
Fatty Pancreas and the Development of Type 2 Diabetes
The English friar and philosopher William of Ockham (1287-1347) is credited with developing the fundamental problem solving principle known as lex parsimoniae or Occam’s Razor. This principle holds that the hypothesis with the fewest assumptions is most often right. The simplest explanation is usually the most correct.
Albert Einstein is quoted as saying, “Everything should be made as simple as possible, but not simpler.” With that in mind, let’s remember that type 2 diabetes reflects two fundamental problems:
Insulin resistance
Beta cell dysfunction
Insulin resistance, an overflow phenomenon, is caused by fatty infiltration of the liver and muscle. Without dietary intervention, defect #2 virtually always follows #1, albeit by many years. Also, #2 is almost never found without #1.
Yet somehow, we are asked to believe that the mechanism behind insulin resistance and beta cell dysfunction are completely and utterly unrelated? Occam’s razor suggests that both defects must be caused by the same underlying mechanism.
Searching for the mechanism
Hyperinsulinemia stimulates de novo lipogenesis transforming excess dietary carbohydrate into new fat. The liver packages and exports this new fat as VLDL making it widely available for other organs. The new fat deposits in skeletal muscles takes up much of this fat, as do the fat cells in and around the abdominal organs leading to the central obesity that is an important component of metabolic syndrome.
As fat begins to deposit within the organs, specifically the liver and muscles, insulin resistance develops, gradually leading
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