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

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Episode 7 – How processed starches affect metabolic responses

The first paper discussed is from 1989 and is called “Insulin and glycemic responses in healthy humans to native starches processed in different ways: correlation with in vitro alpha-amylase hydrolysis” Link: https://www.ncbi.nlm.nih.gov/pubmed/2667315 18 subjects eat 35g of starch that is either raw, gelled (boiled & cooled) or made into a paste (via mechanical extrusion). In vitro α-hydrolysis with α-amylase of differently processed starches correlate strongly (r2 = 0.95, p < 0.0001) with the glycemic and insulin responses of 18 human subjects

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Episode 6 – why bariatric surgery improves metabolic parameters quickly

Episode 5 of the Break Nutrition Show Gabor and I  had a discussion about the paper called “Mechanisms facilitating weight loss and resolution of type 2 diabetes following bariatric surgery”. Mechanisms facilitating weight loss and resolution of type 2 diabetes following bariatric surgery Link: https://www.ncbi.nlm.nih.gov/pubmed/20133150 Bariatric surgery is more akin to metabolic surgery than a procedure to mechanically restricting food intake The 3 classical categories of bariatric surgery (1) restrictive (2) malabsorptive (3) hybrid of 1 & 2 Improvement of metabolic

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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

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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

Episode 2 – trafficking fatty acids properly to avoid ectopic fat deposition

In Episode 2 of the BreakNutrition Show we talked about how dysregulated cycling of fat between fat cells, the liver and the fat we eat can lead to obesity, here is the paper: Downregulation of adipose tissue fatty acid trafficking in obesity: a driver for ectopic fat deposition? Link: http://www.ncbi.nlm.nih.gov/pubmed/20943748

Episode 1 – Linking dysregulated adipocyte fat flow to diabetes

In Episode 1 of the BreakNutrition Show we talked about how how dysregulated fat flow from fat cells can drive the creation of new glucose in the liver and lead to diabetes, here is the paper: Hepatic acetyl CoA links adipose tissue inflammation to hepatic insulin resistance and type 2 diabetes. link: https://www.ncbi.nlm.nih.gov/pubmed/25662011