Rat studies show that feeding sucrose (table sugar) to rats can induce insulin resistance. In fact studies using intakes of sucrose equivalent to the upper range of human intakes show the development of insulin resistance in just a few weeks (here). Sucrose is thought to lead to insulin resistance because it overloads the liver with energy and this energy shifts the metabolism of the liver to one of lipid synthesis. In particular the sucrose induces the de novo lipogenesis pathway and increases the rate of fatty acid synthesis. These fatty acids enter the circulation and are deposited in tissues such as the liver and skeletal muscle. Here the lipids interfere with the insulin signal cascade and this results in a reduction in insulin sensitivity. Epidemiological data supports the contention that sucrose are detrimental to insulin function as associations exist between sugar consumption and the risk of type 2 diabetes and obesity. Human clinical studies also show that sucrose consumption is detrimental to insulin function.
Sucrose contains both a fructose and a glucose moiety, and either or both could be responsible for the detrimental effects of sucrose. However, evidence suggests it is the fructose that is detrimental. For example, in one study1, researchers investigated the insulin to insulin receptor binding rate in healthy human volunteers. The healthy young subjects were fed their usual diets plus either 1000 kcal of glucose per day or 1000 kcal of fructose per day. Subjects consumed the diets for just 1 week and during this time there was no detrimental effects for glucose on the insulin sensitivity of the subjects. However, those subjects consuming fructose experienced a significant reduction in the binding of insulin to the insulin receptor and of whole body insulin sensitivity. Analysis of the data showed that the reduction in insulin binding and the reduction in insulin sensitivity correlated linearly. The authors concluded that fructose was the likely component of sucrose that is responsible for the detrimental effects on the insulin system.
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