Journal
PEPTIDES
Volume 29, Issue 12, Pages 2169-2174Publisher
ELSEVIER SCIENCE INC
DOI: 10.1016/j.peptides.2008.09.010
Keywords
Melanocyte-stimulating hormone; Corticotropin-releasing factor; Feeding; Anorexia
Funding
- Ministry of Education, Science and Culture of Japan [18591014]
- Grants-in-Aid for Scientific Research [18591014] Funding Source: KAKEN
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Alpha-melanocyte-stimulating hormone (alpha-MSH) and its receptors are critical and indispensable for maintaining appropriate feeding behavior and energy homeostasis in both mice and humans. Corticotropin-releasing factor (CRF) is a candidate for mediating the anorexic effect of alpha-MSH. In the present study, we examined whether CRF and its receptors are involved in the anorexic effect of alpha-MSH, using CRF-deficient (CRFKO) mice and a CRF receptor antagonist. Intracerebroventricular administration of NDP-MSH, a synthetic alpha-MSH analogue, suppressed food intake in wild-type (WT) mice. This effect was abolished by pretreatment with a non-selective CRF receptor antagonist, astressin, suggesting that the effect of alpha-MSH-induced anorexia was mediated by a CRF receptor. In CRFKO mice, administration with NDP-MSH did not affect food intake at an early phase (0-4 h). In addition, CRF mRNA levels in the hypothalamus were significantly increased in NDPMSH-treated mice. Therefore, our findings, using CRFKO, strongly support evidence that CRF is involved in the acute anorexic effect of alpha-MSH. On the other hand, NDP-MSH administered to CRFKO mice led to suppressed food intake at the late phase (4-12 h), similar to the effect in WT mice. Further, NDP-MSH similarly reduced food intake during the late phase in all types of mice, including WT, CRFKO, and CRFKO with corticosterone replacement. The results would suggest that a-MSH-induced suppression of food intake at late phase was independent of glucocorticoids and CRF. (c) 2008 Elsevier Inc. All rights reserved.
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