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Discussion Starter #1
"An often ignored point is that insulin inhibits hepatic gluconeogenesis. The reduction in insulin secretion while working is a significant factor in the promotion of gluconeogenesis. The importance of this is obvious when we consider diabetes. Diabetic hyperglycemia is partially due to glucagon-stimulated hepatic glucose synthesis which occurs in spite of the high blood glucose levels that follow the loss of insulin or insulin resistance. Inhibition of hepatic gluconeogenesis with metformin is an important component of treatment for type 2 diabetes."

Insulin and Glucagon

So, supposing you have the type of IR that is predominantly hyper-gluconeogenesis ... and they keep giving you PILLS? Hmmmmm.
 

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... and from the same page (seems to be a lecture) ...

Hypothalamic KATP Channels Regulate Hepatic Gluconeogenesis and Postprandial Blood Glucose Levels.

Blood sugar levels are dependent upon glucose uptake after meals and hepatic release of glucose between meals. The sugar released from the liver comes either from stored glycogen or production of glucose from lactate and amino acids. This production of glucose is largely responsible for stabilization of postprandial blood sugar levels. The hyperglycemia noted in type 2 diabetes partially results from lack of control over hepatic glucose formation due to resistance to insulin. It has recently become clear that part of this insulin effect occurs indirectly through insulin-sensitive receptors in the brain (more precisely, in the hypothalamus). In a very recent article in Nature, Alessandro Pocai and coauthors presented convincing data that couples insulin-stimulation of hypothalamic KATP channels with neural control of hepatic gluconeogenesis (Nature 434, 1026-1031, 2005; and an overview by Nature's editors ((click here)). Insulin stimulated opening of hypothalamic KATP channels results in vagal nerve signaling to the liver and inhibition of gluconeogenesis. This is part of the normal response to meals and following insulin release from the pancreatic ß-cells. Thus, signaling from the brain is one of the important control mechanisms which establish correct "between-meal" blood sugar levels. Hypothalamic insulin resistance and therefore loss of control over hepatic gluconeogenesis may well be one of the important factors involved in development of type 2 diabetes. This model is summarized in this figure from the overview in Nature .
 

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Thanks, Foxl. I've bookmarked that site for later study. Food for thought, yes, but my brain is in low gear today, so I have indigestion of the frontal lobes.
 

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HAH!

He is against the paleo or low carb diet, be forewarned (without any justification!).

But his explanations of the pathophys are great.
 

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Hello Linda :D, Here's an apple for your efforts in your lecture as like other students in this class, I have information overload in my frontal lobes too. The .PDF files will be something to show my endo when I see him. :D:p
 
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