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Steroidogenic Factor-1 Is Essential for Compensatory Adrenal Growth Following Unilateral Adrenalectomy

Division of Endocrinology and Metabolism (F.B., C.M., D.L.B., G.D.H.), Department of Internal Medicine, University of Michigan, Ann Arbor, Michigan 48109-0678; Departments of Surgery and Neuroscience (Y.M.U.-L., W.C.E.), University of Minneapolis, Minneapolis, Minnesota 55455; and Division of Genetics (C.K.), Department of Pediatrics, University of Michigan, Ann Arbor, Michigan 48109-0318

Address all correspondence and requests for reprints to: Gary D. Hammer, M.D., Ph.D., Division of Endocrinology and Metabolism, Department of Internal Medicine, 5560A MSRB II, 1150 West Medical Center Dr, University of Michigan, Ann Arbor, Michigan 48109-0678. E-mail: . ghammer{at}umich.edu

While the orphan nuclear receptor steroidogenic factor-1 (SF-1) has been shown to function as an induction factor to define adrenocortical cell lineage, it remains unclear whether SF-1 plays an additional role as a growth promoting agent in the adult adrenal cortex. The proliferative potential of the adrenal cortex in adult SF-1^+/- mice was examined using the model of compensatory adrenal growth following unilateral adrenalectomy (uADX). While the right adrenal gland of wild-type (wt) mice grew significantly after uADX, the adrenal of SF-1^+/- mice exhibited a blunted, statistically nonsignificant weight increase. Accordingly, a profound increase in the proliferation marker proliferating cell nuclear antigen could be detected only in wt mice after uADX but not in the SF-1^+/- mice. The proposed key regulator in adrenal compensatory growth, the recently cloned adrenal secretory serine protease was up-regulated in the remaining adrenal of wt mice, whereas this increase was blunted in SF-1^+/- mice. While no differences in preadipocyte factor-1, the presumed marker of primitive adrenocortical cells, were detectable in the adrenals of wt and SF-1^+/- mice, an increase in the ACTH receptor as well as agouti-related protein was observed only in wt animals but not in the SF-1^+/- mice following uADX. Taken together, these results reflect a primary inability of adrenal cortical cells of SF-1^+/- mice to undergo compensatory adrenal growth in response to uADX.

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