Dieting results in long term changes to hormones and muscle fibers.

[eridani]

226. There has been no increase in the number of people genetically predisposed toward diabetes

You are born diabetic, period. What is changing in a really disturbing way is the age of onset of symptoms, and on a worldwide basis, not just in America. Back when most people did a lot of physical work on short rations, diabetics very rarely developed problems with sugar control before they died of something else. Since the industrial revolution, it became more common to see symptoms in late middle age. Now symptoms are showing up in kids and teenagers.

Americans are unique mainly because of the high levels of inequality, lack of universal health care, and lack of a strong labor movement. Stress hormones are very well known antagonists of insulin.

Don't blame me because you don't know anything about current research. For starters--

http://mdn.mainichi.jp/mdnnews/news/20120105p2a00m0na006000c.html

Team of Japanese scientists discovers insulin-resistant protein

A team of Japanese scientists has identified an insulin-resistant protein that could be a major cause of obesity and diabetes, a discovery that could help medical practitioners diagnose and treat lifestyle diseases.

Using a method called "comparative proteomic analysis," the team of scientists from Kobe University, Shimadzu Corp. and other groups found the insulin-resistant protein in mice after conducting detailed analysis of various kinds of protein. The analysis showed that the levels of the insulin-resistant protein in the blood of obese mice were twice to three times higher than normal. When the protein was injected into other mice, those mice that were not obese became resistant to insulin.

Moreover, those mice that were made incapable of producing the protein did not become obese even when they were fed fatty foods and showed no resistance to insulin. The same protein exists in humans and it is known to be effective in treating inflammation and injuries...


http://www.thedailybeast.com/articles/2012/01/17/no-proof-paula-deen-s-high-fat-southern-cooking-caused-her-diabetes.html

After eight years, there was no statistically significant difference in the rate at which type 2 diabetes occurred among women in the two groups. (The women who reduced their caloric intake weighed an average of four pounds less than they did at the beginning of the trial.) This study is the most powerful evidence yet that there simply is no causal relationship between dietary fat intake and developing type 2 diabetes.

Indeed, diabetes is primarily a genetic disease. If one identical twin doesn’t develop diabetes, the odds are less than 1 percent that the other will, while if one such twin does have the disease, the odds are better than 75 percent that the other twin will develop it as well. It is also a disease of affluence and old age: in poor countries beset by chronic undernourishment, diabetes is unusual, in large part because most of the population dies before getting old enough to develop it.

It is true that there’s a strong correlation between higher weight and diabetes. This does not, however, mean that higher weight causes diabetes. Rather, it appears that both higher weight and higher diabetes risk are caused by the same underlying genetic mechanism: the so-called thrifty gene that leads some people to store caloric energy far more efficiently than others.


http://www.sciencedaily.com/releases/1999/03/990305073924.htm
Washington D.C. - A team of Canadian scientists has identified a potentially useful target for drugs to treat type II diabetes and obesity. In the scientists' experiments, genetically engineered mice lacking a specific enzyme were able to resist weight gain and to avoid the decreased sensitivity to insulin that characterizes type II diabetes, even when fed an extremely high calorie, high fat diet. The results are reported in the 5 March issue of Science.

Previous research has suggested that an enzyme known as PTP-1B might somehow play a role in reducing insulin's ability to regulate blood sugar levels. To investigate this possibility, Mounib Elchebly of McGill University and his colleagues "knocked out" the mouse gene responsible for the production of this enzyme. Compared to normal mice, the mice lacking the enzyme had significantly lower amounts of glucose in their blood after eating and even lower amounts of insulin. Thus, deleting the PTP-1B enzyme appeared to increase the mice's sensitivity to insulin: they were able to use smaller amounts of the hormone to efficiently move glucose from the bloodstream into the cells.

To further probe the insulin signaling process, the scientists fed both normal and knockout mice a diet extremely high in calories, 50 percent of which were from fat. As expected, normal mice quickly gained extra weight and developed obesity-related insulin resistance. In contrast, the knockout mice did not gain much weight and had normal insulin and glucose levels.