Decreased<i>β</i>- Adrenergic Receptors in Rat Heart in Streptozotocin-Induced Diabetes: Role of Thyroid Hormones^*

TLDR

The study aimed to determine how streptozotocin‑induced diabetes alters β‑adrenergic receptor‑coupled adenylate cyclase activity in rat heart. This was investigated by examining rat heart particulate fractions. Streptozotocin‑induced diabetes reduced myocardial β‑adrenergic receptor numbers by 34% and slightly lowered cAMP production, but insulin or l‑T4 restored receptor levels; the effect appears mediated by thyroid hormones, as thyroidectomy abolished the diabetes‑induced receptor loss. Endocrinology 1984;114:1358.

Abstract

The effect of streptozotocin-induced diabetes on the β-adrenergic receptor-coupled adenylate cyclase was studied in rat heart particulate fractions. Streptozotocin treatment decreased the number of myocardial β-adrenergic receptors by 34% with no change in the apparent affinity of these receptors for [3H]dihydroalprenolol. The maximal isoproterenol-activated accumulation of cAMP in steptozotocin-treated rat hearts was decreased by only 10%. Insulin administration to streptozotocin-treated rats increased the number of myocardial β-adrenergic receptors to near or above control levels. Administration of l-T4 to streptozotocintreated rats had the same effect. Total T4, free T4) and total T3 levels were all significantly decreased in the diabetic animals. Administration of insulin to streptozotocin-treated rats increased the serum thyroid hormone levels toward or above the levels found in control animals. Streptozotocin-induced diabetes had no significant effect on cardiac β-adrenergic receptor number in thyroidectomized rats. Insulin did not elevate cardiac β-adrenergic receptor number in thyroidectomized diabetic rats. The decrease in the number of myocardial β-adrenergic receptors occurring in diabetes mellitus is probably mediated through thyroid hormones. (Endocrinology114: 1358, 1984)