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dc.relation.isnodouble80a4e7cb-2592-4ece-87f7-47b158a12a69*
hal.structure.identifierCentre des Sciences du Goût et de l'Alimentation [Dijon] [CSGA]
dc.contributor.authorCARNEIRO, Lionel
hal.structure.identifierService d'Endocrinologie, Diabétologie et Métabolisme
dc.contributor.authorASRIH, Mohamed
hal.structure.identifierDepartment of Physiology
dc.contributor.authorREPOND, Cendrine
hal.structure.identifierUniversité Catholique de Louvain = Catholic University of Louvain [UCL]
dc.contributor.authorSEMPOUX, Christine
dc.contributor.authorSTEHLE, Jean-Christophe
hal.structure.identifierCentre des Sciences du Goût et de l'Alimentation [Dijon] [CSGA]
dc.contributor.authorLELOUP, Corinne
hal.structure.identifierService d'Endocrinologie, Diabétologie et Métabolisme
dc.contributor.authorJORNAYVAZ, François R.
hal.structure.identifierDépartement de Physiologie
dc.contributor.authorPELLERIN, Luc
dc.date.accessioned2021-10-07T16:28:24Z
dc.date.available2021-10-07T16:28:24Z
dc.date.issued2017-12
dc.identifier.issn2212-8778
dc.identifier.urihttps://oskar-bordeaux.fr/handle/20.500.12278/112594
dc.description.abstractEnObjective: Hepatic steatosis is the first step leading to non-alcoholic fatty liver disease, which represents a major complication of obesity. Here, we show that MCT1 haploinsufficient mice resist to hepatic steatosis development when fed a high fat diet. They exhibit a reduced hepatic capacity to metabolize monocarboxylates such as lactate compared to wildtype mice. Methods: To understand how this resistance to steatosis develops, we used HFD fed wildtype mice with hepatic steatosis and MCT1 haploinsufficient mice to study hepatic metabolism. Results: AMPK is constitutively activated in the liver of MCT1 haploinsufficient mice, leading to an inactivation of SREBP1. Therefore, expression of key transcription factors for lipid metabolism, such as PPARα and γ, CHREB, or SREBP1 itself, as well as several enzymes including FAS and CPT1, was not upregulated in these mice when fed a high fat diet. It is proposed that reduced hepatic lactate metabolism is responsible for the protection against hepatic steatosis in MCT1 haploinsufficient mice via a constitutive activation of AMPK and repression of several major elements involved in hepatic lipid metabolism. Conclusion: Our results support a role of increased lactate uptake in hepatocytes during HFD that, in turn, induce a metabolic shift stimulating SREBP1 activity and lipid accumulation. AMPK activation caused by reduced liver lactate metabolism protects against hepatic steatosis in MCT1 haploinsufficient mice (PDF Download Available). Available from: https://www.researchgate.net/publication/320544573_AMPK_activation_caused_by_reduced_liver_lactate_metabolism_protects_against_hepatic_steatosis_in_MCT1_haploinsufficient_mice [accessed Jan 16 2018].
dc.language.isoen
dc.publisherElsevier
dc.rights.urihttp://creativecommons.org/licenses/by/
dc.subject.enAMPK
dc.subject.enHepatic steatosis
dc.title.enAMPK activation caused by reduced liver lactate metabolism protects against hepatic steatosis in MCT1 haploinsufficient mice
dc.typeArticle de revue
dc.identifier.doi10.1016/j.molmet.2017.10.005
dc.subject.halSciences du Vivant [q-bio]/Médecine humaine et pathologie
bordeaux.journalMolecular metabolism
bordeaux.page1625 - 1633
bordeaux.volume6
bordeaux.hal.laboratoriesCentre de Résonance Magnétique des Systèmes Biologiques (CRMSB) - UMR 5536*
bordeaux.issue12
bordeaux.institutionUniversité de Bordeaux
bordeaux.institutionCNRS
bordeaux.peerReviewedoui
hal.identifierhal-01685459
hal.version1
hal.origin.linkhttps://hal.archives-ouvertes.fr//hal-01685459v1
bordeaux.COinSctx_ver=Z39.88-2004&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.jtitle=Molecular%20metabolism&rft.date=2017-12&rft.volume=6&rft.issue=12&rft.spage=1625%20-%201633&rft.epage=1625%20-%201633&rft.eissn=2212-8778&rft.issn=2212-8778&rft.au=CARNEIRO,%20Lionel&ASRIH,%20Mohamed&REPOND,%20Cendrine&SEMPOUX,%20Christine&STEHLE,%20Jean-Christophe&rft.genre=article


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