31 Jul 2018 The True Cause of Type 2 Diabetes and Insulin Resistance
studies cited and relevant articles
Glucose uptake is not inhibited in type 2 diabetes and insulin resistance:
https://www.jci.org/articles/view/116226
https://academic.oup.com/bja/article/85/1/69/263650
https://www.ncbi.nlm.nih.gov/pubmed/11431133
https://www.jci.org/articles/view/111258
Glucose oxidation is inhibited in type 2 diabetes and insulin resistance:
https://www.jci.org/articles/view/116226
https://www.ncbi.nlm.nih.gov/pubmed/9216960
https://www.ncbi.nlm.nih.gov/pubmed/17472434
http://science.sciencemag.org/content/300/5622/1140
https://academic.oup.com/edrv/article/25/5/807/2355272
Hepatic glucose production is responsible for fasting hyperglycemia in type 2 diabetes and insulin resistance, and insulin lowers fasting hyperglycemia in these conditions by inhibiting hepatic glucose production rather than increasing glucose uptake:
https://academic.oup.com/bja/article/85/1/69/263650
https://www.ncbi.nlm.nih.gov/pubmed/11431133
https://www.jci.org/articles/view/111258
Issues with low-carb and ketogenic diets:
https://jayfeldmanwellness.com/carbs-vs-fats-which-is-the-better-fuel/
https://jayfeldmanwellness.com/carbs-vs-fats-hormonal-effects/
Nicki
Posted at 08:34h, 22 OctoberHi Jay, I’m a nutritional therapist and have been digging into your work and reading your references. What I’d like some help with is the the following: let’s say that the reason diabetics and pre diabetics are suffering from hyperglycaemia is because the mitochondria are dysfunctional and that this dysfunction is down to a mix of the following: ROS, the xenobiotics in our environment, infection from microbes and endotoxins, and pufas. What I’d like some clarity on is what is the mechanism that is causing the hyperinsulinaemia to fail to switch off the hepatic production of glucose from gluconeogenesis, proteolysis and ketogenesis. The Sonksen and Sonksen article was describing how this is the main function of insulin; to put the brakes on hepatic glucose production. So clearly the insulin is not doing this, hence more insulin is produced by the beta cells in the pancreas. At the top of my question we have a picture of insulin resistance at the level of the mitochondria where the Krebs and the ETC can’t oxidise the glucose. But at the level of the hepatic inhibition of glucose production, what is stopping the insulin from inhibiting that production. I’m not sure the mitochondria would have that role? What does insulin resistance really mean here?
Jay Feldman
Posted at 22:06h, 24 OctoberHi Nicki. Great question! The hyperinsulinemia does actually turn off the hepatic glucose output, but normal amounts of insulin don’t. I would largely blame this on the elevated stress hormones (cortisol, adrenaline, and especially glucagon) that are seen in this state due to the impairment in energy production. Higher amounts of insulin are needed to counteract the gluconeogenic effects of the excessive cortisol/adrenaline/glucagon at the liver.
We discussed the role of hyperglucagonemia in diabetes/insulin resistance in this podcast episode and will be digging further into insulin resistance in future episodes: https://www.jayfeldmanwellness.com/ep-86-robb-wolf-on-ray-peat-and-the-bioenergetic-view-stress-blood-sugar/