Featured Publications
Downregulation of hepatic ceruloplasmin ameliorates NAFLD via SCO1-AMPK-LKB1 complex
Xie L, Yuan Y, Xu S, Lu S, Gu J, Wang Y, Wang Y, Zhang X, Chen S, Li J, Lu J, Sun H, Hu R, Piao H, Wang W, Wang C, Wang J, Li N, White M, Han L, Jia W, Miao J, Liu J. Downregulation of hepatic ceruloplasmin ameliorates NAFLD via SCO1-AMPK-LKB1 complex. Cell Reports 2022, 41: 111498. PMID: 36261001, PMCID: PMC10153649, DOI: 10.1016/j.celrep.2022.111498.Peer-Reviewed Original ResearchConceptsNon-alcoholic fatty liver diseaseFatty liver diseaseLipid metabolism diseasesLipid catabolismHepatic lipid catabolismFatty acid oxidationDetectable hepatotoxicityCopper deficiencyNAFLD developmentLiver diseaseMetabolic diseasesMetabolism diseasesNormal levelsDiseaseMitochondrial biogenesisAcid oxidationAMPK activityAMPKAblationDeficiencyCatabolismLKB1Hepatotoxicity
2007
Plasma insulin levels predict the development of atherosclerosis when IRS2 deficiency is combined with severe hypercholesterolemia in apolipoprotein E-null mice.
Gonzalez-Navarro H, Vila-Caballer M, Pastor M, Vinue A, White M, Burks D, Andres V. Plasma insulin levels predict the development of atherosclerosis when IRS2 deficiency is combined with severe hypercholesterolemia in apolipoprotein E-null mice. Frontiers In Bioscience-Landmark 2007, 12: 2291-8. PMID: 17127239, DOI: 10.2741/2231.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsApolipoproteins EAtherosclerosisBlood GlucoseDiabetes Mellitus, Type 2Diabetic AngiopathiesFemaleHypercholesterolemiaInsulinInsulin Receptor Substrate ProteinsIntracellular Signaling Peptides and ProteinsLipidsMacrophagesMaleMiceMice, KnockoutMuscle, Smooth, VascularPhosphoproteinsConceptsInsulin receptor substrate 2ApoE-/- miceDevelopment of atherosclerosisIrs2-/- miceSevere hypercholesterolemiaInsulin levelsType 2 diabetic patientsAtherosclerotic lesion burdenPre-diabetic patientsPlasma insulin levelsFat-fed miceAbsence of hyperglycaemiaDefective insulin signalingDiabetic patientsLesion burdenClinical manifestationsInsulin resistanceModerate hypercholesterolemiaApolipoprotein EGlucose levelsAtherosclerotic lesionsAtherosclerosisHypercholesterolemiaNull miceImportant modulator
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