The question to me isn't whether highly palatable processed foods are a factor in diabetes/obesity etc., but how they are.
One example of a possible explanation--palatable food encourages snacking, as opposed to eating discrete meals. Give a mouse or rat high-fat, high sugar food, and instead of eating mostly at night, which is normal for these species, they'll eat smaller amounts of food, around the clock. This out of synch eating has been shown to increase obesity, diabetes and cancer in these animals, making food available only at the time of day when these animals would eat less pleasing food protects against these outcomes--in fact prevents all of the damage of a high fat/high sugar diet. And how do people eat these days? In discrete meals, or constantly nibbling, often right up to bed-time?
So insulin is elevated constantly throughout the day, instead of two or three times a day. Having large portions of the day when insulin is not elevated might be more important than worrying about just how high insulin goes at any one meal. Maybe constantly elevated insulin--rather than occasionally high insulin--matters more to the development of insulin resistance.
Also--inject insulin into the brain, and appetite decreases. So insulin is a satiety hormone.... but this is a case where the level of insulin is raised in the brain, but not in the periphery. What happens when you raise insulin locally? Locally, cells are better fed. This is illustrated in those cases where diabetics inject insulin in the same spot for decades, and develop large fatty pads at the injection site.
In the case of the brain, it's just the brain getting the insulin--and just a small part of the hypothalamus, mostly, at that. The insulin does its work, the cells draw in more glucose and amino acids, the brain cells are under the false impression that the body is well-fed--when this is the case, suppression of appetite makes sense, so that's what happens. There isn't an increased need for glucose because of this application of insulin, because, after all, only a small fraction of the body is being given that insulin signal to take up glucose.
If you think about this--if I'm making any sense at all, then insulin doesn't have to be any kind of a satiety hormone at all, under normal function, this could just be a weird little phenomenon when insulin is administered in a very unnatural way. The same goes for centrally administered leptin--which by the way results in a sort of osteoporosis. Feed those cells in the hypothalamus a little bit better, and they pretend the body's well-nourished, whether that's the case or not.
The peripheral insulin that the diabetic is taking is a different story. Cells all over the body are taking up glucose--and there had better be enough to go around.
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