effects of fish oil on the studied variables in the intervention group. In the placebo group, serum triglyceride significantly increased and high-density lipoprotein cholesterol significantly decreased (p = 0.01 and p = 0.009, respectively). By repeated measurement analysis after adjustments, the overall decrease in serum triglycerides compared with placebo was significant (p = 0.04).
CONCLUSION:
Supplementation with low dose n-3 fatty acids for 6 months could significantly protect elderly Iranians from a rise in serum triglycerides.]]></description>
<dc:subject>supplements fish oil EPA cholesterol dyslipidemia high risk benefit blood lipids insulin resistance aging peer-reviewed research in vivo human clinical trial</dc:subject>
<dc:source>https://pinboard.in/</dc:source>
<dc:identifier>https://pinboard.in/u:Michael.Massing/b:bc160aa33533/</dc:identifier>
<taxo:topics><rdf:Bag>	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:supplements"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:fish"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:oil"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:EPA"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:cholesterol"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:dyslipidemia"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:high"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:risk"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:benefit"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:blood"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:lipids"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:insulin"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:resistance"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:aging"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:peer-reviewed"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:research"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:in"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:vivo"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:human"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:clinical"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:trial"/>
</rdf:Bag></taxo:topics>
</item>
<item rdf:about="http://www.diabetesselfmanagement.com/blog/one-day-low-carb-diet-decreases-insulin-resistance-study-finds/">
    <title>One Day of a Low-Carb Diet Decreases Insulin Resistance, Study Finds - Diabetes Self-Management</title>
    <dc:date>2016-11-23T18:43:05+00:00</dc:date>
    <link>http://www.diabetesselfmanagement.com/blog/one-day-low-carb-diet-decreases-insulin-resistance-study-finds/</link>
    <dc:creator>Michael.Massing</dc:creator><dc:subject>insulin resistance self treatment diabetes type 2 T2D prediabetes low carb carbohydrate diet peer-reviewed research in vivo human clinical trial</dc:subject>
<dc:source>https://pinboard.in/</dc:source>
<dc:identifier>https://pinboard.in/u:Michael.Massing/b:94dac91c6863/</dc:identifier>
<taxo:topics><rdf:Bag>	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:insulin"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:resistance"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:self"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:treatment"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:diabetes"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:type"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:2"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:T2D"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:prediabetes"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:low"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:carb"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:carbohydrate"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:diet"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:peer-reviewed"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:research"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:in"/>
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	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:human"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:clinical"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:trial"/>
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</item>
<item rdf:about="http://eatingacademy.com/quick-faq">
    <title>Quick FAQ - The Eating Academy | Peter Attia, M.D. The Eating Academy | Peter Attia, M.D.</title>
    <dc:date>2016-09-02T17:36:13+00:00</dc:date>
    <link>http://eatingacademy.com/quick-faq</link>
    <dc:creator>Michael.Massing</dc:creator><description><![CDATA[The conventional wisdom is that sugar is no more harmful, calorie per calorie, than any other nutrient in the diet. And yet virtually every diet, even low-fat diets, restrict sugar consumption considerably. (And by sugar, I mean both the white powdered stuff, sucrose, that we put in our coffee and tea, and the ubiquitous high fructose corn syrup in all juices and processed foods.)

