Insulin characterized by abnormally high blood glucose concentrations, and generalized body wasting. In type 2 diabetes mellitus the destruction of beta cells is less pronounced than in type 1 diabetes, and is not due to an autoimmune process. Instead there is an accumulation of amyloid in the pancreatic islets, which likely disrupts their anatomy and physiology. The pathogenesis of type 2 diabetes is not well understood but patients exhibit a reduced population of islet beta-cells, reduced secretory function of islet beta-cells that survive, and peripheral tissue insulin resistance. Type 2 diabetes is characterized by high rates of glucagon secretion into the
Insulin resistance (generally caused by insulin resistance), this down-regulation acts as a kind of positive feedback, increasing the need for insulin. Exercise reverses this process in muscle tissue, but if it is left unchecked, it may contribute to insulin resistance. Elevated blood levels of glucose—regardless of cause—lead to increased glycation of proteins with changes, only a few of which are understood in any detail, in protein function throughout the body. Insulin resistance often is found in people with visceral adiposity (i.e., a high degree of fatty tissue within the abdomen—as distinct from subcutaneous adiposity or fat between the skin and the muscle