title: Neuromedin U-induced anorexigenic action is mediated by the corticotropin-releasing hormone receptor-signaling pathway in goldfish.
abstract: Our recent research has indicated that neuromedin U (NMU) orthologs exist in goldfish, and that NMU consisting of 21 amino acid residues (NMU-21) can potently inhibit food intake in goldfish, as is the case in rodents. However, the anorexigenic pathway of NMU-21 has not yet been clarified in this species. Corticotropin-releasing hormone (CRH), CRH-related peptides and alpha-melanocyte-stimulating hormone (alpha-MSH), which exert potent anorexigenic effects, are important mediators involved in feeding regulation in fish. We examined whether CRH or alpha-MSH mediates NMU-21-induced anorexigenic action in goldfish. We first investigated the effect of intracerebroventricular (ICV) administration of NMU-21 at 100 pmol/g body weight (BW), which is enough to suppress food intake, on expression levels of mRNA for CRH and proopiomelanocortin (POMC) in the hypothalamus. ICV-injected NMU-21 induced a significant increase in the expression level of CRH mRNA, but not that of POMC mRNA. We also examined the effects of ICV administration of the CRH 1/2 receptor antagonist, alpha-helical CRH((9-41)), and the melanocortin 4 receptor antagonist, HS024, on the anorexigenic action of ICV-injected NMU-21. The anorexigenic effect of NMU-21 was blocked by treatment with alpha-helical CRH((9-41)) at 400 pmol/g BW, but not HS024 at 200 pmol/g BW. These results suggest that the anorexigenic action of NMU-21 is mediated by the CRH 1 or 2 receptor-signaling pathway in goldfish.
authors.affiliation: Laboratory of Regulatory Biology, Graduate School of Science and Engineering, University of Toyama, 3190-Gofuku, Toyama 930-8555, Japan.
authors.forename: Keisuke
authors.initials: K
authors.lastname: Maruyama
authors.forename: Kohei
authors.initials: K
authors.lastname: Wada
authors.forename: Kotaro
authors.initials: K
authors.lastname: Ishiguro
authors.forename: Sei-Ichi
authors.initials: S
authors.lastname: Shimakura
authors.forename: Tatsuya
authors.initials: T
authors.lastname: Wakasugi
authors.forename: Minoru
authors.initials: M
authors.lastname: Uchiyama
authors.forename: Seiji
authors.initials: S
authors.lastname: Shioda
authors.forename: Kouhei
authors.initials: K
authors.lastname: Matsuda
mesh_terms: D000818:Animals; D001067:Appetite Depressants / Q000494:pharmacology*; D003346:Corticotropin-Releasing Hormone / Q000235:genetics / Q000494:pharmacology; D006054:Goldfish; D006727:Hormone Antagonists / Q000494:pharmacology; D009479:Neuropeptides / Q000494:pharmacology; D011333:Pro-Opiomelanocortin / Q000235:genetics; D018019:Receptors, Corticotropin-Releasing Hormone / Q000037:antagonists & inhibitors / Q000378:metabolism*; D015398:Signal Transduction / Q000187:drug effects*; D000521:alpha-MSH / Q000378:metabolism
chemical_list: D001067:Appetite Depressants; D006727:Hormone Antagonists; D009479:Neuropeptides; D018019:Receptors, Corticotropin-Releasing Hormone; C069206:alpha helical corticotropin-releasing hormone; C056900:neuromedin U; D000521:alpha-MSH; D011333:Pro-Opiomelanocortin; D003346:Corticotropin-Releasing Hormone