The pathogenesis of diabetes mellitus type I

With type I diabetes the most important stage of the pathogenesis is the activation of T lymphocytes against specific antigens present on the beta cells of the patient. These activated T cells contribute to the slow destruction of beta cells by enlarging the pool of T-and B-lymphocytes, macrophages and cytokines.

Morphological study of the pancreases of children who died of acute diabetes debut, showed inflammatory infiltrate of mononuclear cells, did not extend beyond the island - the so-called insulin. In the end, over the years comes complete destruction of beta cells. Detection of serum child high titer of autoantibodies to insulotsitam a predictor of progression of type I diabetes. Different antigen expressed beta-cells, are involved as targets for autoimmune attack. Such antigens include both the insulin and the protein molecular weight of 64 kilodaltons (now known as glutamic acid decarboxylase, or DHA).

Starting factor for activation of T cells against these self antigens is unknown, but may participate in the process of environmental factors, which are identical to autoantigens by antigenically. T-cells activated against the antigen from the environment can then be cross-react with an antigen on the surface of the beta-cells - a process called molecular mimicry.

As for type I diabetes, the potential activators of the environment include viruses, toxins and food products. For example, assume that the consumption of cow's milk during the first weeks of life, b plays a role in the development of type I diabetes in genetically susceptible children to him. Viruses can trigger type I diabetes through molecular mimicry or by direct changes in beta-cells that cause abnormal expression of autoantigens, or by direct destruction of beta cells.

Pathogenesis of type II diabetes

Pathogenesis of type II diabetes is unclear, but apparently, it is multifactorial. The earliest defect that can be detected by a resistive tentnost insulin, manifested by elevated levels of insulin in the blood plasma - and fasting or after oral or intravenous tolerance test glucose.

This anomaly can be observed even in late adolescence, and it may precede the development of diabetes, one or two decades. At this early stage rezistentiost insulin is obvious, even if not obese. Prospective studies indicate that the inheritance of insulin resistance is an obligate, but not sufficient for the development of diabetes. Diabetes does not develop in genetically predisposed people to him, if they maintain body weight close to ideal. Ill usually just genetically predisposed to diabetes are people suffering from obesity. Obesity, especially obesity, the body is associated with insulin resistance and is said to have high requirements of beta-cells.

As for people who are genetically predisposed to type II diabetes, the beta cells are essentially able to compensate for insulin resistance. However, over the years, beta cells lose this ability. This case is failure of the function of beta cells is common, when put clinical diagnosis of diabetes.

The transition from insulin resistance to failure of beta cells can clearly be seen in humans. Similarly, we can predict diabetes mellitus type II, as reproduced in animals, which progresses through various stages of insulin resistance and insulin deficiency.