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The effect of beta-adrenergic stimulation on insulin binding was studied in human fat cells in vitro. Isoproterenol rapidly (approximately 5 min) reduced insulin binding through a beta-adrenergic and dose-dependent mechanism. The reduced binding was enhanced by the addition of adenosine deaminase and was also elicited by the addition of dibutyryl cAMP. This effect was due to a decreased number of binding sites. The reduction was rapidly reversed by propranolol (t1/2 approximately 10 min) and other beta-adrenoreceptor blocking agents. Insulin binding was also measured in fat cells from 6 patients with a phaeochromocytoma. A significant negative correlation between tracer binding and the log value of total urinary catecholamine excretion was found (r = -0.821, p less than 0.05). Mean tracer insulin binding was reduced about 30% as compared to cells from 16 carefully matched control subjects. Decreased insulin binding was again mainly attributable to a decreased number of binding sites. Thus, beta-adrenergic stimulation, both in vitro and in vivo, leads to a decreased number of binding sites for insulin in human fat cells.

diabetologia

Reduced insulin binding to human fat cells following beta-adrenergic stimulation ? experimental evidence and studies in patients with a phaeochromocytoma