Fifty years of biochemistry, though, suggests that sugar is the ultimate cause of insulin resistance (because of the metabolic load it puts on the liver) and so perhaps the ultimate cause of obesity, diabetes and the diseases that associate with them, including cancer and Alzheimer’s disease.
]]></description>
<dc:subject>LCHF diabetes sugar ketosis nutrition insulin resistance liver diet health low carb high fat Peter Attia Alzheimer's</dc:subject>
<dc:source>https://twitter.com/</dc:source>
<dc:identifier>https://pinboard.in/u:Michael.Massing/b:a5eeb6aea6ed/</dc:identifier>
<taxo:topics><rdf:Bag>	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:LCHF"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:diabetes"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:sugar"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:ketosis"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:nutrition"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:insulin"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:resistance"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:liver"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:diet"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:health"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:low"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:carb"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:high"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:fat"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:Peter"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:Attia"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:Alzheimer's"/>
</rdf:Bag></taxo:topics>
</item>
<item rdf:about="https://www.kickstarter.com/projects/951782667/unspeakably-wonderful-a-new-feature-film">
    <title>Unspeakably Wonderful - A new feature film by Alex Tweddle — 
Kickstarter</title>
    <dc:date>2016-06-14T20:51:45+00:00</dc:date>
    <link>https://www.kickstarter.com/projects/951782667/unspeakably-wonderful-a-new-feature-film</link>
    <dc:creator>Michael.Massing</dc:creator><description><![CDATA[RT @UnspeakablyW: Please help us tell the extraordinary story of #insulin 's discovery. #diabetes #movie #crowdfunding ]]></description>
<dc:subject>movie diabetes crowdfunding insulin</dc:subject>
<dc:source>https://twitter.com/</dc:source>
<dc:identifier>https://pinboard.in/u:Michael.Massing/b:cbc4d644906d/</dc:identifier>
<taxo:topics><rdf:Bag>	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:movie"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:diabetes"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:crowdfunding"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:insulin"/>
</rdf:Bag></taxo:topics>
</item>
<item rdf:about="http://www.docfoc.com/ir-and-hyperinsulinemia-insulin-resistance-a-survival-mechanism-gone-awry">
    <title>IR and Hyperinsulinemia Insulin Resistance: A Survival Mechanism, Gone Awry Stan Schwartz MD,FACP Affiliate, Main Line Health System Emeritus, Clinical. - Documents</title>
    <dc:date>2016-06-11T18:51:47+00:00</dc:date>
    <link>http://www.docfoc.com/ir-and-hyperinsulinemia-insulin-resistance-a-survival-mechanism-gone-awry</link>
    <dc:creator>Michael.Massing</dc:creator><dc:subject>insulin resistance evolution human</dc:subject>
<dc:source>https://pinboard.in/</dc:source>
<dc:identifier>https://pinboard.in/u:Michael.Massing/b:59a71670d9a3/</dc:identifier>
<taxo:topics><rdf:Bag>	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:insulin"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:resistance"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:evolution"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:human"/>
</rdf:Bag></taxo:topics>
</item>
<item rdf:about="http://www.diabetesincontrol.com/insulin-resistance-a-survival-mechanism-gone-awry-part-5/">
    <title>Insulin Resistance - A Survival Mechanism Gone Awry, Part 5</title>
    <dc:date>2016-06-11T18:50:43+00:00</dc:date>
    <link>http://www.diabetesincontrol.com/insulin-resistance-a-survival-mechanism-gone-awry-part-5/</link>
    <dc:creator>Michael.Massing</dc:creator><dc:subject>insulin resistance evolution human</dc:subject>
<dc:source>https://pinboard.in/</dc:source>
<dc:identifier>https://pinboard.in/u:Michael.Massing/b:5b6174f369cf/</dc:identifier>
<taxo:topics><rdf:Bag>	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:insulin"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:resistance"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:evolution"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:human"/>
</rdf:Bag></taxo:topics>
</item>
