Episode 27 – Adipocytes and insulin resistance

Show notes: 60% of US adults are overweight to moderately obese but within that group there is great heterogeneity in their response to insulin ⇒ their degree of insulin sensitivity can vary more than sixfold at any given BMI within this range Adults constantly form and replace adipose cells, called turnover 2 places to measure fat are the femoral (leg fat) and subcutaneous (under your skin and predominantly white) adipose tissues For IMGU (insulin mediated glucose uptake), the higher the

Continue Reading

Episode 26 – Dr.Bikman: well behaved fat and good insulin signaling FTW

Discuss further on: https://ask.breaknutrition.com Show notes: Here’s Dr.Bikman’s Twitter profile The Bikman lab is in The College of Life Sciences of Brigham Young University It focuses on identifying first “the molecular mechanisms that explain the increased risk of disease that accompanies weight gain, with particular emphasis on the etiology of insulin resistance and disrupted mitochondrial function. Second, we hope to reveal novel cellular processes that are responsible for fat development” Dr.Bikman enumerates some of the metabolic drugs used in disease

Continue Reading

Why controlling gluconeogenesis is important for reversing diabetes?

Introduction: our very own sugar factory Step into the low-carb world and soon enough you’ll hear the term GlucoNeoGenesis. GNG for short, is your body’s ability to construct glucose, a kind of sugar, out of molecules that aren’t glucose. It does this to ensure that, if you don’t eat any carbs, the cells in your body that need glucose will still get enough of it. It’s one reason why humans are so good at fasting or delaying death from starvation

Continue Reading

Episode 8 – starch digestibility and limitations of the glycemic response

In episode 8 of the Break Nutrition show we discuss 2 papers which explore the glycemic, insulin and incretin responses and how the digestibility of starch as well as the apportioning of endogenous vs exogenous glucose comes into play. The paper from 2012 is “Slowly and rapidly digestible starchy foods can elicit a similar glycemic response because of differential tissue glucose uptake in healthy men” http://www.ncbi.nlm.nih.gov/pubmed/22990033. The paper from 2015 is “Plasma glucose kinetics and response of insulin and GIP

Continue Reading

Episode 5 – how enlarged adipocytes overloaded with lipids lead to insulin resistance

 Episode 5 of the Break Nutrition Show Gabor and I  had a discussion about the paper called “Lipid-overloaded enlarged adipocytes provoke insulin resistance independent of inflammation”, covering the following points (and more): Link: http://www.ncbi.nlm.nih.gov/pubmed/25733684 The concept of IR occurring after the lipid-derived enlargement of adipocytes (as opposed to the other model of IR preceding it) The difference in mild/early-stage obesity versus severe/late-stage obesity Mechanisms whereby adipocyte-focused inflammation appears necessary to make adipocytes more insulin resistance in severe/late-stage obesity but not in

Continue Reading

Episode 4 – the rate at which sugar is absorbed by the gastro intestinal system affects obesity, diabetes and metabolic health

In episode 4 we discuss why the rate at which you absorb sugar may affect obesity, diabetes and general metabolic health, here is the 2 papers discussed: Effects of small intestinal glucose on glycaemia, insulinaemia and incretin hormone release are load-dependent in obese subjects Link: http://www.ncbi.nlm.nih.gov/pubmed/27840416 Accelerated intestinal glucose absorption in morbidly obese humans: relationship to glucose transporters, incretin hormones, and glycemia Link: http://www.ncbi.nlm.nih.gov/pubmed/25423571

Episode 3 – Affecting fat loss in rodents by caloric restriction, knocking out insulin genes and seeing how incretin hormones play into it

In Episode 3 of the Break Nutrition show we discussed rodent studies showing an insulin gene dosage-dependent effect on adiposity, the interplay between caloric restriction & circulating insulin, as well as how incretin hormones affect fat loss dynamics. Caloric Restriction Paradoxically Increases Adiposity in Mice With Genetically Reduced Insulin. Link: https://www.ncbi.nlm.nih.gov/m/pubmed/27145011/ Suppression of hyperinsulinaemia in growing female mice provides long-term protection against obesity. Link: https://www.ncbi.nlm.nih.gov/m/pubmed/26155745/?i=3&from=/27145011/related

Site Footer