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dc.rights.licenseopenen_US
dc.contributor.authorVILY-PETIT, Justine
dc.contributor.authorSOTY-ROCA, Maud
dc.contributor.authorSILVA, Marine
dc.contributor.authorMICOUD, Manon
dc.contributor.authorEVRARD, Félicie
dc.contributor.authorBRON, Clara
dc.contributor.authorRAFFIN, Margaux
dc.contributor.authorBEIROA, Daniel
dc.contributor.authorNOGUEIRAS, Rubén
dc.contributor.authorROUSSEL, Damien
dc.contributor.authorGAUTIER-STEIN, Amandine
dc.contributor.authorRAJAS, Fabienne
hal.structure.identifierNeurocentre Magendie : Physiopathologie de la Plasticité Neuronale [U1215 Inserm - UB]
dc.contributor.authorCOTA, Daniela
dc.contributor.authorMITHIEUX, Gilles
dc.date.accessioned2025-07-02T11:19:37Z
dc.date.available2025-07-02T11:19:37Z
dc.date.issued2024-04
dc.identifier.issn1930-7381en_US
dc.identifier.urihttps://oskar-bordeaux.fr/handle/20.500.12278/207180
dc.description.abstractEnObjective: Intestinal gluconeogenesis (IGN), via the initiation of a gut-brain nervous circuit, accounts for the metabolic benefits linked to dietary proteins or fermentable fiber in rodents and has been positively correlated with the rapid amelioration of body weight after gastric bypass surgery in humans with obesity. In particular, the activation of IGN moderates the development of hepatic steatosis accompanying obesity. In this study, we investigated the specific effects of IGN on adipose tissue metabolism, independent of its induction by nutritional manipulation. Methods: We used two transgenic mouse models of suppression or overexpression of G6pc1, the catalytic subunit of glucose-6 phosphatase, which is the key enzyme of endogenous glucose production specifically in the intestine. Results: Under a hypercaloric diet, mice overexpressing IGN showed lower adiposity and higher thermogenic capacities than wild-type mice, featuring marked browning of white adipose tissue (WAT) and prevention of the whitening of brown adipose tissue (BAT). Sympathetic denervation restricted to BAT caused the loss of the antiobesity effects associated with IGN. Conversely, IGN-deficient mice exhibited an increase in adiposity under a standard diet, which was associated with decreased expression of markers of thermogenesis in both BAT and WAT. Conclusions: IGN is sufficient to activate the sympathetic nervous system and prevent the expansion and the metabolic alterations of BAT and WAT metabolism under a high-calorie diet, thereby preventing the development of obesity. These data increase knowledge of the mechanisms of weight reduction in gastric bypass surgery and pave the way for new approaches to prevent or cure obesity. © 2024 The Obesity Society.
dc.description.sponsorshipLe Signal Glucose Portal protège du Diabèteen_US
dc.language.isoENen_US
dc.subject.enHumans
dc.subject.enControlled Study
dc.subject.enGenetics
dc.subject.enAnimal Experiment
dc.subject.enMouse
dc.subject.enImmunohistochemistry
dc.subject.enComplication
dc.subject.enNuclear Magnetic Resonance Imaging
dc.subject.enMetabolism
dc.subject.enCytokine Release
dc.subject.enWestern Blotting
dc.subject.enHistopathology
dc.subject.enObesity
dc.subject.enAnimal Model
dc.subject.enAnimal Tissue
dc.subject.enFatty Liver
dc.subject.enElectron Microscopy
dc.subject.enLipid Storage
dc.subject.enTransmission Electron Microscopy
dc.subject.enEnergy Metabolism
dc.subject.enTransgenic Mouse
dc.subject.enOxidative Phosphorylation
dc.subject.enFat Mass
dc.subject.enAdrenergic System
dc.subject.enSympathetic Nervous System
dc.subject.enEnergy Expenditure
dc.subject.enThermogenesis
dc.subject.enAdipose Tissue
dc.subject.enAntiobesity Activity
dc.subject.enBrown Adipose Tissue
dc.subject.enGluconeogenesis
dc.subject.enGlucose 6 Phosphatase
dc.subject.enHigh Calorie Diet
dc.subject.enIntestine Function
dc.subject.enTissue Metabolism
dc.title.enAntiobesity effects of intestinal gluconeogenesis are mediated by the brown adipose tissue sympathetic nervous system
dc.title.alternativeObesity (Silver Spring)en_US
dc.typeArticle de revueen_US
dc.identifier.doi10.1002/oby.23985en_US
dc.subject.halSciences du Vivant [q-bio]/Neurosciences [q-bio.NC]en_US
dc.identifier.pubmed38311801en_US
bordeaux.journalObesityen_US
bordeaux.page710 – 722en_US
bordeaux.volume32en_US
bordeaux.hal.laboratoriesNeurocentre Magendie - U1215en_US
bordeaux.issue4en_US
bordeaux.institutionUniversité de Bordeauxen_US
bordeaux.institutionINSERMen_US
bordeaux.teamPhysiopathologie de l'équilibre énergétique et obésitéen_US
bordeaux.peerReviewedouien_US
bordeaux.inpressnonen_US
hal.popularnonen_US
hal.audienceInternationaleen_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=Obesity&rft.date=2024-04&rft.volume=32&rft.issue=4&rft.spage=710%20%E2%80%93%20722&rft.epage=710%20%E2%80%93%20722&rft.eissn=1930-7381&rft.issn=1930-7381&rft.au=VILY-PETIT,%20Justine&SOTY-ROCA,%20Maud&SILVA,%20Marine&MICOUD,%20Manon&EVRARD,%20F%C3%A9licie&rft.genre=article


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