Adrenergic modulation of insulin secretion in vivo dependent on thyroid states.

Abstract

Insulin secretory responses via adrenergic mechanisms were studied in vivo with hyperthyroid rats prepared by daily injections with thyroxine and with rats rendered hypothyroid by the addition of methylthiouracil in the drinking water. Isoproterenol, a beta-adrenergic agent, caused hyperinsulinemia in hyperthyroid rats more markedly than in euthyroid rats, but failed to induce hyperinsulinemia in hypothyroid rats. The isoproterenol-induced hyperinsulinemia was abolished by a beta-adrenergic receptor blocker in hyperthyroid as well as in euthyroid rats. The glucose-induced hyperinsulinemia was enhanced in hyperthyroid, was not essentially affected in euthyroid, and was inhibited in hypothyroid rats, by an alpha- and beta-adrenergic agent such as epinephrine. It is concluded that the relative function of alpha- to beta-adrenergic receptors responsible for the pancreatic secretion of insulin is dependent on the thyroid state; beta-adrenergic actions are predominant over alpha-actions in hyperthyroidism and vice versa in hypothyroidism.