Ablation of LMO4 in glutamatergic neurons impairs leptin control of fat metabolism

FieldValue
dc.contributor.authorChen, Hsiao-Huei
dc.contributor.authorZhou, Xun
dc.contributor.authorGomez-Smith, Mariana
dc.contributor.authorQin, Zhaohong
dc.contributor.authorDuquette, Philippe M.
dc.contributor.authorCardenas-Blanco, Arturo
dc.contributor.authorRai, Punarpreet S.
dc.contributor.authorHarper, Mary-Ellen
dc.contributor.authorTsai, Eve C.
dc.contributor.authorAnisman, Hymie
dc.date.accessioned2012-02-27T20:35:57Z
dc.date.available2012-02-27T20:35:57Z
dc.date.created2012
dc.date.issued2012-02-27
dc.identifier.urihttp://hdl.handle.net/10393/20718
dc.identifier.urihttp://www.springerlink.com/content/k7231q2141443894/fulltext.pdf
dc.description.abstractThe LIM domain only 4 (LMO4) protein is expressed in the hypothalamus, but its function there is not known. Using mice with LMO4 ablated in postnatal glutamatergic neurons, including most neurons of the paraventricular (PVN) and ventromedial (VMH) hypothalamic nuclei where LMO4 is expressed, we asked whether LMO4 is required for metabolic homeostasis. LMO4 mutant mice exhibited early onset adiposity. These mice had reduced energy expenditure and impaired thermogenesis together with reduced sympathetic outflow to adipose tissues. The peptide hormone leptin, produced from adipocytes,activates Jak/Stat3 signaling at the hypothalamus to control food intake, energy expenditure, and fat metabolism. Intracerebroventricular infusion of leptin suppressed feeding similarly in LMO4 mutant and control mice.However, leptin-induced fat loss was impaired and activation of Stat3 in the VMH was blunted in these mice. Thus, our study identifies LMO4 as a novel modulator of leptin function in selective hypothalamic nuclei to regulate fat metabolism.
dc.language.isoen
dc.subjectAdiposity
dc.subjectObesity
dc.subjectSympathetic outflow
dc.subjectHypothalamus
dc.subjectLeptin
dc.titleAblation of LMO4 in glutamatergic neurons impairs leptin control of fat metabolism
dc.typeArticle
dc.identifier.doi10.1007/s00018-011-0794-3
CollectionIRHO - Publications // OHRI - Publications
Publications en libre accès financées par uOttawa // uOttawa financed open access publications

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