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dc.rights.licenseopenen_US
hal.structure.identifierNeurocentre Magendie : Physiopathologie de la Plasticité Neuronale [U1215 Inserm - UB]
dc.contributor.authorALLARD, Camille
hal.structure.identifierNeurocentre Magendie : Physiopathologie de la Plasticité Neuronale [U1215 Inserm - UB]
dc.contributor.authorMIRALPEIX, Cristina
hal.structure.identifierNeurocentre Magendie : Physiopathologie de la Plasticité Neuronale [U1215 Inserm - UB]
dc.contributor.authorLÓPEZ-GAMBERO, Antonio J.
hal.structure.identifierNeurocentre Magendie : Physiopathologie de la Plasticité Neuronale [U1215 Inserm - UB]
dc.contributor.authorCOTA, Daniela
dc.date.accessioned2025-05-19T09:05:53Z
dc.date.available2025-05-19T09:05:53Z
dc.date.issued2024-04
dc.identifier.issn1759-5029en_US
dc.identifier.urihttps://oskar-bordeaux.fr/handle/20.500.12278/206648
dc.description.abstractEnIn eukaryotic cells, the mammalian target of rapamycin complex 1 (sometimes referred to as the mechanistic target of rapamycin complex 1; mTORC1) orchestrates cellular metabolism in response to environmental energy availability. As a result, at the organismal level, mTORC1 signalling regulates the intake, storage and use of energy by acting as a hub for the actions of nutrients and hormones, such as leptin and insulin, in different cell types. It is therefore unsurprising that deregulated mTORC1 signalling is associated with obesity. Strategies that increase energy expenditure offer therapeutic promise for the treatment of obesity. Here we review current evidence illustrating the critical role of mTORC1 signalling in the regulation of energy expenditure and adaptive thermogenesis through its various effects in neuronal circuits, adipose tissue and skeletal muscle. Understanding how mTORC1 signalling in one organ and cell type affects responses in other organs and cell types could be key to developing better, safer treatments targeting this pathway in obesity. © Springer Nature Limited 2024.; The protein complex mTORC1 is a key regulator of cellular metabolism in response to energy availability. This Review discusses the role of mTORC1 in regulating energy expenditure and the implications for the development and treatment of obesity. © Springer Nature Limited 2024..; Mammalian target of rapamycin complex 1 (mTORC1) plays different and complex roles in the regulation of energy expenditure. mTORC1 cell-specific actions affect other cells and organs by altering cellular metabolism and the use of energy substrates while modifying inter-organ communication. mTORC1 activation is required for central sympathetic nervous system (SNS) stimulation and SNS effects on white adipose tissue (WAT), brown adipose tissue (BAT) and skeletal muscle, which lead to WAT browning and increased energy expenditure. mTORC1 stimulates non-shivering thermogenesis in BAT and skeletal muscle. mTORC1 is a master regulator of skeletal muscle metabolism and it is crucial for skeletal muscle mass maintenance. © Springer Nature Limited 2024..
dc.language.isoENen_US
dc.subject.enInsulin
dc.subject.enHuman
dc.subject.enMetabolism
dc.subject.enObesity
dc.subject.enPhysiology
dc.subject.enInsulin
dc.subject.enSignal Transduction
dc.subject.enRegulatory Mechanism
dc.subject.enSkeletal Muscle
dc.subject.enEnergy Metabolism
dc.subject.enNerve Cell
dc.subject.enHypothalamus
dc.subject.enEnergy Expenditure
dc.subject.enCell Interaction
dc.subject.enMammalian Target Of Rapamycin Complex 1
dc.subject.enAdipose Tissue
dc.subject.enCell Metabolism
dc.subject.enCells By Body Anatomy
dc.subject.enFibroblast Growth Factor 21
dc.subject.enGrowth Differentiation Factor 15
dc.subject.enMechanistic Target Of Rapamycin Complex 1
dc.subject.enSacral Nerve Stimulation
dc.subject.enThermogenesis
dc.title.enmTORC1 in energy expenditure: consequences for obesity
dc.title.alternativeNat Rev Endocrinolen_US
dc.typeArticle de revueen_US
dc.identifier.doi10.1038/s41574-023-00934-0en_US
dc.subject.halSciences du Vivant [q-bio]/Neurosciences [q-bio.NC]en_US
dc.identifier.pubmed38225400en_US
bordeaux.journalNature Reviews Endocrinologyen_US
bordeaux.page239 – 251en_US
bordeaux.volume20en_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
dc.rights.ccPas de Licence CCen_US
bordeaux.COinSctx_ver=Z39.88-2004&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.jtitle=Nature%20Reviews%20Endocrinology&rft.date=2024-04&rft.volume=20&rft.issue=4&rft.spage=239%20%E2%80%93%20251&rft.epage=239%20%E2%80%93%20251&rft.eissn=1759-5029&rft.issn=1759-5029&rft.au=ALLARD,%20Camille&MIRALPEIX,%20Cristina&L%C3%93PEZ-GAMBERO,%20Antonio%20J.&COTA,%20Daniela&rft.genre=article


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