Featured Publications
1632-P: Effects of MTOR Signaling in Muscle-Specific Irs1/2 Knockout Mice
STOEHR O, COPPS K, TAO R, WHITE M. 1632-P: Effects of MTOR Signaling in Muscle-Specific Irs1/2 Knockout Mice. Diabetes 2023, 72 DOI: 10.2337/db23-1632-p.Peer-Reviewed Original ResearchMTKO miceGlucose uptakeMTOR pathwayMdKO miceReduced ejection fractionCardiac fatty acid uptakeHigh-fat dietInsulin-resistant heartMuscle glucose uptakeDays of lifeWhite adipose tissueCardiac glucose uptakeFatty acid uptakeEffects of mTORInsulin-stimulated conditionsEjection fractionFat dietFat massMuscle atrophyIRS2 expressionCardiac hypertrophyEarly deathCardiac energyKnockout miceAdipose tissue
2019
282-LB: Dysregulated FGF21 Links Hepatic Insulin Resistance to Dysfunctional BAT
STOEHR O, TAO R, COPPS K, WHITE M. 282-LB: Dysregulated FGF21 Links Hepatic Insulin Resistance to Dysfunctional BAT. Diabetes 2019, 68 DOI: 10.2337/db19-282-lb.Peer-Reviewed Original ResearchHepatic insulin resistanceFGF-21Insulin resistanceHFD feedingControl miceDiabetic phenotypeGlucose metabolismFGF-21 serum levelsWhole-body glucose metabolismGlucose uptakeInsulin-resistant liverImproved glucose toleranceWild-type miceHepatic glucose productionSevere diabetic phenotypeNormal glucose uptakeHealthy batsBAT dysfunctionSerum levelsGlucose toleranceBAT functionType miceNormal rangeInsulin actionAdenoviral infection
2018
Metabolic Dysfunction within Brown Adipose Tissue and Skeletal Muscle Caused by Complete Hepatic Insulin Resistance Is Reversible by FGF-21 Treatment
STOEHR O, TAO R, COPPS K, WHITE M. Metabolic Dysfunction within Brown Adipose Tissue and Skeletal Muscle Caused by Complete Hepatic Insulin Resistance Is Reversible by FGF-21 Treatment. Diabetes 2018, 67 DOI: 10.2337/db18-1873-p.Peer-Reviewed Original ResearchHepatic insulin resistanceFGF-21Insulin resistanceGlucose toleranceSkeletal muscleGlucose uptakeAdipose tissue markersFGF-21 treatmentSkeletal muscle dysfunctionSystemic insulin resistanceBetter glucose toleranceSystemic glucose homeostasisDouble knockout miceBrown adipose tissueDeletion of FoxO1Hepatokine secretionThermogenesis markersHepatic infectionBody core temperatureGlucose intoleranceMuscle dysfunctionSevere hyperglycemiaControl miceInsulin sensitivityMetabolic dysfunction
2008
Muscle-Specific IRS-1 Ser→Ala Transgenic Mice Are Protected From Fat-Induced Insulin Resistance in Skeletal Muscle
Morino K, Neschen S, Bilz S, Sono S, Tsirigotis D, Reznick RM, Moore I, Nagai Y, Samuel V, Sebastian D, White M, Philbrick W, Shulman GI. Muscle-Specific IRS-1 Ser→Ala Transgenic Mice Are Protected From Fat-Induced Insulin Resistance in Skeletal Muscle. Diabetes 2008, 57: 2644-2651. PMID: 18633112, PMCID: PMC2551673, DOI: 10.2337/db06-0454.Peer-Reviewed Original ResearchMeSH KeywordsAlanineAmino Acid SubstitutionAnimalsBlotting, WesternDietary FatsFemaleGlucose Clamp TechniqueGlucose Tolerance TestImmunoprecipitationInsulinInsulin Receptor Substrate ProteinsInsulin ResistanceMaleMiceMice, Inbred C57BLMice, TransgenicMuscle, SkeletalPhosphorylationSerineTriglyceridesConceptsSerine phosphorylationIRS-1IRS-1-associated phosphatidylinositolSkeletal muscleInsulin-stimulated IRS-1-associated phosphatidylinositolWild-type transgenic miceFat-induced insulin resistanceInsulin receptor substrateTransgenic miceReceptor substrateInsulin signalingAkt phosphorylationPhosphorylationCellular mechanismsCritical roleGlucose uptakeHigh-fat feedingInsulin resistanceMuscle glucose uptakeInsulin actionVivoSerInsulin-stimulated muscle glucose uptakeImportant rolePhosphatidylinositol
2005
Reduced mitochondrial density and increased IRS-1 serine phosphorylation in muscle of insulin-resistant offspring of type 2 diabetic parents