<item rdf:about="http://www.diabetesincontrol.com/insulin-resistance-a-survival-mechanism-gone-awry-part-4/">
    <title>Insulin Resistance - A Survival Mechanism Gone Awry, Part 4</title>
    <dc:date>2016-06-11T18:50:16+00:00</dc:date>
    <link>http://www.diabetesincontrol.com/insulin-resistance-a-survival-mechanism-gone-awry-part-4/</link>
    <dc:creator>Michael.Massing</dc:creator><dc:subject>insulin resistance evolution human</dc:subject>
<dc:source>https://pinboard.in/</dc:source>
<dc:identifier>https://pinboard.in/u:Michael.Massing/b:4e9226a454ba/</dc:identifier>
<taxo:topics><rdf:Bag>	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:insulin"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:resistance"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:evolution"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:human"/>
</rdf:Bag></taxo:topics>
</item>
<item rdf:about="http://www.diabetesincontrol.com/insulin-resistance-a-survival-mechanism-gone-awry-part-3/">
    <title>Insulin Resistance - A Survival Mechanism Gone Awry, Part 3</title>
    <dc:date>2016-06-11T18:49:49+00:00</dc:date>
    <link>http://www.diabetesincontrol.com/insulin-resistance-a-survival-mechanism-gone-awry-part-3/</link>
    <dc:creator>Michael.Massing</dc:creator><dc:subject>insulin resistance evolution human</dc:subject>
<dc:source>https://pinboard.in/</dc:source>
<dc:identifier>https://pinboard.in/u:Michael.Massing/b:72b274ab9caf/</dc:identifier>
<taxo:topics><rdf:Bag>	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:insulin"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:resistance"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:evolution"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:human"/>
</rdf:Bag></taxo:topics>
</item>
<item rdf:about="http://www.diabetesincontrol.com/insulin-resistance-a-survival-mechanism-gone-awry-part-2/">
    <title>Insulin Resistance - A Survival Mechanism Gone Awry, Part 2</title>
    <dc:date>2016-06-11T18:49:00+00:00</dc:date>
    <link>http://www.diabetesincontrol.com/insulin-resistance-a-survival-mechanism-gone-awry-part-2/</link>
    <dc:creator>Michael.Massing</dc:creator><dc:subject>insulin resistance evolution human</dc:subject>
<dc:source>https://pinboard.in/</dc:source>
<dc:identifier>https://pinboard.in/u:Michael.Massing/b:6275bc8b22ac/</dc:identifier>
<taxo:topics><rdf:Bag>	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:insulin"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:resistance"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:evolution"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:human"/>
</rdf:Bag></taxo:topics>
</item>
<item rdf:about="http://www.diabetesincontrol.com/insulin-resistance-a-survival-mechanism-gone-awry-part-1/">
    <title>Insulin Resistance - A Survival Mechanism Gone Awry, Part 1</title>
    <dc:date>2016-06-11T18:48:33+00:00</dc:date>
    <link>http://www.diabetesincontrol.com/insulin-resistance-a-survival-mechanism-gone-awry-part-1/</link>
    <dc:creator>Michael.Massing</dc:creator><dc:subject>insulin resistance evolution human</dc:subject>
<dc:source>https://pinboard.in/</dc:source>
<dc:identifier>https://pinboard.in/u:Michael.Massing/b:784e36efb361/</dc:identifier>
<taxo:topics><rdf:Bag>	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:insulin"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:resistance"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:evolution"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:human"/>
</rdf:Bag></taxo:topics>
</item>
<item rdf:about="http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3781574/">
    <title>Favorable Effects of Insulin Sensitizers Pertinent to Peripheral Arterial Disease in Type 2 Diabetes</title>
    <dc:date>2016-06-11T01:56:15+00:00</dc:date>
    <link>http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3781574/</link>
    <dc:creator>Michael.Massing</dc:creator><description><![CDATA[The Bypass Angioplasty Revascularization Investigation 2 Diabetes (BARI 2D) trial randomly assigned participants to insulin sensitization (IS) therapy versus insulin-providing (IP) therapy for glycemic control. Results showed similar 5-year mortality in the two glycemic treatment arms. In secondary analyses reported here, we examine the effects of treatment assignment on the incidence of PAD. A total of 1,479 BARI 2D participants with normal ankle-brachial index (ABI) (0.91–1.30) were eligible for analysis. The following PAD-related outcomes are evaluated in this article: new low ABI ≤0.9, a lower-extremity revascularization, lower-extremity amputation, and a composite of the three outcomes.

