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

The effect of β-adrenergic stimulation on insulin binding was studied in human fat cells in vitro. Isoproterenol rapidly (∼ 5 min) reduced insulin binding through a β-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 ∼ 10 min) and other β-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<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, β-adrenergic stimulation, both in vitro and in vivo, leads to a decreased number of binding sites for insulin in human fat cells.