Type 1 diabetes mellitus (biochemistry)

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

The disease results from the selective destruction of pancreatic islet β-cells 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 stage of β-cell destruction tends to be very rapid, so diabetes is manifested by classic acute symptoms (including ketoacidosis). At a later age, the disease tends to have a much slower onset and only eventually results in complete insulin dependence. Insulin secretion may be reduced for several years, but sufficient to prevent ketoacidosis. The clinical course of the disease therefore resembles type 2 diabetes mellitus and it is stated that about one in ten patients originally classified as type 2 diabetes has slow-onset 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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