Enjoyed your blog post
@tim2000s
Yours covers overlapping territory to mine.
Certainly a minimally understood and challenging subject area.
It's been blowing my mind trying to understand it and debate it!
Indeed it does, and I think we have to tread carefully in this respect. I can fully understand the perspective that Roger Unger has opened up based on my experiences of food consumption. I've started a debate with my diabetic team relating to Amylin and Glucagon, so it will be interesting to see where that one goes.
Reading your glucose/insulin/glucagon article, what stood out to me is that it doesn't pick up on the roles that insulin (and Amylin) have in suppressing Glucagon response and potentially why both T1 and T2 diabetics are more susceptible to GNG than non-diabetics as a result of Insulin resistance.
I've not yet found clear clinical studies relating to lack of satiety in Type 2 diabetics as a result of insulin and maybe amylin resistance (or maybe depletion as a result of high BG levels resulting in damage to the beta cells) but I think this is also linked in to the equation.
What I've also found is that by increasing basal insulin, I've been able to limit GNG caused by the (relatively) higher protein content of my diet. Now this could be down to one of two factors. Either a) It stops the liver undertaking GNG autonomously or b) it either regulates glucagon release or inhibits the reaction to glucagon in the liver and restricts GNG in the process. Either way, it has an impact, which is why I want to try Symlin (Synthetic Amylin) and see what the results are.