Diabetes (db), which occurred in an inbred strain of mouse, is inherited as a unit autosomal recessive and is characterized by a metabolic disturbance resembling diabetes mellitus in man. Abnormal deposition of fat at 3 to 4 weeks of age is followed shortly by hyperglycemia, polyuria, and glycosuria. Accompanying morphological changes in the islets of Langerhans suggest neogenesis to compensate for insulin depletion.

The mutation, diabetes:,(db), that occurred in the C57BL/Ks strain of mice is a unit autosomal recessive gene with full penetrance, and causes metabolic disturbances in homozygous mice resembling diabetes mellitus in man. Abnormal deposition of fat at 3 to 4 weeks of age is followed by hyperglycemia, polyuria and glycosuria. The diabetic condition appears to develop in two

A new congenie strain of obese mice, C57BK/KsJ-ob, has been developed for comparison with the C57BL/6J-ob eongenie strain. While obese mlee of both strains are characterized by obesity, hyperphagia, and hyperglycemia, the C57BL/Ks obese mice have severe diabetes, marked hyperglycemia, temporarily elevated plasma insulin concentrations, and typical degenerative changes in the islets of Langerhans. In contrast, the C57BL/6J obese mice have mild hyperglycemia and marked h3q3erinsulinemia eoupled with hypertrophy and hyperplasia of the islets of Langerhans. The severe diabetic condition produced by obese (ob) on the C57BL/KsJ background is similar, if not identical, to tha~ produced by the diabetes (db) gene on the same background. The metabolic disorder produced by these mutations is associated with the capaeit, y of the islets to respond to an increased demand for insulin. The islet response, whei,her atrophy or hypertrophy, appears to be due to the interaction of the obese and diabetes genes with modifiers in the genetic background rather than the specific consequences of the particular gene. The markedly differen~ diabetic syndromes that result when the obese mutation is on different genetic backgrounds emphasize the importance of strict genetic control in studies with obesehyperglycemic mutants.

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