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dc.contributor.authorWu, Zhaofei
dc.contributor.authorXu, Yuanzhong
dc.contributor.authorZhu, Yaming
dc.contributor.authorSutton, Amy K.
dc.contributor.authorZhao, Rongjie
dc.contributor.authorLowell, Bradford Barr
dc.contributor.authorOlson, David Paul
dc.contributor.authorTong, Qingchun
dc.date.accessioned2013-04-10T20:08:39Z
dc.date.issued2012
dc.identifier.citationWu, Zhaofei, Yuanzhong Xu, Yaming Zhu, Amy K. Sutton, Rongjie Zhao, Bradford B. Lowell, David P. Olson, and Qingchun Tong. 2012. An obligate role of oxytocin neurons in diet induced energy expenditure. PLoS ONE 7(9): e45167.en_US
dc.identifier.issn1932-6203en_US
dc.identifier.urihttp://nrs.harvard.edu/urn-3:HUL.InstRepos:10524337
dc.description.abstractOxytocin neurons represent one of the major subsets of neurons in the paraventricular hypothalamus (PVH), a critical brain region for energy homeostasis. Despite substantial evidence supporting a role of oxytocin in body weight regulation, it remains controversial whether oxytocin neurons directly regulate body weight homeostasis, feeding or energy expenditure. Pharmacologic doses of oxytocin suppress feeding through a proposed melanocortin responsive projection from the PVH to the hindbrain. In contrast, deficiency in oxytocin or its receptor leads to reduced energy expenditure without feeding abnormalities. To test the physiological function of oxytocin neurons, we specifically ablated oxytocin neurons in adult mice. Our results show that oxytocin neuron ablation in adult animals has no effect on body weight, food intake or energy expenditure on a regular diet. Interestingly, male mice lacking oxytocin neurons are more sensitive to high fat diet-induced obesity due solely to reduced energy expenditure. In addition, despite a normal food intake, these mice exhibit a blunted food intake response to leptin administration. Thus, our study suggests that oxytocin neurons are required to resist the obesity associated with a high fat diet; but their role in feeding is permissive and can be compensated for by redundant pathways.en_US
dc.language.isoen_USen_US
dc.publisherPublic Library of Scienceen_US
dc.relation.isversionofdoi:10.1371/journal.pone.0045167en_US
dc.relation.hasversionhttp://www.ncbi.nlm.nih.gov/pmc/articles/PMC3445456/pdf/en_US
dash.licenseLAA
dc.subjectBiologyen_US
dc.subjectGeneticsen_US
dc.subjectAnimal Geneticsen_US
dc.subjectModel Organismsen_US
dc.subjectAnimal Modelsen_US
dc.subjectMouseen_US
dc.subjectNeuroscienceen_US
dc.subjectNeural Networksen_US
dc.subjectNeurobiology of Disease and Regenerationen_US
dc.subjectNeurotransmittersen_US
dc.subjectMedicineen_US
dc.subjectEndocrinologyen_US
dc.subjectNeuroendocrinologyen_US
dc.subjectNutritionen_US
dc.subjectEating Disordersen_US
dc.subjectObesityen_US
dc.titleAn Obligate Role of Oxytocin Neurons in Diet Induced Energy Expenditureen_US
dc.typeJournal Articleen_US
dc.description.versionVersion of Recorden_US
dc.relation.journalPLoS ONEen_US
dash.depositing.authorLowell, Bradford Barr
dc.date.available2013-04-10T20:08:39Z
dc.identifier.doi10.1371/journal.pone.0045167*
dash.contributor.affiliatedOlson, David Paul
dash.contributor.affiliatedLowell, Bradford


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