Effects of Streptozocin-Induced Diabetes on Glucose Metabolism and Lactate Release by Isolated Fat Cells From Young Lean and Older, Moderately Obese Rats

Streptozocin-induced diabetes (STZ-D) was produced in male Wistar rats at two stages of development: young, lean rats, weighing 150–220 g (6–8 wk), and older, moderately obese rats, weighing 450–500 g (6–8 mo). A comparable degree of hyperglycemia (420–500 mg/dl) without ketosis was generated by injection of 50 mg/kg i.v. STZ for young, lean rats and 30 mg/kg i.v. for older, fatter rats. The animals were killed 8–11 days after injection. Insulin binding by the isolated adipocytes of both groups was not significantly altered on a per-cell basis by the presence of diabetes. Total adipocyte glucose metabolism, both basal and insulin stimulated, was reduced (63 and 88%, respectively) by the induction of diabetes in young, lean rats. In contrast, the induction ofdiabetes in the older, moderately obese rats had no suppressive effect on total glucose metabolismby their fat cells. Diabetes increased the relative conversion of glucose to lactate by fat cells from both groups of rats, but in absolute terms, the fat cells from the obese diabetic rats produced significantly more lactate from glucose than cells from the lean diabetic rats, both in the absence and presence of insulin. Diabetes did not alter the glucose concentration at which peak insulin response occurred in either group. We conclude that STZ-D in rats, at different stages of development and degrees of adiposity, results in quantitatively different alterations of adipocyte metabolism, which appear to be postreceptor in nature and result in an increase in glucose conversion to lactate.