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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
5
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pubmed:dateCreated |
2009-11-3
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pubmed:abstractText |
The hypothalamic paraventricular nucleus (PVN) functions as a center to integrate various neuronal activities for regulating feeding behavior. Nesfatin-1, a recently discovered anorectic molecule, is localized in the PVN. However, the anorectic neural pathway of nesfatin-1 remains unknown. Here we show that central injection of nesfatin-1 activates the PVN and brain stem nucleus tractus solitarius (NTS). In the PVN, nesfatin-1 targets both magnocellular and parvocellular oxytocin neurons and nesfatin-1 neurons themselves and stimulates oxytocin release. Immunoelectron micrographs reveal nesfatin-1 specifically in the secretory vesicles of PVN neurons, and immunoneutralization against endogenous nesfatin-1 suppresses oxytocin release in the PVN, suggesting paracrine/autocrine actions of nesfatin-1. Nesfatin-1-induced anorexia is abolished by an oxytocin receptor antagonist. Moreover, oxytocin terminals are closely associated with and oxytocin activates pro-opiomelanocortin neurons in the NTS. Oxytocin induces melanocortin-dependent anorexia in leptin-resistant Zucker-fatty rats. The present results reveal the nesfatin-1-operative oxytocinergic signaling in the PVN that triggers leptin-independent melanocortin-mediated anorexia.
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pubmed:grant |
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Nov
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pubmed:issn |
1932-7420
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pubmed:author |
pubmed-author:DezakiKatsuyaK,
pubmed-author:DietrichMarcelo OMO,
pubmed-author:FujiwaraKenK,
pubmed-author:HashimotoKoushiK,
pubmed-author:HorvathTamas LTL,
pubmed-author:KohnoDaisukeD,
pubmed-author:KoikeMasatoM,
pubmed-author:MaejimaYukoY,
pubmed-author:MoriMasatomoM,
pubmed-author:NakataMasanoriM,
pubmed-author:Oh-IShinsukeS,
pubmed-author:OnakaTatsushiT,
pubmed-author:SedbazarUdvalU,
pubmed-author:ShimizuHiroyukiH,
pubmed-author:SuyamaShigetomoS,
pubmed-author:TakanoEisukeE,
pubmed-author:TanakaShigeyasuS,
pubmed-author:UchiyamaYasuoY,
pubmed-author:YadaToshihikoT,
pubmed-author:YashiroTakashiT,
pubmed-author:YoshidaNatsuN
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pubmed:issnType |
Electronic
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pubmed:volume |
10
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
355-65
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pubmed:meshHeading |
pubmed-meshheading:19883614-Animals,
pubmed-meshheading:19883614-Anorexia,
pubmed-meshheading:19883614-Autocrine Communication,
pubmed-meshheading:19883614-Leptin,
pubmed-meshheading:19883614-Melanocortins,
pubmed-meshheading:19883614-Mice,
pubmed-meshheading:19883614-Nerve Tissue Proteins,
pubmed-meshheading:19883614-Neuroendocrine Cells,
pubmed-meshheading:19883614-Oxytocin,
pubmed-meshheading:19883614-Paracrine Communication,
pubmed-meshheading:19883614-Paraventricular Hypothalamic Nucleus,
pubmed-meshheading:19883614-Pro-Opiomelanocortin,
pubmed-meshheading:19883614-Rats,
pubmed-meshheading:19883614-Rats, Zucker,
pubmed-meshheading:19883614-Signal Transduction,
pubmed-meshheading:19883614-Solitary Nucleus
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pubmed:year |
2009
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pubmed:articleTitle |
Nesfatin-1-regulated oxytocinergic signaling in the paraventricular nucleus causes anorexia through a leptin-independent melanocortin pathway.
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pubmed:affiliation |
Division of Integrative Physiology, Department of Physiology, Jichi Medical University School of Medicine, Shimotsuke, Tochigi 329-0498, Japan.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't,
Research Support, N.I.H., Extramural
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