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 with insulin resistance. It is hypothesized that increasing cell membrane fluidity by increasing PUFA concentration might result in an enhanced number of insulin receptors, an increased affinity of insulin to its receptors, and a reduced insulin resistance, and vice versa. Many stressing factors may lead to increased cortisol in the bloodstream. Cortisol counteracts insulin, contributes to hyperglycemia-causing hepatic gluconeogenesis, and inhibits the peripheral utilization of glucose, which eventually leads to insulin resistance. It does this by decreasing the translocation of glucose transporters (especially GLUT4) to the cell membrane. Inflammation by itself also seems to be implicated in causing insulin resistance.