Morino K, Petersen KF, Dufour S, Befroy D, Frattini J, Shatzkes N, Neschen S, White MF, Bilz S, Sono S, Pypaert M, Shulman GI. Reduced mitochondrial density and increased IRS-1 serine phosphorylation in muscle of insulin-resistant offspring of type 2 diabetic parents. Journal Of Clinical Investigation 2005, 115: 3587-3593. PMID: 16284649, PMCID: PMC1280967, DOI: 10.1172/jci25151.Peer-Reviewed Original ResearchMeSH KeywordsBiopsyBlood GlucoseBlotting, WesternBody Mass IndexBody WeightDiabetes Mellitus, Type 2DNA, MitochondrialFamily HealthFemaleGene Expression RegulationGlucose Clamp TechniqueGlucose Tolerance TestHumansHyperinsulinismImmunoprecipitationInsulinInsulin Receptor Substrate ProteinsInsulin ResistanceLipidsMaleMicroscopy, ElectronMicroscopy, Electron, TransmissionMitochondriaMusclesPhosphoproteinsPhosphorylationProtein Serine-Threonine KinasesReverse Transcriptase Polymerase Chain ReactionRNA, MessengerSerineSignal TransductionTime FactorsTranscription, GeneticTriglyceridesConceptsInsulin-resistant offspringIR offspringType 2 diabetesInsulin-stimulated muscle glucose uptakeType 2 diabetic parentsIntramyocellular lipid contentHyperinsulinemic-euglycemic clampMuscle glucose uptakeIRS-1 serine phosphorylationMuscle mitochondrial densityMitochondrial densityMuscle biopsy samplesSerine kinase cascadeInsulin-stimulated Akt activationDiabetic parentsInsulin resistanceControl subjectsBiopsy samplesGlucose uptakeLipid accumulationMitochondrial dysfunctionInsulin signalingAkt activationEarly defectsMuscle
2003
Essential role of protein kinase Cζ in the impairment of insulin‐induced glucose transport in IRS‐2‐deficient brown adipocytes
Arribas M, Valverde A, Burks D, Klein J, Farese R, White M, Benito M. Essential role of protein kinase Cζ in the impairment of insulin‐induced glucose transport in IRS‐2‐deficient brown adipocytes. FEBS Letters 2003, 536: 161-166. PMID: 12586357, DOI: 10.1016/s0014-5793(03)00049-8.Peer-Reviewed Original ResearchConceptsGLUT4 translocationIRS-2/PIBrown adipocytesInsulin-induced glucose transportProtein kinase C zetaIRS-2-associated phosphatidylinositolKinase-inactive mutantGlucose uptakeWild-type cellsProtein kinase CζEssential roleInsulin receptor substrate-2-deficient (IRS2(-/-)) miceC zetaPKC-zetaMolecular mechanismsIRS-2Impaired glucose uptakeGlucose transportAdipocytesTranslocationCellsUptakeMutantsPhosphatidylinositolCζ
2000
Essential Role of Insulin Receptor Substrate-2 in Insulin Stimulation of Glut4 Translocation and Glucose Uptake in Brown Adipocytes*
Fasshauer M, Klein J, Ueki K, Kriauciunas K, Benito M, White M, Kahn C. Essential Role of Insulin Receptor Substrate-2 in Insulin Stimulation of Glut4 Translocation and Glucose Uptake in Brown Adipocytes*. Journal Of Biological Chemistry 2000, 275: 25494-25501. PMID: 10829031, DOI: 10.1074/jbc.m004046200.Peer-Reviewed Original ResearchMeSH KeywordsAdipocytesAdipose Tissue, BrownAnimalsArabidopsis ProteinsAzo CompoundsBiological TransportCell DifferentiationCell MembraneCells, CulturedColoring AgentsDose-Response Relationship, DrugGlucoseGlucose Transporter Type 4ImmunoblottingInsulinInsulin Receptor Substrate ProteinsIntracellular Signaling Peptides and ProteinsMiceMice, KnockoutMonosaccharide Transport ProteinsMuscle ProteinsPhosphatidylinositol 3-KinasesPhosphoproteinsPhosphorylationPlant ProteinsPlasmidsPotassium ChannelsPrecipitin TestsProtein Serine-Threonine KinasesProto-Oncogene ProteinsProto-Oncogene Proteins c-aktRetroviridaeSignal TransductionSubcellular FractionsTime FactorsConceptsInsulin-stimulated GLUT4 translocationGLUT4 translocationInsulin-induced glucose uptakeIRS-2Plasma membraneDownstream effectorsWild typeInsulin receptor substrate (IRS) proteinsBrown adipocyte cell lineInsulin stimulationGlycogen synthase kinase-3IRS-2-associated phosphatidylinositolGlucose uptakeAkt-dependent phosphorylationInsulin receptor substrate 2Synthase kinase-3Brown adipocytesMajor downstream effectorActivity of AktMature brown adipocytesAdipocyte cell lineSubstrate proteinsWild-type counterpartsKO cellsKinase 3