Rosiglitazone-Induced Mitochondrial Biogenesis in White Adipose Tissue Is Independent of Peroxisome Proliferator-Activated Receptor γ Coactivator-1α 英文参考文献.docVIP

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Rosiglitazone-Induced Mitochondrial Biogenesis in White Adipose Tissue Is Independent of Peroxisome Proliferator-Activated Receptor γ Coactivator-1α 英文参考文献.doc

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Rosiglitazone-Induced Mitochondrial Biogenesis in White Adipose Tissue Is Independent of Peroxisome Proliferator-Activated Receptor γ Coactivator-1α 英文参考文献

Rosiglitazone-InducedMitochondrialBiogenesisinWhite AdiposeTissueIsIndependentofPeroxisome Proliferator-ActivatedReceptorcCoactivator-1a RosarioPardo1,Nata`liaEnguix1,JaimeLasheras1,JuanE.Feliu1,AnastasiaKralli2,JosepA.Villena1* 1Laboratory of Metabolism and Obesity, Unit of Diabetes and Metabolism, Vall d’Hebron-Institut de Recerca, Universitat Auto`noma de Barcelona, Barcelona, Spain, 2DepartmentofChemicalPhysiology,TheScrippsResearchInstitute,LaJolla,California,UnitedStatesofAmerica Abstract Background:Thiazolidinediones,afamilyofinsulin-sensitizingdrugscommonlyusedtotreattype2diabetes,arethought to exert their effects in part by promoting mitochondrial biogenesis in white adipose tissue through the transcriptional coactivatorPGC-1a(PeroxisomeProliferator-ActivatedReceptorcCoactivator-1a). Methodology/Principal Findings: To assess the role of PGC-1a in the control of rosiglitazone-induced mitochondrial biogenesis,wehavegeneratedamousemodelthatlacksexpressionofPGC-1aspecificallyinadiposetissues(PGC-1a-FAT- KOmice).Wefoundthatexpressionofgenesencodingformitochondrialproteinsinvolvedinoxidativephosphorylation, tricarboxylicacidcycleorfattyacidoxidation,wassimilarinwhiteadiposetissueofwildtypeandPGC-1a-FAT-KOmice. Furthermore,theabsenceofPGC-1adidnotpreventthepositiveeffectofrosiglitazoneonmitochondrialgeneexpression orbiogenesis,butitprecludedtheinductionbyrosiglitazoneofUCP1andotherbrownfat-specificgenesinwhiteadipose tissue. Consistent with the in vivo findings, basal and rosiglitazone-induced mitochondrial gene expression in 3T3-L1 adipocyteswasunaffectedbytheknockdownofPGC-1abutitwasimpairedwhenPGC-1bexpressionwasknockdownby theuseofspecificsiRNA. Conclusions/Significance: These results indicate that in white adipose tissue PGC-1a is dispensable for basal and rosiglitazone-inducedmitochondrial biogenesis butrequired fortherosiglitazone-induced expressionofUCP1andother brownadipocyte-specificmarkers.OurstudysuggeststhatPGC-1aisimportantfortheappearanceofbrowna