Please use this identifier to cite or link to this item: http://hdl.handle.net/2440/100163
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dc.contributor.authorKentish, S.en
dc.contributor.authorVincent, A.en
dc.contributor.authorKennaway, D.en
dc.contributor.authorWittert, G.en
dc.contributor.authorPage, A.en
dc.date.issued2016en
dc.identifier.citationJournal of Neuroscience, 2016; 36(11):3199-3207en
dc.identifier.issn0270-6474en
dc.identifier.issn1529-2401en
dc.identifier.urihttp://hdl.handle.net/2440/100163-
dc.description.abstractRats with high-fat diet (HFD)-induced obesity increase daytime eating, suggesting an alteration in circadian food intake mechanisms. Gastric vagal afferents (GVAs) respond to mechanical stimuli to initiate satiety. These signals are dampened in HFD mice and exhibit circadian variations inversely with food intake in lean mice. Furthermore, leptin shows circadian variation in its circulating level and is able to modulate GVA mechanosensitivity. However, whether leptin's ability to modulate GVAs occurs in a circadian manner is unknown. Therefore, we investigated whether changes in the circadian intake of food in HFD-induced obesity is associated with a disruption in GVA circadian rhythms. Eight-week-old male C57BL/6 mice were fed a standard laboratory diet (SLD) or a HFD for 12 weeks. A subgroup of SLD and HFD mice were housed in metabolic cages. After 12 weeks, ex vivo GVA recordings were taken at 3 h intervals starting at zeitgeber time 0 (ZT0) and stomach content was measured. After 12 weeks, HFD mice consumed more food during the light phase through larger and more frequent meals compared with SLD mice. SLD mice exhibited circadian fluctuation in stomach content, which peaked at ZT18 and reached a nadir at ZT9. At these time points, both tension and mucosal receptor mechanosensitivity were the lowest and highest, respectively. HFD mice exhibited little circadian variation in stomach content or GVA mechanosensitivity. Leptin potentiated mucosal receptor mechanosensitivity only in SLD mice and with reduced potency during the dark phase. In conclusion, loss of circadian variation in GVA signaling may underpin changes in eating behavior in HFD-induced obesityen
dc.description.statementofresponsibilityStephen J. Kentish, Andrew D. Vincent, David J. Kennaway, Gary A. Wittert, and Amanda J. Pageen
dc.language.isoenen
dc.publisherSociety for Neuroscienceen
dc.rightsCopyright © 2016 the authorsen
dc.subjectCircadian; food intake; leptin; obesity; stomach; vagusen
dc.titleHigh-fat diet-induced obesity ablates gastric vagal afferent circadian rhythmsen
dc.typeJournal articleen
dc.identifier.rmid0030045397en
dc.identifier.doi10.1523/JNEUROSCI.2710-15.2016en
dc.relation.granthttp://purl.org/au-research/grants/nhmrc/1046289en
dc.relation.granthttp://purl.org/au-research/grants/nhmrc/1091586en
dc.identifier.pubid239998-
pubs.library.collectionMedicine publicationsen
pubs.library.teamDS14en
pubs.verification-statusVerifieden
pubs.publication-statusPublisheden
dc.identifier.orcidKennaway, D. [0000-0002-5864-3514]en
dc.identifier.orcidWittert, G. [0000-0001-6818-6065]en
dc.identifier.orcidPage, A. [0000-0002-7086-5865]en
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