Abstract
The beta effects of catecholamines are potentiated by thyroid hormones in adipose tissue. In the liver of hypothyroid rats there is an elevation in the number of beta-adrenergic receptors and the ability of catecholamines to increase cyclic AMP accumulation. Just the opposite effect is noted in adipose tissue of hypothyroid rats where there is a marked reduction in the ability of beta catecholamines to elevate cyclic AMP. Thyroid hormones do not appear to regulate the number of binding sites for beta adrenergic antagonists in adipose tissue but do affect agonist displacement of antagonist binding. The major influence of thyroid status on cyclic AMP metabolism in rat adipocytes is mediated through regulation of the ability of lipolytic hormones and even guanine nucleotides to activate adenylate cyclase. In neither liver or adipose tissue is there any evidence that thyroid hormones affect adrenoceptor interconversion. Thyroid status did not affect the alpha-I adrenergic stimulation of glycogenolysis in rat hepatocytes or the alpha-I adrenergic inactivation of glycogen synthase and stimulation of phosphatidylinositol turnover in rat adipocytes. There was also no effect of thyroid hormones on alpha-2 adrenergic inactivation of adenylate cyclase in hamster adipocytes. In these tissues thyroid hormones affect beta adrenergic responses without affecting either alpha-I or alpha-2 responses.
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