2013
Urocortin 2 autocrine/paracrine and pharmacologic effects to activate AMP-activated protein kinase in the heart
Li J, Qi D, Cheng H, Hu X, Miller EJ, Wu X, Russell KS, Mikush N, Zhang J, Xiao L, Sherwin RS, Young LH. Urocortin 2 autocrine/paracrine and pharmacologic effects to activate AMP-activated protein kinase in the heart. Proceedings Of The National Academy Of Sciences Of The United States Of America 2013, 110: 16133-16138. PMID: 24043794, PMCID: PMC3791748, DOI: 10.1073/pnas.1312775110.Peer-Reviewed Original ResearchMeSH KeywordsAcetyl-CoA CarboxylaseAMP-Activated Protein KinasesAnalysis of VarianceAnimalsAntibodies, NeutralizingCorticotropin-Releasing HormoneEnzyme ActivationImmunoblottingImmunohistochemistryMiceMyocardiumPeptide FragmentsPhosphorylationReceptors, Corticotropin-Releasing HormoneReperfusion InjurySignal TransductionUrocortinsConceptsIschemia/reperfusionIschemia/reperfusion injuryUCN2 treatmentReperfusion injuryContractile dysfunctionRegional ischemia/reperfusionAMPK activationHeart muscleIschemic AMPK activationAutocrine/paracrine pathwayCardiac contractile dysfunctionAutocrine/paracrine factorCorticotropin-releasing factor (CRF) familyIsolated heart muscleCRFR2 antagonistAcetyl-CoA carboxylase phosphorylationCardiac damageMyocardial injuryCRF receptorsPharmacologic effectsUrocortin 2ΕV1-2Activation of AMPParacrine pathwaysReperfusion
2004
Role of the nitric oxide pathway in AMPK-mediated glucose uptake and GLUT4 translocation in heart muscle
Li J, Hu X, Selvakumar P, Russell RR, Cushman SW, Holman GD, Young LH. Role of the nitric oxide pathway in AMPK-mediated glucose uptake and GLUT4 translocation in heart muscle. AJP Endocrinology And Metabolism 2004, 287: e834-e841. PMID: 15265762, DOI: 10.1152/ajpendo.00234.2004.Peer-Reviewed Original ResearchMeSH KeywordsAminoimidazole CarboxamideAMP-Activated Protein KinasesAnimalsBiological TransportEnzyme ActivationGlucoseGlucose Transporter Type 4Hypoglycemic AgentsIn Vitro TechniquesMaleMonosaccharide Transport ProteinsMultienzyme ComplexesMuscle ProteinsNitric OxideNitric Oxide SynthaseNitric Oxide Synthase Type IIIPapillary MusclesProtein Serine-Threonine KinasesProtein TransportRatsRats, Sprague-DawleyRibonucleotidesConceptsGLUT4 translocationAMPK stimulationGlucose transportAMPK catalytic subunitGlucose uptakeCell surfaceGlucose transporter GLUT4Serine-threonine kinaseEndothelial NO synthasePotential downstream mediatorsVesicular traffickingCatalytic subunitProtein kinaseAICAR treatmentCellular metabolismNitric oxide pathwayAMPKDownstream mediatorTranslocationEssential roleHeart muscleOxide pathwayCyclase pathwayPathwayAICARCardiac myocyte‐specific HIF‐1α deletion alters vascularization, energy availability, calcium flux, and contractility in the normoxic heart
Huang Y, Hickey RP, Yeh JL, Liu D, Dadak A, Young LH, Johnson RS, Giordano FJ. Cardiac myocyte‐specific HIF‐1α deletion alters vascularization, energy availability, calcium flux, and contractility in the normoxic heart. The FASEB Journal 2004, 18: 1138-1140. PMID: 15132980, DOI: 10.1096/fj.04-1510fje.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCalcium SignalingCoronary CirculationDNA-Binding ProteinsEnergy MetabolismGene DeletionGene Expression RegulationHeart Function TestsHypoxia-Inducible Factor 1Hypoxia-Inducible Factor 1, alpha SubunitMiceMice, Inbred C57BLMice, KnockoutMyocardial ContractionMyocardiumMyocytes, CardiacNeovascularization, PhysiologicNuclear ProteinsOxygen ConsumptionReverse Transcriptase Polymerase Chain ReactionRNA, MessengerTranscription FactorsTranscription, GeneticConceptsCardiac functionCalcium fluxHypoxia-inducible transcription factor HIF-1alphaCardiac oxygen deliveryDisease statesHIF-1alphaSkeletal muscleCardiac contractile dysfunctionHigh-energy phosphate contentCardiovascular disease statesResting pulse rateTranscription factor HIF-1alphaCoronary vasodilatationMyocardial demandContractile dysfunctionMyocardial hibernationNormoxic heartsOxygen supplyGene expressionCalcium handlingOxygen deliveryPulse rateHeart muscleCardiac muscleMolecular pathology
1993
Response of rat heart and skeletal muscle protein in vivo to insulin and amino acid infusion
McNulty PH, Young LH, Barrett EJ. Response of rat heart and skeletal muscle protein in vivo to insulin and amino acid infusion. American Journal Of Physiology 1993, 264: e958-e965. PMID: 8333520, DOI: 10.1152/ajpendo.1993.264.6.e958.Peer-Reviewed Original ResearchConceptsAmino acid infusionMuscle protein synthesisContinuous infusionAcid infusionNet muscle protein synthesisSaline-treated ratsSkeletal muscle protein synthesisInfusion of insulinPlasma specific activitySkeletal muscle proteinsProtein synthesisAmino acid solutionMature ratsInfusionRat heartInsulinBolusTracer infusionHeart muscleSkeletal muscleTracer infusion methodRatsPhysiological concentrationsAmino acids
1989
Physiologic hyperinsulinemia stimulates lactate extraction by heart muscle in the conscious dog
Young L, Zaret B, Barrett E. Physiologic hyperinsulinemia stimulates lactate extraction by heart muscle in the conscious dog. Metabolism 1989, 38: 1115-1119. PMID: 2682138, DOI: 10.1016/0026-0495(89)90049-8.Peer-Reviewed Original ResearchConceptsPhysiologic hyperinsulinemiaConscious dogsFree fatty acidsArterial free fatty acid concentrationMumol/minHeart muscleArterial plasma insulinMyocardial lactate uptakeFree fatty acid concentrationsArterial lactate concentrationHyperinsulinemic-euglycemic clampMyocardial glucose uptakeHyperinsulinemia increasesEuglycemic hyperinsulinemiaNormal heart muscleEuglycemic clampFatty acidsPlasma insulinBasal measurementsBlood glucoseLactate extractionFatty acid concentrationsMyocardial uptakeLactate uptakeHyperinsulinemia