Journal of Clinical Endocrinology & Metabolism, Vol 55, 910-915, Copyright © 1982 by Endocrine Society

ARTICLES

Hypercortisolism and insulin resistance: comparative effects of prednisone, hydrocortisone, and dexamethasone on insulin binding of human erythrocytes

K Yasuda, E Hines 3d and AE Kitabchi

We have studied the effects of 3 days of hydrocortisone (30 mg every 8 h), dexamethasone (1 mg every 8 h), and prednisone (7.5 mg every 8 h) ingestion on glucose intolerance and insulin resistance in three groups of lean normal volunteers and compared these parameters to specific insulin binding in erythrocytes. All three glucocorticoids caused significant reduction of glucose tolerance as assessed by glucose and insulin areas under oral glucose tolerance text curves and insulin sensitivity in response to 0.1 U insulin/kg BW, iv. Although both hydrocortisone and dexamethasone caused significant reduction in insulin binding compared to that during the pretreatment period (11.0 +/- 0.7 vs. 9.0 +/- 0.5% (P less than 0.01) and 11.8 +/- 0.7 vs. 9.0 +/- 0.5% (P less than 0.05), respectively), prednisone ingestion did not significantly alter insulin binding (10.6 +/- 0.6 before vs. 9.4 +/- 0.5% after). Decreased insulin binding with hydrocortisone and dexamethasone was caused by decreased binding affinity rather than by a decreased number of receptors. In two subjects in whom receptor binding was measured daily for 3 days during prednisone (one subject) or hydrocortisone (one subject) ingestion, the inhibition of binding was highest on the first day, with subsequent reduction of this inhibited binding toward normal by the third day. We conclude that although hydrocortisone, dexamethasone, and prednisone all cause deterioration of glucose tolerance and decreased insulin sensitivity, only hydrocortisone and dexamethasone exhibit significant decreases in insulin binding to erythrocytes. This decreased binding is not due to changes in receptor numbers but to decreased affinity brought about by hyperinsulinemia. Prednisone ingestion caused significant insulin resistance with an insignificant decrease in insulin binding. We believe that other mechanisms, such as alteration of postreceptor events, may play a major role in the induction of insulin resistance in hypercortisolism in man.

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