RESULTS

During an average 4.6 years of follow-up, 303 participants experienced one or more of the outcomes listed above. Incidence of the composite outcome was significantly lower among participants assigned to IS therapy than those assigned to IP therapy (16.9 vs. 24.1%; P < 0.001). The difference was significant in time-to-event analysis (hazard ratio 0.66 [95% CI 0.51–0.83], P < 0.001) and remained significant after adjustment for in-trial HbA1c (0.76 [0.59–0.96], P = 0.02).

CONCLUSIONS

In participants with type 2 diabetes who are free from PAD, a glycemic control strategy of insulin sensitization may be the preferred therapeutic strategy to reduce the incidence of PAD and subsequent outcomes.]]></description>
<dc:subject>limb risk amputation PAD peripheral arterial disease clinical research human in vivo retrospective insulin sensitizer mimetic leg foot trial postmarket situ cardiovascular</dc:subject>
<dc:source>https://pinboard.in/</dc:source>
<dc:identifier>https://pinboard.in/u:Michael.Massing/b:3c3ee3aae5a0/</dc:identifier>
<taxo:topics><rdf:Bag>	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:limb"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:risk"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:amputation"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:PAD"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:peripheral"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:arterial"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:disease"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:clinical"/>
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	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:human"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:in"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:vivo"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:retrospective"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:insulin"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:sensitizer"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:mimetic"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:leg"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:foot"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:trial"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:postmarket"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:situ"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:cardiovascular"/>
</rdf:Bag></taxo:topics>
</item>
<item rdf:about="http://www.dlife.com/diabetes-news/viewdetailnews?news_article_id=11347569">
    <title>dLife Diabetes News - Diabetes | Type 1 Diabetes | Type 2 Diabetes - www.dlife.com</title>
    <dc:date>2016-05-19T02:39:45+00:00</dc:date>
    <link>http://www.dlife.com/diabetes-news/viewdetailnews?news_article_id=11347569</link>
    <dc:creator>Michael.Massing</dc:creator><description><![CDATA[Previous research conducted by the same researchers at Lund University in 2009 showed a gene variant to melatonin receptor 1B increases risk for type 2 diabetes. The variant causes the level of the melatonin receptors in beta cells to increase, making them more sensitive to melatonin and stopping them from secreting insulin.
"A third of all people carry this specific gene variant," Hindrik Mulder, a professor at Lund University, said in a press release. "Our results show that the effect of melatonin is stronger in them. We believe that this explains their increased risk of developing type 2 diabetes."
For the study, researchers recruited 23 healthy carriers of the gene variant and 22 people without the variant, treating them with four milligrams of melatonin before bed for three months.
The researchers found insulin secretion was lower among participants with the genetic variation, and that blood glucose levels were higher among all participants after melatonin treatment -- but most significantly in those with the variation.]]></description>
<dc:subject>genetic risk etiology factor T2D type 2 diabetes melatonin correlation peer-reviewed research circadian rhythms hormone drug effects contraindication pancreas insulin beta cells light body clock mutation genetics cause factors</dc:subject>
<dc:source>https://pinboard.in/</dc:source>
<dc:identifier>https://pinboard.in/u:Michael.Massing/b:beace043a3e7/</dc:identifier>
<taxo:topics><rdf:Bag>	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:genetic"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:risk"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:etiology"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:factor"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:T2D"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:type"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:2"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:diabetes"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:melatonin"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:correlation"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:peer-reviewed"/>
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	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:circadian"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:rhythms"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:hormone"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:drug"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:effects"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:contraindication"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:pancreas"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:insulin"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:beta"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:cells"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:light"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:body"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:clock"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:mutation"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:genetics"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:cause"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:factors"/>
</rdf:Bag></taxo:topics>
</item>
<item rdf:about="http://carbsanity.blogspot.com/2012/10/blood-sugar-140-context-is-everything-i.html">
    <title>The Carb-Sane Asylum: Blood Sugar 140: Context is Everything I - Diabetic vs. Non</title>
    <dc:date>2016-05-15T00:54:12+00:00</dc:date>
    <link>http://carbsanity.blogspot.com/2012/10/blood-sugar-140-context-is-everything-i.html</link>
    <dc:creator>Michael.Massing</dc:creator><description><![CDATA[I can think of nothing more harmful to health than the insulin phobia rampant in the LC community.  While the frank type 2 diabetic is baseline hyperinsulinemic, they don't produce the appropriate acute insulin response.  Given the health issues accompanying improper insulin/signaling, it seems a no-brainer that establishing  as normal a level of both insulin and glucose as possible....

