2020
Leptin mediates postprandial increases in body temperature through hypothalamus–adrenal medulla–adipose tissue crosstalk
Perry RJ, Lyu K, Rabin-Court A, Dong J, Li X, Yang Y, Qing H, Wang A, Yang X, Shulman GI. Leptin mediates postprandial increases in body temperature through hypothalamus–adrenal medulla–adipose tissue crosstalk. Journal Of Clinical Investigation 2020, 130: 2001-2016. PMID: 32149734, PMCID: PMC7108915, DOI: 10.1172/jci134699.Peer-Reviewed Original ResearchConceptsBrown adipose tissueLeptin concentrationsBody temperatureAdrenomedullary catecholamine secretionPlasma leptin concentrationsAdipose tissue lipolysisFasting-induced reductionFeeding-induced increaseMeal ingestionPlasma catecholaminesPostprandial increaseCatecholamine secretionObese ratsTissue lipolysisLean ratsAdrenergic activationAdipose tissueTissue crosstalkWeight gainIntragastric infusionRatsLeptinBolusLipolysisFatty acids
2009
The Role of Peroxisome Proliferator-Activated Receptor γ Coactivator-1 β in the Pathogenesis of Fructose-Induced Insulin Resistance
Nagai Y, Yonemitsu S, Erion DM, Iwasaki T, Stark R, Weismann D, Dong J, Zhang D, Jurczak MJ, Löffler MG, Cresswell J, Yu XX, Murray SF, Bhanot S, Monia BP, Bogan JS, Samuel V, Shulman GI. The Role of Peroxisome Proliferator-Activated Receptor γ Coactivator-1 β in the Pathogenesis of Fructose-Induced Insulin Resistance. Cell Metabolism 2009, 9: 252-264. PMID: 19254570, PMCID: PMC3131094, DOI: 10.1016/j.cmet.2009.01.011.Peer-Reviewed Original ResearchMeSH KeywordsAdipose TissueAnimalsDietFructoseGene ExpressionHepatocytesHumansInsulin ResistanceLiverMaleMiceOligonucleotides, AntisensePeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaRatsRats, Sprague-DawleyRNA-Binding ProteinsSterol Regulatory Element Binding Protein 1Transcription FactorsConceptsInsulin resistancePeroxisome proliferator-activated receptor gamma coactivator 1 betaInsulin-stimulated whole-body glucose disposalWhole-body glucose disposalPGC-1betaTreatment of NAFLDFructose-Induced Insulin ResistanceHepatic insulin resistanceWhite adipose tissueDe novo lipogenesisSREBP-1Downstream lipogenic genesReceptor γ coactivatorGlucose disposalInsulin-stimulated statesHepatic lipogenesisNovo lipogenesisTherapeutic targetAdipose tissuePeroxisome proliferatorLipogenic genesΓ coactivatorGlucose uptakePathogenesisMetabolic phenotype
2001
Glucose toxicity and the development of diabetes in mice with muscle-specific inactivation of GLUT4
Kim J, Zisman A, Fillmore J, Peroni O, Kotani K, Perret P, Zong H, Dong J, Kahn C, Kahn B, Shulman G. Glucose toxicity and the development of diabetes in mice with muscle-specific inactivation of GLUT4. Journal Of Clinical Investigation 2001, 108: 153-160. PMID: 11435467, PMCID: PMC353719, DOI: 10.1172/jci10294.Peer-Reviewed Original ResearchMeSH KeywordsAdipose TissueAge of OnsetAnimalsDepression, ChemicalDiabetes Mellitus, Type 2Disease Models, AnimalGlucoseGlucose Transporter Type 4HyperglycemiaInsulinInsulin Infusion SystemsInsulin ResistanceKidney TubulesLiverMaleMiceMice, KnockoutMonosaccharide Transport ProteinsMuscle ProteinsMuscle, SkeletalPhlorhizinPrediabetic StateProtein TransportConceptsDevelopment of diabetesMuscle glucose uptakeKO miceHepatic glucose productionInsulin-stimulated glucose uptakeGlucose toxicityMuscle-specific inactivationGlucose uptakeAdipose tissueInsulin-stimulated muscle glucose uptakeGlucose productionWhole-body glucose uptakeSkeletal muscle glucose uptakeAdipose tissue glucose uptakeSuppress hepatic glucose productionTissue glucose uptakeHyperinsulinemic-euglycemic clampMuscle glucose transportInsulin resistanceTransgenic miceDiabetes phenotypeInsulin actionPhloridzin treatmentInsulin's abilityDiabetes