Differential Roles of Each Orexin Receptor Signaling in Obesity

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dc.contributor.authorKakizaki, Miyoko
dc.contributor.authorTsuneoka, Yousukeko
dc.contributor.authorTakase, Kenkichiko
dc.contributor.authorKim, Staci Jakyongko
dc.contributor.authorChoi, Jinhwanko
dc.contributor.authorIkkyu, Ayako
dc.contributor.authorAbe, Manabuko
dc.contributor.authorSakimura, Kenjiko
dc.contributor.authorYanagisawa, Masashiko
dc.contributor.authorFunato, Hiromasako
dc.date.accessioned2024-04-24T03:00:15Z-
dc.date.available2024-04-24T03:00:15Z-
dc.date.created2024-04-24-
dc.date.created2024-04-24-
dc.date.created2024-04-24-
dc.date.created2024-04-24-
dc.date.issued2019-10-
dc.identifier.citationISCIENCE, v.20, pp.1 - 13-
dc.identifier.issn2589-0042-
dc.identifier.urihttp://hdl.handle.net/10203/319221-
dc.description.abstractOrexins are hypothalamic neuropeptides that regulate feeding, energy expenditure, and sleep. Although orexin-deficient mice are susceptible to obesity, little is known about the roles of the orexin receptors in long-term energy metabolism. Here, we performed the metabolic characterization of orexin receptor-deficient mice. Ox1r-deficient mice were resistant to diet-induced obesity, and their food intake was similar between chow and high-fat food. Ox2r-deficient mice exhibited less energy expenditure than wild-type mice when fed a high-fat diet. Neither Ox1r-deficient nor Ox2r-deficient mice showed body weight gain similar to orexin-deficient mice. Although the presence of a running wheel suppressed diet-induced obesity in wild-type mice, the effect was weaker in orexin neuron-ablated mice. Finally, we did not detect abnormalities in brown adipose tissues of orexin-deficient mice. Thus, each orexin receptor signaling has a unique role in energy metabolism, and orexin neurons are involved in the interactive effect of diet and exercise on body weight gain.-
dc.languageEnglish-
dc.publisherCELL PRESS-
dc.titleDifferential Roles of Each Orexin Receptor Signaling in Obesity-
dc.typeArticle-
dc.identifier.wosid000493388000001-
dc.identifier.scopusid2-s2.0-85072344335-
dc.type.rimsART-
dc.citation.volume20-
dc.citation.beginningpage1-
dc.citation.endingpage13-
dc.citation.publicationnameISCIENCE-
dc.identifier.doi10.1016/j.isci.2019.09.003-
dc.contributor.localauthorKim, Staci Jakyong-
dc.contributor.nonIdAuthorKakizaki, Miyo-
dc.contributor.nonIdAuthorTsuneoka, Yousuke-
dc.contributor.nonIdAuthorTakase, Kenkichi-
dc.contributor.nonIdAuthorChoi, Jinhwan-
dc.contributor.nonIdAuthorIkkyu, Aya-
dc.contributor.nonIdAuthorAbe, Manabu-
dc.contributor.nonIdAuthorSakimura, Kenji-
dc.contributor.nonIdAuthorYanagisawa, Masashi-
dc.contributor.nonIdAuthorFunato, Hiromasa-
dc.description.isOpenAccessN-
dc.type.journalArticleArticle-
dc.subject.keywordPlusDIET-INDUCED OBESITY-
dc.subject.keywordPlusFOOD-CONSUMPTION-
dc.subject.keywordPlusKNOCKOUT MICE-
dc.subject.keywordPlusNARCOLEPSY-
dc.subject.keywordPlusNEURONS-
dc.subject.keywordPlusANTAGONIST-
dc.subject.keywordPlusSLEEP-
dc.subject.keywordPlusDYSFUNCTION-
dc.subject.keywordPlusHYPOCRETIN-
dc.subject.keywordPlusADDICTION-
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