Induction of diabetic alterations by goldthioglucose-obesity in KK, ICR and C57BL mice

Abstract

The effect of goldthioglucose (GTG) obesity on development of diabetes was investigated in genetically diabetic (KK) and normal (ICR and C57BL) mice. GTG obesity intensified diabetic traits in KK mice from chemical diabetes to overt diabetes, as was already demonstrated in obesity induced by either dietary or genetical means. GTG obesity caused diabetic changes likewise in ICR mice as manifested by hyperglycemia, glucosuria, hyperinsulinemia, and depressed insulin sensitivity. In vitro glucose oxidation was also decreased to about half of the untreated controls and became less sensitive to added insulin in the epididymal adipose tissue from GTG-obese ICR mice. Hypertrophy of pancreatic islets associated with degranulation of B cells was also recognized in the obese mice. By contrast, either hyperglycemia or glucosuria did not develop in GTG-obese C57BL mice, although the other diabetic changes observed in GTG-obese ICR mice were induced but only in lesser extents. These results indicate that mice inherit their own diabetic potentials and add further experimental evidence for the concept that obesity accelerates the development of diabetes. © 1972 Springer-Verlag.