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Endocrinology Vol. 140, No. 1 310-317
Copyright © 1999 by The Endocrine Society

ARTICLES

Glucocorticoid Replacement, but not Corticotropin-Releasing Hormone Deficiency, Prevents Adrenalectomy-Induced Anorexia in Mice1

Lauren Jacobson

Division of Endocrinology, Department of Medicine, Harvard Medical School, Boston, Massachusetts 02115

Address all correspondence and requests for reprints to: Dr. Lauren Jacobson, Division of Endocrinology, Children’s Hospital, 300 Longwood Avenue, Boston, Massachusetts 02115. E-mail: jacobson{at}a1.tch.harvard.edu

There is considerable evidence that CRH can suppress food intake. As hypothalamic CRH, a main site of CRH expression, is also negatively regulated by glucocorticoids, it is unclear whether anorexia and weight loss in adrenal insufficiency are attributable to elevated CRH or to decreased glucocorticoid levels. To distinguish these possibilities, we have measured food intake and body weight in wild-type and CRH-deficient mice after sham adrenalectomy (Sham ADX) or adrenalectomy (ADX) with and without corticosterone (B) replacement. CRH deficiency neither increased basal food intake and body weight nor attenuated decreases in food intake after ADX or Sham ADX. B replacement producing plasma levels above the circadian peak completely blocked ADX-induced decreases in feeding and body weight in all mice and frequently stimulated food intake in CRH-deficient mice. Plasma levels of insulin and leptin, two other hormones involved in appetite regulation, did not differ between genotypes; however, the relationship between food intake and circulating leptin was significantly less negative at B doses that preserved appetite. B replacement levels slightly below circadian peak concentrations did not prevent hypophagia after ADX. We conclude that factors other than or in addition to CRH are more important in mediating appetite responses to adrenalectomy.




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