Normal individuals eating a "normal" diet will regularly exceed 140 mg/dL, though not necessarily by much, to no apparent detriment.  Neuropathy would simply be far more common in occur in younger populations if BG's over 140 damaged nerves to any significant level. 

In a diabetic, however, not only do postprandial glucose levels climb higher, they tend to stay elevated for longer periods of time, thus if the hyperglycemia is toxic per se, the exposure is greater.  The glucose levels also may never fall below, say, 100 or even far higher depending on the degree of glycemic control.  Therefore it is not surprising that IGT or diabetes was diagnosed by OGTT in 2/3rds of subjects presenting with neuropathy in this study.    I shall discuss the implications of that finding in a separate post as well.

In someone with impaired insulin secretion (T1 = none/insignificant, T1.5 = insufficient, T2 = varying depending) if blood glucose goes over 140, it likely climbs considerably over that and takes longer to clear (and/or is added to by inappropriate endogenous glucose production).  The more carbs ingested the higher the glucose spike in somewhat proportional fashion.  This is because insulin is not secreted properly and the glucose will be cleared by non-insulin dependent mechanisms.  A person with normal insulin secretion will almost never get a glucose spike over around 180 because their glucose stimulated insulin secretion (GSIS) is proportional to the glucose ingested.  So a diabetic consumes 50g carb or 100g carb and their BG level climbs quite a lot higher after the 100g load, but a non-diabetic consumes 50g or 100g or 200g, and their BG level may climb 10 or 20 points higher at the high dose, but their GSIS will just increase proportionally to handle the load to avoid runaway glucose levels....

Eating sugar or carbohydrates in general does not cause diabetes.  The pancreas has more than enough insulin making capacity to last more than a lifetime.  It's not like eggs in your ovaries as I've seen the analogy drawn.  Yes, with aging comes some declining function, just as sarcopenia can become an issue, but that decline is not due to having used up some insulin reservoir.   Eating a low carb diet to avoid getting diabetes on this basis is, frankly, downright foolish.  Equally foolish, IMO, is looking at thresholds and studies in diabetics and applying those same measures to the non-diabetic.    A non-diabetic will simply rarely if ever exceed around 180 mg/dL no matter what, and this includes "compensators" -- those with IR for whom an exaggerated GSIS compensates for impaired transport to achieve normoglycemia.   So long as one is not continually adding to whatever has caused the IR, there's little indication the pancreas can't keep on keeping on.  Remember, the LIRKO mouse is hyperglycemic throughout most of its shortened life, but hyperinsulinemic to the bitter end.   We can argue over the glucose and/or insulin being toxic in this mouse, but it's pretty clear that at least in the mouse, raging chronic hyperglycemia didn't kill off its beta cells.

In summary, then, application of thresholds and targets aimed at diabetics to non-diabetics should be qualified and are often so out of context as to be irrelevant.  I would agree that maintaining more truly normal glycemic control in the diabetic -- keeping glucose spikes under 200 and 2 hr readings below 140 -- may well be a more effective means to prevent diabetic complications.  I'd sure as heck aim for that myself were I diabetic.  But I don't see any reason for a non-diabetic to worry or obsess over postprandial spikes exceeding that magic 140 mg/dL number.    If your low carb diet has rendered your formerly non-diabetic metabolism into a functionally diabetic one, it may be time to rethink things a bit.  Insulin does more than stimulate glucose transport into your cells.... 

The last [study cited by a correspondent] is very interesting [link] What Is the Best Predictor of Future Type 2 Diabetes?

"The insulin secretion/insulin resistance index is useful as a predictor of future development of type 2 diabetes."

