The effects of hypothalamics lesions in genetically diabetic mice

Abstract

Genetically diabetic (db/db) and normal (+/+) mice were lesioned in the ventromedial nucleus by either gold thioglucose or electrocauterization. The normal mice responded typically to either of these treatments by becoming hyperphagic, obese, and by exhibiting moderately elevated plasma insulin concentrations coupled with near normal blood sugar concentrations. In diabetic mice, destruction of the ventromedial nucleus prevented the development of severe hyperglycemia and had a therapeutic effect in those mice with established, but moderate, hyperglycemia. Hyperphagia and rapid accumulation of adipose tissue continued unabated as expected. Regranulation of the β-cells of the endocrine pancreas was associated with the maintenance of blood sugar at normal concentrations. The marked improvement of the diabetic aspects of this syndrome in mice lends support to the hypothesis that the primary defect in diabetic mice may involve a defective hypothalamus, particularly in the regions of the satiety centers. © 1970 Springer-Verlag.