Effects of chronic glucocorticoid excess in man on insulin binding to circulating cells: differences between endogenous and exogenous hypercorticism.
We measured [125I]insulin binding to circulating monocytes or erythrocytes from 16 patients with chronic glucocorticoid excess, 9 chronically treated with prednisone and 7 with adrenocortical hyperfunction. With monocytes, [125I]insulin binding was iincreased in all patients. Analysis of binding data indicated that increased binding in patients treated with prednisone was due to an ncrease in receptor concentration, whereas in patients with adrenocortical hyperfunction, it was due to an increase in receptor affinity. With erythrocytes from patients with adrenocortical hyperfunction there was an increase in receptor affinity and a decrease in receptor concentration, so that the binding of [125I]insulin was normal. The disparity of results between endogenous and exogenous hypercorticism, between the two cell types, and between the present studies and previous studies suggest that the effects of glucocorticoid excess on the insulin receptor are extremely complex and wide-ranging and that in this condition, extrapolations in humans from data with circulating cells to liver and muscle may not be appropriate.
D000293:Adolescent; D000308:Adrenocortical Hyperfunction / Q000378:metabolism*; D000328:Adult; D001773:Blood Cells / Q000378:metabolism*; D004912:Erythrocytes / Q000378:metabolism; D005260:Female; D005938:Glucocorticoids / Q000378:metabolism* / Q000494:pharmacology; D006801:Humans; D007328:Insulin / Q000378:metabolism*; D008297:Male; D008875:Middle Aged; D008954:Models, Biological; D009000:Monocytes / Q000378:metabolism; D011241:Prednisone / Q000494:pharmacology; D011972:Receptor, Insulin / Q000032:analysis / Q000187:drug effects / Q000378:metabolism*; D011965:Receptors, Glucocorticoid / Q000378:metabolism
D005938:Glucocorticoids; D007328:Insulin; D011965:Receptors, Glucocorticoid; D011972:Receptor, Insulin; D011241:Prednisone