How do diabetes are occur

Diabetes is a complex syndrome causes, all can lead to a lack of insulin or insulin resistance factors that can make the genetic susceptibility to diabetes mellitus ontogeny. Thus, since insulin B cells in the synthesis, secretion, blood circulation through the role of transit and target cells in the entire process, a part of any unusual occurrence of diabetes can be. Is divided into three aspects of the brief. (1) islet B-cell level: ① insulin gene mutations. At present, the application of RFLP and DNA recombinant technology, found that due to insulin gene mutation caused by particle password abnormal insulin There are two types: A insulin structural abnormalities. Section 11 of the short arm of chromosome mutation of insulin, B cells, synthesis of insulin mutation. Variability of insulin is still considered a normal immune activity, but very low biological activity. Normal insulin molecules and receptor-binding part of the biological activity of the insulin molecule area, so far have been reported abnormal structure of insulin are B25 phenylalanine was replaced by leucine. B24 phenylalanine replaced by serine, A3 leucine valine was replaced by three variations of insulin syndrome, are manifested in NIDDM. Clinical characterized by high blood glucose, hyperinsulinemia, external source of insulin response to normal insulin receptor to normal, there is no insulin in serum antibodies and insulin receptor antibodies. B Proinsulin excessive. Under normal circumstances, islet B cell secretion of insulin in the proinsulin containing about 5 percent. Insulin gene mutation, B cells, synthesis of proinsulin C-peptide and insulin in the connection point is arginine, histidine has been replaced. Proinsulin role as protease hydrolysis is not complete, a large number of proinsulin into insulin and failed to enter the blood circulation. Proinsulin Bioactive only five percent of insulin, but the immune response in the radiation cross-reaction with insulin, so the determination showed hyperinsulinemia. Clinical manifestations of impaired glucose tolerance or NIDDM. Synthesis and secretion of insulin ② abnormal. Islet B cells by auto-immune response or the destruction of chemical substances, the cells decrease in the number of synthetic insulin reduced or absent, while there is an absolute lack of insulin in IDDM. Another B cell membrane receptor abnormal glucose, the blood glucose concentration is not sensitive; or decreased synthesis of insulin, the cells stored in little insulin. After the intake of glucose, insulin secretion after the peak-shift, does not appear early rapid phase, thereby increasing blood sugar after a meal, often manifested in NIDDM patients. (2) blood circulation in the fight against insulin material increase: blood circulation, the fight against insulin hormones material can be divided into categories with non-hormone, two types of confrontation can be the role of insulin, so that elevated blood sugar. ① hormonal substances: such as glucagon, catecholamines, growth hormone, ACTH, adrenocorticotropic hormone, thyroid stimulating hormone, thyroxine, etc., in which certain hormones in the blood concentration of any unusual increase in the role of insulin-confrontation, by hyperglycemia. ② non-hormonal substances: such as insulin antibody and insulin receptor antibody. In patients with acanthosis nigricans can be found in serum insulin receptor antibody. Receptor and its corresponding antibody binding, the insulin receptor binding and can not, can not play a physiological role of insulin. Black acanthosis nigricans with insulin receptor antibodies in patients with familial, high blood sugar and insulin resistance, such as serious features, are autoimmune diseases.
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