JOE
HOME HELP CONTACT US SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


Journal of Endocrinology (1994) 140, 327-332    DOI: 10.1677/joe.0.1400327
© 1994 Society for Endocrinology

This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Rolla, M
Right arrow Articles by Müller, E E
Right arrow Search for Related Content
PubMed
Right arrow Articles by Rolla, M
Right arrow Articles by Müller, E E

Corticotrophin-releasing hormone does not inhibit growth hormone-releasing hormone-induced release of growth hormone in control subjects but is effective in patients with eating disorders

M Rolla, A Andreoni, D Bellitti, M Ferdeghini, E Ghigo and E E Müller

Previous studies have shown that corticotrophin-releasing hormone (CRH) inhibits GH secretion in response to GH-releasing hormone (GHRH) in normal women and men, and animal studies suggest that this effect is mediated by an increased release of somatostatin from the hypothalamus. It has been reported that there are abnormalities in the neuroendocrine regulation of the hypothalamo-pituitary-somatotrophic axis and the hypothalamo-pituitary-adrenocortical axis in patients with eating disorders. The present study therefore investigated the ability of CRH to inhibit the GH response to GHRH in eight young women with anorexia nervosa (AN) and in seven young women with eating disorders which were not otherwise specified (NOS). We also compared the effect of CRH in the patients with the response it caused in ten control women. In contrast to a previous report, combined i.v. administration of 50 µg human CRH (hCRH) and 50 µg GHRH(1–29) caused a GH response in control women which was higher, although not significantly so, than that induced by GHRH alone (area under the curve (AUC) 988·5 ±506·0 compared with 1568·4 ±795·6 (S.E.M.) ng/ml per 120 min for GHRH alone and GHRH plus hCRH respectively).

Conversely, the administration of hCRH given together with GHRH markedly inhibited the GH response induced by the latter in both AN patients (AUC 2253·0 ±385·7 compared with 1224·4 ±265·7 ng/ml per 120 min for GHRH and GHRH plus hCRH respectively; P<0·005 and NOS patients (AUC 2827·4±281·1 compared with 308·5 ± 183·4 ng/ml per 120 min for GHRH and GHRH plus hCRH respectively; P<0·0001). These results (1) refute the suggestion that there is an inhibitory influence of CRH over GH secretion under normal conditions, (2) indicate that this inhibitory influence exists in patients with eating disorders, and (3) imply that, in the latter, hypothalamic somatostatinergic function is, at least in part, preserved.

Journal of Endocrinology (1994) 140, 327–332




This article has been cited by other articles:


Home page
Physiol. Rev.Home page
E. E. Muller, V. Locatelli, and D. Cocchi
Neuroendocrine Control of Growth Hormone Secretion
Physiol Rev, April 1, 1999; 79(2): 511 - 607.
[Abstract] [Full Text] [PDF]




HOME HELP CONTACT US SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 1994 by the Society for Endocrinology.