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dc.rights.licenseopenen_US
dc.contributor.authorSOTY, Maud
dc.contributor.authorVILY-PETIT, Justine
hal.structure.identifierNeurocentre Magendie : Physiopathologie de la Plasticité Neuronale [U1215 Inserm - UB]
dc.contributor.authorCASTELLANOS-JANKIEWICZ, Ashley
hal.structure.identifierNeurocentre Magendie : Physiopathologie de la Plasticité Neuronale [U1215 Inserm - UB]
dc.contributor.authorGUZMAN-QUEVEDO, Omar
dc.contributor.authorRAFFIN, Margaux
hal.structure.identifierNeurocentre Magendie : Physiopathologie de la Plasticité Neuronale [U1215 Inserm - UB]
dc.contributor.authorCLARK, Samantha
dc.contributor.authorSILVA, Marine
dc.contributor.authorGAUTIER-STEIN, Amandine
hal.structure.identifierNeurocentre Magendie : Physiopathologie de la Plasticité Neuronale [U1215 Inserm - UB]
dc.contributor.authorCOTA, Daniela
dc.contributor.authorMITHIEUX, Gilles
dc.date.accessioned2022-01-25T16:36:55Z
dc.date.available2022-01-25T16:36:55Z
dc.date.issued2021
dc.identifier.issn0028-3835 1423-0194en_US
dc.identifier.urihttps://oskar-bordeaux.fr/handle/20.500.12278/124618
dc.description.abstractEnIntroduction: Intestinal gluconeogenesis (IGN) exerts metabolic benefits in energy homeostasis via the neural sensing of portal glucose. Objective: The aim of this work was to determine central mechanisms involved in the effects of IGN on the control of energy homeostasis. Methods: We investigated the effects of glucose infusion into the portal vein, at a rate that mimics IGN, in conscious wild-type, leptin-deficient Ob/Ob and calcitonin gene-related peptide (CGRP)-deficient mice. Results: We report that portal glucose infusion decreases food intake and plasma glucose and induces in the hypothalamic arcuate nucleus (ARC) the phosphorylation of STAT3, the classic intracellular messenger of leptin signaling. This notably takes place in POMC-expressing neurons. STAT3 phosphorylation does not require leptin, since portal glucose effects are observed in leptin-deficient Ob/Ob mice. We hypothesized that the portal glucose effects could require CGRP, a neuromediator previously suggested to suppress hunger. In line with this hypothesis, neither the metabolic benefits nor the phosphorylation of STAT3 in the ARC take place upon portal glucose infusion in CGRP-deficient mice. Moreover, intracerebroventricular injection of CGRP activates hypothalamic phosphorylation of STAT3 in mice, and CGRP does the same in hypothalamic cells. Finally, no metabolic benefit of dietary fibers (known to depend on the induction of IGN), takes place in CGRP-deficient mice. Conclusions: CGRP-induced phosphorylation of STAT3 in the ARC is part of the neural chain determining the hunger-modulating and glucose-lowering effects of IGN/portal glucose.
dc.language.isoENen_US
dc.subject.enCalcitonin generelated peptide
dc.subject.enFood intake
dc.subject.enIntestinal glucose production
dc.subject.enNeural glucose sensing
dc.title.enCalcitonin gene-related peptide-induced phosphorylation of STAT3 in arcuate neurons is a link in the metabolic benefits of portal glucose
dc.typeArticle de revueen_US
dc.identifier.doi10.1159/000509230en_US
dc.subject.halSciences du Vivant [q-bio]/Neurosciences [q-bio.NC]en_US
dc.identifier.pubmed32516785en_US
bordeaux.journalNeuroendocrinologyen_US
bordeaux.page555-567en_US
bordeaux.volume111en_US
bordeaux.hal.laboratoriesNeurocentre Magendie - UMR-S 1215en_US
bordeaux.issue6en_US
bordeaux.institutionUniversité de Bordeauxen_US
bordeaux.institutionINSERMen_US
bordeaux.peerReviewedouien_US
bordeaux.inpressnonen_US
hal.exportfalse
dc.rights.ccPas de Licence CCen_US
bordeaux.COinSctx_ver=Z39.88-2004&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.jtitle=Neuroendocrinology&rft.date=2021&rft.volume=111&rft.issue=6&rft.spage=555-567&rft.epage=555-567&rft.eissn=0028-3835%C2%A01423-0194&rft.issn=0028-3835%C2%A01423-0194&rft.au=SOTY,%20Maud&VILY-PETIT,%20Justine&CASTELLANOS-JANKIEWICZ,%20Ashley&GUZMAN-QUEVEDO,%20Omar&RAFFIN,%20Margaux&rft.genre=article


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