Dysfunction and/or loss of pancreatic beta cells can result in different forms of diabetes mellitus

Diabetes mellitus is the most common metabolic disorder worldwide. In industrialized countries it is the leading cause of blindness, renal failure and lower limb amputations and is a major risk factor for cardiovascular disease and stroke. Due to population ageing and increasing trends towards obesity and sedentary lifestyles, the number of affected individuals is expected to rise dramatically in the coming years.
Insulin secretion from pancreatic beta cells plays an essential role in the control of blood glucose levels. Production of insufficient amounts of insulin to cover the metabolic demand results in different forms of diabetes mellitus. Type 1 diabetes is due to autoimmune destruction of beta cells. Type 2 diabetes is initiated by a diminished sensitivity of insulin target tissues often linked to obesity. This insulin resistance state is normally compensated by an increased secretory activity of beta cells and by expansion of the functional beta cell mass. However, in genetically predisposed individuals this adaptive mechanism fails, leading to insufficient hormone supply and overt hyperglycemia. Exposure of beta cells to chronically elevated concentrations of glucose, free fatty acids, cytokines and adipokines has a deleterious impact on their functions. This causes defective insulin secretion, partial loss of the cells by apoptosis and diabetes manifestation. The mechanisms underlying beta cell dysfunction and the development of diabetes are not well understood. A better knowledge of the molecular events responsible for these phenomena is needed to allow the design of innovative therapies for prevention and treatment of diabetes.
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