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
2018
Inactivating hepatic follistatin alleviates hyperglycemia
Tao R, Wang C, Stöhr O, Qiu W, Hu Y, Miao J, Dong X, Leng S, Stefater M, Stylopoulos N, Lin L, Copps K, White M. Inactivating hepatic follistatin alleviates hyperglycemia. Nature Medicine 2018, 24: 1058-1069. PMID: 29867232, PMCID: PMC6039237, DOI: 10.1038/s41591-018-0048-0.Peer-Reviewed Original ResearchConceptsHepatic glucose productionAdipose tissue insulinGlucose toleranceTissue insulinSuppression of HGPGastric bypass surgeryFed obese miceHepatic insulin resistanceWhite adipose tissuePotential clinical significanceInsulin receptor substrate-1Bypass surgeryGlucose intoleranceHepatic inactivationObese miceInsulin resistanceObese individualsGlycated hemoglobinTranscription factor FOXO1Insulin sensitivityNormal suppressionClinical significanceReceptor substrate-1Adipose tissueExpression of Fst
2004
Insulin resistance in thermally-injured rats is associated with post-receptor alterations in skeletal muscle, liver and adipose tissue.
Carter E, Burks D, Fischman A, White M, Tompkins R. Insulin resistance in thermally-injured rats is associated with post-receptor alterations in skeletal muscle, liver and adipose tissue. International Journal Of Molecular Medicine 2004, 14: 653-8. PMID: 15375597, DOI: 10.3892/ijmm.14.4.653.Peer-Reviewed Original ResearchConceptsUrinary C-peptide excretionC-peptide excretionPost-receptor alterationsInsulin resistanceInsulin receptor bindingSkeletal muscleInsulin infusionBurn injuryAdipose tissueFull-thickness scald injuryGlucose productionSham-treated control animalsReceptor bindingHepatic glucose productionIRS-1 expressionWestern blot methodBinding of insulinAbsence of changesScald injuryBolus injectionRat modelPossible molecular mechanismsControl animalsInjuryThermal injury
2000
Contrasting Effects of IRS-1 Versus IRS-2 Gene Disruption on Carbohydrate and Lipid Metabolism in Vivo *
Previs S, Withers D, Ren J, White M, Shulman G. Contrasting Effects of IRS-1 Versus IRS-2 Gene Disruption on Carbohydrate and Lipid Metabolism in Vivo *. Journal Of Biological Chemistry 2000, 275: 38990-38994. PMID: 10995761, DOI: 10.1074/jbc.m006490200.Peer-Reviewed Original ResearchMeSH KeywordsAdipose TissueAnimalsCarbohydrate MetabolismFatty Acids, NonesterifiedFood DeprivationGas Chromatography-Mass SpectrometryGlucoseGlycerolInsulinInsulin Receptor Substrate ProteinsIntracellular Signaling Peptides and ProteinsLipid MetabolismLiverMaleMiceMusclesMutationPhenotypePhosphoproteinsRadioimmunoassayTime FactorsConceptsLipid metabolismInsulin resistanceIRS-2Glucose utilizationPlasma free fatty acid concentrationsWhole-body glucose utilizationGlycerol turnoverFree fatty acid concentrationsMarked insulin resistancePeripheral glucose metabolismPeripheral glucose utilizationHyperinsulinemic-euglycemic clampEndogenous glucose productionIRS-1Effect of insulinHepatic glycogen synthesisWT miceFatty acid concentrationsInsulin receptor substrateGlucose metabolismFasted miceAdipose tissueReduced suppressionGlucose productionMiceTissue-specific insulin resistance in mice with mutations in the insulin receptor, IRS-1, and IRS-2
Kido Y, Burks D, Withers D, Bruning J, Kahn C, White M, Accili D. Tissue-specific insulin resistance in mice with mutations in the insulin receptor, IRS-1, and IRS-2. Journal Of Clinical Investigation 2000, 105: 199-205. PMID: 10642598, PMCID: PMC377430, DOI: 10.1172/jci7917.Peer-Reviewed Original ResearchMeSH KeywordsAdipose TissueAnimalsBlood GlucoseCell SizeDiabetes Mellitus, Type 2Disease Models, AnimalHeterozygoteHomozygoteHyperglycemiaInsulinInsulin Receptor Substrate ProteinsInsulin ResistanceIntracellular Signaling Peptides and ProteinsIslets of LangerhansLiverMaleMiceMice, KnockoutMuscle, SkeletalMutationOrgan SpecificityPhosphatidylinositol 3-KinasesPhosphoproteinsReceptor, InsulinConceptsBeta-cell hyperplasiaSevere insulin resistanceInsulin resistanceSkeletal muscleInsulin actionAltered beta-cell functionCompensatory beta-cell hyperplasiaMild insulin resistanceTissue-specific insulin resistanceBeta-cell functionUnderlying metabolic abnormalitiesType 2 diabetesInsulin receptorHeterozygous null mutationsDiabetic miceMetabolic abnormalitiesInsulin receptor substrateAdipose tissueRole of IRSType 2MiceHyperplasiaLiverMuscleIRS-2