Insulin Sensitivity In Obese Rats Research Articles

Effect of adrenalectomy on in vivo glucose metabolism in insulin resistant Zucker obese rats.

Lean (Fa/?) and obese (fa/fa) Zucker rats were adrenalectomized (ADX) in order to assess the contribution of adrenal hormones to insulin resistance of the obese Zucker rat. Glucose utilization was measured using an insulin suppression test. Sham-operated obese rats gained almost twice as much weight as sham-operated lean littermates. However, body weight gain of ADX animals was comparable in both genotypes. It was significantly less than that of the respective sham-operated controls. Body weight differences can be accounted for almost entirely by a marked loss of adipose tissue. Although insulin resistance may be attributable to obesity in part, steroid hormones are thought to be directly antagonistic to insulin for glucose metabolism. Adrenalectomy resulted in a decrease in serum glucose concentrations for both lean and obese Zucker rats compared with their respective sham-operated groups. Serum insulin concentration of lean ADX rats was 23% of sham-operated controls; in obese ADX rats, it was 9% of controls. Elevated levels of steady state serum glucose (SSSG) levels in sham-operated obese rats demonstrate a marked resistance to insulin induced glucose uptake compared with sham-operated lean animals. Adrenalectomy caused a marked improvement in insulin sensitivity of obese rats. The hyperglycemic SSSG levels of the obese rats were reduced 2.5 times by ADX. These results indicate that insulin resistance of Zucker obese rats can be ameliorated by ADX, suggesting adrenal hormones contribute to insulin resistance in these animals.

Insulin sensitivity and carbohydrate metabolism of rats with hypothalamic obesity.

SUMMARY A fixed dose of glucose, irrespective of body weight, used for i.v. glucose tolerance tests in rats with hypothalamic obesity and in non-obese control rats caused almost identical blood glucose increments in both kinds of rats, and the K values (coefficients of glucose assimilation) were not significantly different. Glucose doses proportional to body weight caused much larger increments of blood glucose in the obese animals but the K value was not significantly different from that for the controls. On the other hand, the insulin sensitivity of obese rats was found to be less than that of control rats when a fixed dose of the hormone was given. When the insulin dosage was proportional to body weight, the fall of fasting blood glucose produced in the obese animals was not significantly different from that in the control group. In vitro, the diaphragm muscle of the obese animals was insensitive to the action of insulin as compared with controls. There was no evidence of insulin insensitivity of the obese animals' adipose tissue; the very low metabolic activity of the adipose tissue of both the control and obese animals may have been responsible. The interpretation of these findings is discussed in the light of similar work in human obesity.