Deletion of the diabetes candidate gene Slc16a13 in mice attenuates diet-induced ectopic lipid accumulation and insulin resistance
Schumann T, König J, von Loeffelholz C, Vatner DF, Zhang D, Perry RJ, Bernier M, Chami J, Henke C, Kurzbach A, El-Agroudy NN, Willmes DM, Pesta D, de Cabo R, O´Sullivan J, Simon E, Shulman GI, Hamilton BS, Birkenfeld AL. Deletion of the diabetes candidate gene Slc16a13 in mice attenuates diet-induced ectopic lipid accumulation and insulin resistance. Communications Biology 2021, 4: 826. PMID: 34211098, PMCID: PMC8249653, DOI: 10.1038/s42003-021-02279-8.Peer-Reviewed Original ResearchMeSH KeywordsAMP-Activated Protein KinasesAnimalsDiabetes Mellitus, Type 2Diet, High-FatGene ExpressionGenetic Predisposition to DiseaseHumansInsulin ResistanceLipid MetabolismLiverMice, Inbred C57BLMice, KnockoutMitochondriaMonocarboxylic Acid TransportersNon-alcoholic Fatty Liver DiseaseObesityOxygen ConsumptionConceptsMitochondrial respirationGenome-wide association studiesNovel susceptibility genesLipid accumulationPlasma membraneAMPK activationAssociation studiesPhysiological functionsEctopic lipid accumulationReduced hepatic lipid accumulationSusceptibility genesLactate transporterMonocarboxylate transportersPotential targetGenesTransportersDeletionLipid contentHepatic lipid accumulationPotential importanceKnockout miceRespirationHepatic insulin sensitivityMCT13Accumulation