Effect of short- and long-term experimental hyperthyroidism on plasma glucose level and insulin secretion during an intravenous glucose load and on insulin binding, insulin receptor kinase activity, and insulin action in adipose tissue.

Glucose disposal, insulin secretion, and insulin action in adipose tissue were measured in rats treated for 10 or 30 days with high doses of thyroxine (T4). Acutely induced hyperthyroidism produced a high rate of glucose disposal after an intravenous glucose tolerance test (IVGTT), accompanied by a high glucose-stimulated insulin secretion. In addition, in these rats the following phenomena were observed: (1) high insulin binding to isolated adipocytes due to an increase in the insulin receptor number; (2) high insulin binding to partially purified fat insulin receptors; (3) normal tyrosine kinase activity of fat insulin receptors; and (4) high insulin action in isolated adipocytes, such as glucose transport and lipogenesis. Chronically induced hyperthyroidism produced high rates of glucose disposal after an IVGTT, accompanied by an increase of basal and glucose-stimulated insulin secretion. These rats showed (1) normal insulin binding to either isolated adipocytes or partially purified insulin receptors; (2) normal tyrosine kinase activity of fat insulin receptors; (3) normal insulin action in isolated adipocytes. In conclusion, exogenous hyperthyroidism induced an increase in glucose disposal, probably due in part to high insulin secretion. In short-term T4-treated rats an additional increase of insulin action in adipocytes was also observed.