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Effects of Chronic Glucocorticoid Excess in Man on Insulin Binding to Circulating Cells: Differences between Endogenous and Exogenous Hypercorticism

Diabetes Branch, National Institute of Arthritis, Diabetes, Digestive, and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20205

Address all correspondence and requests for reprints to: Dr. Jesse Roth, Chief, Diabetes Branch, National Institute of Arthritis, Diabetes, Digestive, and Kidney Diseases, Building 10, Room 8-South-243, National Institutes of Health, Bethesda, Maryland 20205.

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 increased in all patients. Analysis of binding data indicated that increased binding in patients treated with prednisone was due to an increase 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. (J Clin Endocrinol Metab 56: 1169,1983)

^* Present address: Chair of Metabolic Diseases, University of Verona, Policlinico Borgo Roma, Verona, Italy.

Received April 3, 1980.