Acute Regulation of Cardiac Metabolism by the Hexosamine Biosynthesis Pathway and Protein O-GlcNAcylation 英文参考文献.docVIP

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Acute Regulation of Cardiac Metabolism by the Hexosamine Biosynthesis Pathway and Protein O-GlcNAcylation 英文参考文献.doc

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Acute Regulation of Cardiac Metabolism by the Hexosamine Biosynthesis Pathway and Protein O-GlcNAcylation 英文参考文献

AcuteRegulationofCardiacMetabolismbythe HexosamineBiosynthesisPathwayandProtein O-GlcNAcylation Bogla′rkaLaczy1.,NorbertFu¨lo¨p1,2.,ArzuOnay-Besikci3,ChristineDesRosiers4,JohnC.Chatham1* 1DivisionofCardiovascularDisease,DepartmentofMedicine,UniversityofAlabamaatBirmingham,Birmingham,Alabama,UnitedStatesofAmerica,2Departmentof Nephrology, Kaposi Mo′r County Hospital, Kaposva′r, Hungary, 3Department of Pharmacology, University of Ankara, Ankara, Turkey, 4Montreal Heart Institute and DepartmentofNutrition,Universite′ deMontre′al,Montreal,Quebec,Canada Abstract Objective:Thehexosaminebiosynthesispathway(HBP)fluxandproteinO-linkedN-acetyl-glucosamine(O-GlcNAc)levels have been implicated in mediating the adverse effects of diabetes in the cardiovascular system. Activation of these pathwayswithglucosaminehasbeenshowntomimicsomeofthediabetes-inducedfunctionalandstructuralchangesin the heart; however, the effect on cardiac metabolism is not known. Therefore, the primary goal of this study was to determinetheeffectsofglucosamineoncardiacsubstrateutilization. Methods:Isolatedratheartswereperfusedwithglucosamine(0–10mM)toincreaseHBPfluxundernormoxicconditions. Metabolic fluxes were determined by 13C-NMR isotopomer analysis; UDP-GlcNAc a precursor of O-GlcNAc synthesis was assessedbyHPLCandimmunoblotanalysiswasusedtodetermineO-GlcNAclevels,phospho-andtotallevelsofAMPKand ACC,andmembranelevelsofFAT/CD36. Results:GlucosaminecausedadosedependentincreaseinbothUDP-GlcNAcandO-GlcNAclevels,whichwasassociated withasignificantincreaseinpalmitateoxidationwithaconcomitantdecreaseinlactateandpyruvateoxidation.Therewas noeffectofglucosamineonAMPKorACCphosphorylation;however,membranelevelsofthefattyacidtransportprotein FAT/CD36wereincreasedandpreliminarystudiessuggestthatFAT/CD36isapotentialtargetforO-GlcNAcylation. Conclusion/Interpretation:ThesedatademonstratethatacutemodulationofHBPandproteinO-GlcNAcylationintheheart stimulates fatty acid oxidation, possibly by increasing plasma membran