High-fat diet-induced obesity ablates gastric vagal afferent circadian rhythms

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dc.contributor.authorKentish, S.J.
dc.contributor.authorVincent, A.D.
dc.contributor.authorKennaway, D.J.
dc.contributor.authorWittert, G.A.
dc.contributor.authorPage, A.J.
dc.date.issued2016
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 obesity
dc.description.statementofresponsibilityStephen J. Kentish, Andrew D. Vincent, David J. Kennaway, Gary A. Wittert, and Amanda J. Page
dc.identifier.citationJournal of Neuroscience, 2016; 36(11):3199-3207
dc.identifier.doi10.1523/JNEUROSCI.2710-15.2016
dc.identifier.issn0270-6474
dc.identifier.issn1529-2401
dc.identifier.orcidKentish, S.J. [0000-0002-5479-2643]
dc.identifier.orcidVincent, A.D. [0000-0002-6428-1070]
dc.identifier.orcidKennaway, D.J. [0000-0002-5864-3514]
dc.identifier.orcidWittert, G.A. [0000-0001-6818-6065]
dc.identifier.orcidPage, A.J. [0000-0002-7086-5865]
dc.identifier.urihttp://hdl.handle.net/2440/100163
dc.language.isoen
dc.publisherSociety for Neuroscience
dc.relation.granthttp://purl.org/au-research/grants/nhmrc/1046289
dc.relation.granthttp://purl.org/au-research/grants/nhmrc/1091586
dc.rightsCopyright © 2016 the authors. Authors grant JNeurosci a license to publish their work and copyright remains with the author. For articles published after 2014, the Society for Neuroscience (SfN) retains an exclusive license to publish the article for 6 months; after 6 months, the work becomes available to the public to copy, distribute, or display under the terms of the Creative Commons Attribution 4.0 International License (CC-BY). This license allows data and text mining, use of figures in presentations, and posting the article online, provided that the original article is credited.
dc.source.urihttps://doi.org/10.1523/jneurosci.2710-15.2016
dc.subjectCircadian; food intake; leptin; obesity; stomach; vagus
dc.titleHigh-fat diet-induced obesity ablates gastric vagal afferent circadian rhythms
dc.typeJournal article
pubs.publication-statusPublished

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