Diabetes mellitus type 1 (biochemistry)

Type 1 diabetes mellitus is characterized by an absolute or almost complete lack of endogenous insulin and lifelong dependence on the application of exogenous insulin. Patients are prone to ketoacidosis.

The disease arises as a result of the selective destruction of β-cells of the Langerhans islets in pancreas by an autoimmune process in genetically predisposed individuals. The triggering mechanism of the autoimmune process is probably a viral infection or contact with another exogenous or endogenous agent.

The clinical picture of type 1 diabetes mellitus depends on the aggressiveness of the autoimmune process. In childhood and adolescence, when most diseases develop, the last phase of β-cell destruction tends to be very rapid, so diabetes manifests itself with classic acute symptoms (including ketoacidosis). At a later age, the disease has a significantly slower onset and only after some time results in complete dependence on insulin. Insulin secretion may be reduced for several years, but sufficient to prevent ketoacidosis. The clinical course of the disease is therefore similar to type 2 diabetes mellitus, and it is reported that about one in ten patients originally classified as type 2 diabetes has a slowly progressing type 1 diabetes – latent autoimmune diabetes of adults (LADA)..

Type 1 DM is a less common form of diabetes that occurs in about 7% of diabetics. The classic symptoms of type 1 DM are thirst, polyuria and weight loss.

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