I think I'll do a quick blog post on this paper in the next day or so. If insulin is a better predictor it *may* mean that it is the primary factor in the etiology. This is what I believe based on my reading of the literature (especially recently) demonstrating that postprandial insulin production is impaired early on in the progression of the disease.]]></description>
<dc:subject>insulin normoglycemia euglycemia blood glucose excursions cycle postprandial diabetes type 2 T2D normal standards threshold eitiology etiology cause factor risk target range management</dc:subject>
<dc:source>https://pinboard.in/</dc:source>
<dc:identifier>https://pinboard.in/u:Michael.Massing/b:71955e71ee19/</dc:identifier>
<taxo:topics><rdf:Bag>	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:insulin"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:normoglycemia"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:euglycemia"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:blood"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:glucose"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:excursions"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:cycle"/>
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	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:standards"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:threshold"/>
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	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:etiology"/>
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	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:factor"/>
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	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:management"/>
</rdf:Bag></taxo:topics>
</item>
<item rdf:about="http://www.wsj.com/articles/tech-savvy-families-use-home-built-diabetes-device-1462728637">
    <title>Tech-Savvy Families Use Home-Built Diabetes Device - WSJ</title>
    <dc:date>2016-05-09T03:24:43+00:00</dc:date>
    <link>http://www.wsj.com/articles/tech-savvy-families-use-home-built-diabetes-device-1462728637</link>
    <dc:creator>Michael.Massing</dc:creator><description><![CDATA[The latest >  Tech-Savvy Families Use Home-Built Diabetes Device     - WSJ , see more ]]></description>
<dc:subject>OpenAPS closed-loop artificial pancreas DIYPS #WeAreNotWaiting T1D type 1 diabetes juvenile insulin DIY</dc:subject>
<dc:source>https://pinboard.in/</dc:source>
<dc:identifier>https://pinboard.in/u:Michael.Massing/b:db4c26caff4a/</dc:identifier>
<taxo:topics><rdf:Bag>	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:OpenAPS"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:closed-loop"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:artificial"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:pancreas"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:DIYPS"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:#WeAreNotWaiting"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:T1D"/>
	<rdf:li rdf:resource="https://pinboard.in/u:Michael.Massing/t:type"/>
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<item rdf:about="https://www.researchgate.net/publication/262789337_Exaggerated_effects_of_particulate_matter_air_pollution_in_genetic_type_II_diabetes_mellitus">
    <title>Exaggerated effects of particulate matter air pollution in genetic type II diabetes mellitus (PDF Download Available)</title>
    <dc:date>2016-04-10T02:12:25+00:00</dc:date>
    <link>https://www.researchgate.net/publication/262789337_Exaggerated_effects_of_particulate_matter_air_pollution_in_genetic_type_II_diabetes_mellitus</link>
    <dc:creator>Michael.Massing</dc:creator><description><![CDATA[Researchers found that exposure to air pollution, over a period of 24 weeks, exaggerates insulin resistance and fat inflammation. “[O]besity has reached epidemic proportions with 34% of adults in the US, ages 20 and over, meeting the criteria...Obesity and diabetes are very prevalent in urban areas and there have been no studies evaluating the impact of poor air quality on these related conditions until now.”
Type 2 diabetes...has soared worldwide with a projected 221 million people expected to suffer from this disease in 2010, a 46 percent increase compared to 1995...[S]cientists fed male mice a diet high in fat over a 10-week period to induce obesity and then exposed them to either filtered air or air with particulate matter for six hours a day, five days a week, over a 24-week period...The air pollution level inside the chamber containing particulate matter was comparable to levels a commuter may be exposed to in...many metropolitan areas in the U.S.
[description by Diabetes in Control - expired link]]]></description>
<dc:subject>in vivo animal correlation pollution environment risk body fat inflammation heart circulation insulin epidemic poison etiology resistance T2D diabetes type 2 research peer-reviewed environmental factor public health genetic genetics cause epidemiology factors geiography</dc:subject>
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<item rdf:about="http://www.med.unc.edu/www/newsarchive/2011/april/unc-study-helps-clarify-link-between-high-fat-diet-and-type-2-diabetes">
    <title>UNC study helps clarify link between high-fat diet and type 2 diabetes — UNC School of Medicine</title>
    <dc:date>2016-04-10T01:14:07+00:00</dc:date>
    <link>http://www.med.unc.edu/www/newsarchive/2011/april/unc-study-helps-clarify-link-between-high-fat-diet-and-type-2-diabetes</link>
    <dc:creator>Michael.Massing</dc:creator><description><![CDATA[New research from the University of North Carolina at Chapel Hill School of Medicine adds clarity to the connection. The study published online April 10 in the journal Nature Immunology finds that saturated fatty acids but not the unsaturated type can activate immune cells to produce an inflammatory protein, called interleukin-1beta.

