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Effect of Dexamethasone and Cortisone on Insulin Receptors in Normal Human Male^*

ROBERTO DE PIRRO, ALDO BERTOLI, ANGELO FUSCO, IVANO TESTA, ALDO V. GRECO and RENATO LAURO

Seconda Clinica Medica, Policlinico Umberto 1°, 00161 Roma, Italy

Address all correspondence and requests for reprints to: Roberto De Pirro, M.D.,2nd Clinica Medica, Policlinico Umberto 1°, Viale del Policlinico, 00161 Roma, Italy.

Results of a recent study suggested that depending upon the glucocorticoid or the model used, opposite changes occur in insulin binding; in fact, the increase in insulin receptor number on monocytes after prednisone ingestion in man appears to contrast with previous reports in animals in which a decrease was shown after dexamethasone. To establish whether this apparent discrepancy depends upon the model used in human studies (i.e. monocytes), the effect of dexamethasone and cortisone intake on normal men was evaluated.

A significant decrease was observed in insulin binding on circulating monocytes 24,48,and 72 h after both steroids, mainly due to reduced receptor affinity. Furthermore, steroid treatment increased insulinemia which did not appear to be related to insulin binding.

These data are in agreement with results in animal studies and appear to suggest that previous data on prednisone do not depend upon the model used (i.e. monocytes) but upon the hormone itself, thus indicating that glucocorticoids, depending upon their chemical structure, may produce opposite changes in membrane insulin binding sites. Furthermore, since dexamethasone and cortisone affect plasma insulin levels in the same fashion as previously reported with prednisone, it is suggested that the variation in insulin binding observed after glucocorticoid treatment is not due to variations in insulinemia.

^* This work was supported in part by a grant from ISIS, sezione scientifica.

Present address: Clinica Medica, Universita di Ancona, Ancona, Italy.

Received January 11, 1980.

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