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The function of the pancreatic B-cell was studied in relation to the development of the diabetic syndrome in a new variety of the diabetic mutant mouse, which was produced at The Jackson Laboratory, Bar Harbor, Maine, U.S.A. by outcrossing of a c57bl/ksJ-db stock with C57BL/6J mice. The expression of the db-gene in the resulting strain was evaluated by measurements of the body weights and the concentrations of serum glucose and serum insulin at different ages of the animals. In the diabetic mice the body weights increased rapidly between 5 and 25 weeks of age to a weight twice that of the lean controls. During the same time hyperglycaemia and hyperinsulinaemia occurred, the maximal serum glucose and insulin values being observed between 17 and 25 weeks of age. Later on the serum glucose and serum insulin concentrations gradually decreased. Islets were isolated with collagenase from animals 5, 10 or 20 weeks old, and studied with respect to insulin content, glucose oxidation and the secretion and synthesis of insulin. The results were compared with data from control experiments with islets isolated from non-diabetic littermates. No major differences were found between islets from diabetic and control mice with regard to the glucose oxidation rate, whereas an exaggerated insulin response to glucose was observed in islets from 5 weeks old diabetic mice. In the 20 weeks old diabetic animals there was a significantly decreased islet insulin content and a considerably lowered insulin biosynthesis.

Function of the pancreatic B-cell during the development of hyperglycaemia in mice homozygous for the mutations ?diabetes? (db) and ?Misty? (m)