“The cellular path that mediates fatty acid metabolism is also the one that causes interleukin-1beta production,” says senior study co-author Jenny Y. Ting, PhD, William Kenan Rand Professor in the Department of Microbiology and Immunology.

“Interleukin-1beta then acts on tissues and organs such as the liver, muscle and fat (adipose) to turn off their response to insulin, making them insulin resistant.  As a result, activation of this pathway by fatty acid can lead to insulin resistance and type 2 diabetes symptoms.”  Ting is also a member of the UNC Lineberger Comprehensive Cancer Center, and the UNC Inflammatory Diseases Institute.]]></description>
<dc:subject>insulin resistance mechanism risk factor diabetes type 2 T2D inflammation correlation etiology saturated fat peer-reviewed research diet food earnest liver fatty body metabolic syndrome disorder public health cause chicken-and-egg</dc:subject>
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<item rdf:about="http://www.endocrineweb.com/conditions/type-2-diabetes/type-2-diabetes-risk-factors">
    <title>Type 2 Diabetes Risk Factors - What Risk Factors Do You Have?</title>
    <dc:date>2016-03-28T00:50:39+00:00</dc:date>
    <link>http://www.endocrineweb.com/conditions/type-2-diabetes/type-2-diabetes-risk-factors</link>
    <dc:creator>Michael.Massing</dc:creator><dc:subject>risk factors diabetes type 2 T2D insulin resistance</dc:subject>
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<dc:identifier>https://pinboard.in/u:Michael.Massing/b:1e9c60781377/</dc:identifier>
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<item rdf:about="http://f1000research.com/articles/5-136/v1">
    <title>GPR21 KO mice demonstrate no resistance to high fat diet induced obesity or improved glucose tolerance - F1000Research</title>
    <dc:date>2016-03-24T00:02:33+00:00</dc:date>
    <link>http://f1000research.com/articles/5-136/v1</link>
    <dc:creator>Michael.Massing</dc:creator><description><![CDATA[failed replication: glucose metabolism improvement or obesity resistance in mice correlated with high-fat diet]]></description>
<dc:subject>glucose tolerance insulin sensitivity in vivo high fat diet metabolism animal peer-reviewed research correlation failed replication obesity</dc:subject>
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<dc:identifier>https://pinboard.in/u:Michael.Massing/b:870e67bc9f63/</dc:identifier>
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<item rdf:about="http://care.diabetesjournals.org/content/27/8/2047.short?rss=1&amp;amp%3bssource=mfr">
    <title>Caffeine Impairs Glucose Metabolism in Type 2 Diabetes</title>
    <dc:date>2016-03-14T03:17:22+00:00</dc:date>
    <link>http://care.diabetesjournals.org/content/27/8/2047.short?rss=1&amp;amp%3bssource=mfr</link>
    <dc:creator>Michael.Massing</dc:creator><description><![CDATA[[related research appended]]]></description>
<dc:subject>caffeine coffee risk benefit type 2 diabetes T2D insulin resistance glucose metabolism peer-reviewed research human in vivo</dc:subject>
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<item rdf:about="http://www.nature.com/nm/journal/vaop/ncurrent/full/nm.4057.html">
    <title>A branched-chain amino acid metabolite drives vascular fatty acid transport and causes insulin resistance : Nature Medicine : Nature Publishing Group</title>
    <dc:date>2016-03-09T23:28:29+00:00</dc:date>
    <link>http://www.nature.com/nm/journal/vaop/ncurrent/full/nm.4057.html</link>
    <dc:creator>Michael.Massing</dc:creator><dc:subject>insulin resistance mechanism peer-reviewed research</dc:subject>
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<dc:identifier>https://pinboard.in/u:Michael.Massing/b:e6ef07668f5f/</dc:identifier>
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