2021
Short-term overnutrition induces white adipose tissue insulin resistance through sn-1,2-diacylglycerol – PKCε – insulin receptorT1160 phosphorylation
Lyu K, Zhang D, Song J, Li X, Perry RJ, Samuel VT, Shulman GI. Short-term overnutrition induces white adipose tissue insulin resistance through sn-1,2-diacylglycerol – PKCε – insulin receptorT1160 phosphorylation. JCI Insight 2021, 6: e139946. PMID: 33411692, PMCID: PMC7934919, DOI: 10.1172/jci.insight.139946.Peer-Reviewed Original ResearchConceptsInsulin resistanceInsulin actionAdipose tissue insulin resistanceTissue insulin resistanceWT control miceHyperinsulinemic-euglycemic clampShort-term HFDTissue insulin actionAdipose tissue insulin actionDiet-fed ratsPotential therapeutic targetHFD feedingControl miceInsulin sensitivityTherapeutic targetLipolysis suppressionImpairs insulinHFDPKCε activationGlucose uptakeΕ activationMiceDiacylglycerol accumulationRecent evidenceProtein kinase C
2014
Targeting steroid receptor coactivator 1 with antisense oligonucleotides increases insulin-stimulated skeletal muscle glucose uptake in chow-fed and high-fat-fed male rats
Cantley JL, Vatner DF, Galbo T, Madiraju A, Petersen M, Perry RJ, Kumashiro N, Guebre-Egziabher F, Gattu AK, Stacy MR, Dione DP, Sinusas AJ, Ragolia L, Hall CE, Manchem VP, Bhanot S, Bogan JS, Samuel VT. Targeting steroid receptor coactivator 1 with antisense oligonucleotides increases insulin-stimulated skeletal muscle glucose uptake in chow-fed and high-fat-fed male rats. AJP Endocrinology And Metabolism 2014, 307: e773-e783. PMID: 25159329, PMCID: PMC4216948, DOI: 10.1152/ajpendo.00148.2014.Peer-Reviewed Original ResearchMeSH KeywordsAdipose TissueAnimalsBiological TransportDiet, High-FatEnzyme InhibitorsGene Expression Regulation, EnzymologicGlucose IntoleranceGlucose Transporter Type 4Insulin ResistanceIntracellular Signaling Peptides and ProteinsIntramolecular OxidoreductasesLipocalinsLiverMaleMuscle, SkeletalNuclear Receptor Coactivator 1Oligodeoxyribonucleotides, AntisensePhosphoenolpyruvate Carboxykinase (GTP)Prostaglandin D2Protein Interaction Domains and MotifsProteolysisRats, Sprague-DawleyConceptsMuscle glucose uptakeSteroid receptor coactivator-1Endogenous glucose productionInsulin-stimulated muscle glucose uptakeReceptor coactivator-1Glucose uptakeGlucose homeostasisInsulin-stimulated skeletal muscle glucose uptakeAntisense oligonucleotideBasal endogenous glucose productionInsulin-stimulated whole-body glucose disposalCoactivator-1Whole-body glucose disposalSkeletal muscle glucose uptakeLipocalin-type prostaglandin D2 synthaseSprage-Dawley ratsGluconeogenic enzymes
2001
Disruption of Sur2-containing KATP channels enhances insulin-stimulated glucose uptake in skeletal muscle
Chutkow W, Samuel V, Hansen P, Pu J, Valdivia C, Makielski J, Burant C. Disruption of Sur2-containing KATP channels enhances insulin-stimulated glucose uptake in skeletal muscle. Proceedings Of The National Academy Of Sciences Of The United States Of America 2001, 98: 11760-11764. PMID: 11562480, PMCID: PMC58803, DOI: 10.1073/pnas.201390398.Peer-Reviewed Original ResearchMeSH KeywordsAnalysis of VarianceAnimalsATP-Binding Cassette TransportersBiological TransportBlood GlucoseDeoxyglucoseExonsGlucoseGlucose Clamp TechniqueGlucose Tolerance TestGlucose Transporter Type 4InsulinIntronsMiceMice, KnockoutMonosaccharide Transport ProteinsMuscle ProteinsMuscle, SkeletalPolymerase Chain ReactionPotassium ChannelsPotassium Channels, Inwardly RectifyingReceptors, DrugRNA, MessengerSignal TransductionSodium-Potassium-Exchanging ATPaseSulfonylurea ReceptorsTriglyceridesWeight GainConceptsSkeletal muscleInsulin-stimulated glucose transportGene-targeting strategiesGlucose uptake mechanismsInsulin-stimulated glucose uptakeHomozygous null miceRegulatory subunitInsertional mutagenesisWild typeEnhanced glucose useProtection of tissuesDiverse arrayGlucose transportChannel activityUptake mechanismNull miceATP-sensitive potassium channelsPotassium channelsGlucose uptakeMembrane excitabilityFuture therapeutic approachesWild-type littermatesTarget blood glucose levelsInsulin actionPhysiologic function