A number of genetic and environmental factors determine the development of insulin resistance. In the article “Obesity – insulin resistance – type 2 diabetes” the author points out that one of the most important factors is obesity. A number of studies aimed at assessing which of the components of abdominal fat is most associated with insulin resistance indicate that it is visceral fat. This type of adipose tissue accounts for 7% of total body fat in women and 10% in men, but is an independent risk factor for insulin resistance and other components of the metabolic syndrome. Literature reports also indicate that the abdominal subcutaneous tissue may influence the appearance of insulin resistance. The author of the article emphasizes that the relationship described above illustrates a statistical relationship, and does not prove a cause-and-effect relationship, because it is possible to consider a situation in which abdominal obesity and insulin resistance are caused by the same genetic or environmental factors. Visceral adipose tissue secretes a number of compounds (hormones, metabolites) that are released directly into the hepatic circulation, which have an antagonistic effect on insulin or have an effect that impairs the function of insulin receptors. The released substances also include free fatty acids (FFA – Free Fatty Acids). High levels of FFA inhibit glucose uptake, e.g. in muscle tissues and interferes with the functioning of the insulin receptor. Circulating free fatty acids have the ability to accumulate in pancreatic islets, which in turn may contribute to impaired insulin secretion. The results of clinical trials indicate a relationship between insulin resistance and the level of FFA. The amount of free fatty acids circulating in the body is higher in men with obesity than in women with obesity. Weight loss through the implementation of a reduction diet reduces the concentration of circulating free fatty acids and, as a result, improves insulin sensitivity. Source: Maciej T. Małecki. “Obesity – insulin resistance – type 2 diabetes” Kardiologia Polska 2006; 64:10 (Suppl. 6) |