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
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