NOD mice

The NOD mouse (English Non- Obese Diabetic Mouse) is an inbred strain of color mouse (Mus musculus), which due to a high incidence of spontaneously occurring diabetes mellitus in experimental diabetes research as an animal model for insulin-dependent type 1 diabetes is used. It was first described in 1980 and goes back to attempts at Shionogi in Japan, the original goal was to breed mice with increased susceptibility to cataracts. By means of appropriate investigations it could be shown that the diabetes in the NOD mouse is caused by autoimmune processes and thus has similarities to the occurring mainly in adolescence insulin-dependent type 1 diabetes of man in terms of its etiology.

As for human type 1 diabetes, the diabetes, the NOD mouse is before the onset of the disease, known as insulitis inflammatory infiltration of immune system cells in the islets of Langerhans of the pancreas ( pancreas) advance, which leads to destruction of the insulin-producing beta cells. Genes in the major histocompatibility complex are the most important genetic risk markers of the disease in both the NOD mouse, as well as in humans. Another similarity between the type 1 diabetes of the human and the NOD mouse diabetes, is the occurrence of specific auto-antibodies which are directed against antigens of the islet cells. The outbreak of the disease occurs in the NOD mouse from the 14th week of life. The incidence of diabetes, depending on the colony and housing conditions at 60 to 80 percent for women and 20 to 30 percent for males. In addition to the susceptibility to diabetes, the NOD mouse also shows an increased incidence of other autoimmune diseases such as autoimmune thyroiditis, polyneuropathy and a SLE -like disease.

The NOD mouse is in experimental diabetes research in addition to the BB rat, the dominant animal model for human type 1 diabetes, especially immunological and genetic aspects as well as for the study of new approaches to prevention and treatment of disease. The diabetes of the NOD mouse differs from type 1 diabetes in humans primarily by the gender differences in disease incidence as well as by a relatively mild clinical course of diabetic ketoacidosis.

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