کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
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2008107 | 1066397 | 2008 | 6 صفحه PDF | دانلود رایگان |
![عکس صفحه اول مقاله: Corticotropin-releasing factor (CRF) is involved in the acute anorexic effect of α-melanocyte-stimulating hormone: A study using CRF-deficient mice Corticotropin-releasing factor (CRF) is involved in the acute anorexic effect of α-melanocyte-stimulating hormone: A study using CRF-deficient mice](/preview/png/2008107.png)
Alpha-melanocyte-stimulating hormone (α-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 α-MSH. In the present study, we examined whether CRF and its receptors are involved in the anorexic effect of α-MSH, using CRF-deficient (CRFKO) mice and a CRF receptor antagonist. Intracerebroventricular administration of NDP-MSH, a synthetic α-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 α-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 NDP-MSH-treated mice. Therefore, our findings, using CRFKO, strongly support evidence that CRF is involved in the acute anorexic effect of α-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 α-MSH-induced suppression of food intake at late phase was independent of glucocorticoids and CRF.
Journal: Peptides - Volume 29, Issue 12, December 2008, Pages 2169–2174