Sat, May-07-11, 10:52
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Senior Member
Posts: 2,544
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Plan: VLC
Stats: 265.4/238.8/199
BF:
Progress: 40%
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Quote:
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Originally Posted by Vlad416
So let that sink for you, contrary to GT, rising insulin levels inhibit feeding.
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Hi Vlad:
It seems to me that you've missed the point when you argue about whether the VMN or the arcuate nucleus is the mechanism for the change in appetite. (BTW the wikipedia article you quote doesn't cite the source of the information.) Two sentences beyond the portion you've chosen to highlight and quibble over, Taubes says this (copied and pasted from your own post):
"[I]nsulin secretion in VMH-lesioned animals increases dramatically within seconds of the surgery. The insulin response to eating also goes 'off the scale' with the very first meal. The more insulin secreted in the days after the surgery, the greater the ensuing obesity."
The point of this paragraph is that circulating levels of insulin can now be measured because of new technology, that levels of insulin rise dramatically immediately after the surgery, and that the more insulin is secreted the fatter the animal grows.
Here are a couple of abstracts of studies at the NIH site which seem to indicate that insulin increases hunger and eating:
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The paper reviews studies considering whether hyperinsulinemia, and its resultant effects on adipose tissue mass, can alter perceived hunger, taste, and food consumption. It also describes work addressing the reciprocal question of whether cues associated with food can affect insulin response. Specifically, four general categories of studies are presented. First, studies considering the causes and physiological consequences of chronic hyperinsulinemia are reviewed. Second, work investigating environmental and cognitive influences on insulin secretion are described. These show that high acute levels of insulin can be produced by simply seeing and thinking about food and that individuals showing this response show a greater tendency toward weight gain in a food-abundant environment. Third, studies are covered in which direct manipulations of insulin level, controlling for blood glucose, are performed. These experiments show that elevations in insulin produce increased hunger, heightened perceived pleasantness of sweet taste, and increased food intake. Finally, a study is described that considers how different insulin levels, produced by the type of food ingested, may affect subsequent food intake. Together, these studies show that "overeating" is caused by a complex feedback system of environmental, behavioral, and biological factors.
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http://www.ncbi.nlm.nih.gov/pubmed/3894001
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Rats injected subcutaneously with 5 U/kg of regular insulin increased food intake above control levels in a 2 hr test and showed a median latency to eat of 59 min. One week later, rats were injected again with saline or insulin (5 U/kg), deprived of food and killed 60 +/- 10 min later. Insulin treatment produced a marked reduction in plasma glucose, plasma ketone bodies and liver glycogen, as well as a marked acceleration of gastric emptying. The results indicate that a variety of changes in peripheral metabolism and physiology may underlie the increase in food intake observed after insulin injection and that it is premature to ascribe the hunger-inducing effect of insulin treatment solely to a decline in blood glucose.
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http://www.ncbi.nlm.nih.gov/pubmed/6757987 |
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