Quote:
Originally Posted by nawchem
teaser is it something like when Dr. Fung brings up gastric bypass curing diabetes. Is it the weight loss or the change in diet that cured their diabetes?
|
The Newcastle people suggest that it's the reversal of fatty pancreas and liver that's most important. We do know that the diet they use there, that's similar to the early phase of a gastric bypass diet, where there is a very low calorie diet, reduces fatty liver and pancreas fairly rapidly. Of course, with gastric bypass, early on, most of the overall body fat hasn't been reduced all that much, and people reverse diabetes without becoming what you would necessarily call lean. But even on a standard macronutrient ratio, these people will be eating less carbohydrate, so into the mix goes the fact that it just takes less insulin to handle a smaller amount of food, and walking around with lower glycogen levels, tissues may be more insulin sensitive.
The fat in/fat out conundrum for organs--strategies for defattening the liver include increased export of triglycerides--this actually does happen for a lot of type II diabetics when they first go on insulin, that nastly VLDL that our liver puts out is also doing a good thing, transporting fat out of the liver. Another good strategy that occurs more in starvation or semi-starvation or on a low carb diet is increased oxidation of free fatty acids in the liver. Increase this and fatty liver could be reversed. It's not just because those fats are oxidized--also, the pathways for triglyceride synthesis tend to be reduced when fat oxidative pathways are upregulated and glucose pathways are downregulated. So, you can increase export of triglyceride, or decrease synthesis. Fattening occurs when synthesis outstrips export.
For synthesis--that's where subcutaneous fat and the personal fat threshold comes in. "Overstuffed" fat cells-->increased availability of free fatty acids from spillover for synthesis of triglycerides in the liver and pancreas. In starvation or very low carb, elevated free fatty acids is the physiologic norm. It's a pathological state when accompanied by a high availability of glucose. If the liver is glucose replete, and free fatty acids are elevated, that's a good recipe for fat accumulation in the liver. If free fatty acids are elevated, but glucose is scarce, it's not.
What I'm trying to say here is--I think yes, it's the diet, and yes it's the fat loss. In rodent models, just getting the animals very fat can get them diabetic--but concentrating on a high sugar diet is a more direct path to insulin resistance and diabetes, even though it might not get them as fat as some other diets.