HDL代谢的生理学和病理学意义PPT课件.ppt

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1、HDLandCoronaryHeartDiseasePhysiologyandPathophysiologyofHDLMetabolismStructureofHDLParticleA-IA-IA-IIA-I,A-II=apolipoproteinA-I,A-II;CE=cholesterylester;TG=triglyceridesCETGProductionofHDLbyLiverandIntestineA-IA-IA-IIA-I,A-II=apolipoproteinA-I,A-IILiverIntestineHDLHDLHDLMetabolismandReve

2、rseCholesterolTransportA-ILiverCECECEFCFCLCATFCBileSR-BIA-IABC1=ATP-bindingcassetteprotein1;A-I=apolipoproteinA-I;CE=cholesterylester;FC=freecholesterol;LCAT=lecithin:cholesterolacyltransferase;SR-BI=scavengerreceptorclassBIABC1MacrophageMatureHDLNascentHDLRoleofCETPinHDLMetabolismA-I

3、LiverCECEFCFCLCATFCBileSR-BIA-IABC1MacrophageCEBCETP=cholesterylestertransferproteinLDL=low-densitylipoproteinLDLR=low-densitylipoproteinreceptorVLDL=very-low-densitylipoproteinLDLRVLDL/LDLCETPMatureHDLNascentHDLCESRAOxidationRoleofHepaticLipaseandLipoproteinLipaseinHDLMetabolismCM=chyl

4、omicron;CMR=chylomicronremnant;HDL=high-densitylipoprotein;HL=hepaticlipase;IDL=intermediate-densitylipoprotein;LPL=lipoproteinlipase;PL=phospholipase;TG=triglycerideBKidneyEndotheliumBTGCMR/IDLC-IICM/VLDLHLLPLA-ICETGHDL2PLA-ICEHDL3PLPhospholipidsandapolipoproteinsPrimary(Genetic)Causeso

5、fLowHDL-CApoA-ICompleteapoA-IdeficiencyApoA-Imutations(eg,ApoA-IMilano)LCATCompleteLCATdeficiencyPartialLCATdeficiency(fish-eyedisease)ABC1TangierdiseaseHomozygousHeterozygousFamilialhypoalphalipoproteinemia(somefamilies)UnknowngeneticetiologyFamilialhypoalphalipoproteinemia(mostfamilies)F

6、amilialcombinedhyperlipidemiawithlowHDL-CMetabolicsyndromeCompleteApoA-IDeficiencyMarkedlyreducedHDL-ClevelsandabsentapoA-ICutaneousxanthomas(somepatients)Prematureatheroscleroticvasculardisease(somepatients)ApoA-IMutationsModesttomarkedreductioninHDL-CandapoA-IRapidcatabolismofapoA-ISyst

7、emicamyloidosisPrematureatheroscleroticdisease(rare)LCATDeficiencyandFish-eyeDiseaseBothduetomutationsinLCATgene:LCATdeficiency–completeFish-eyedisease–partialCommontobothtypesofLCATdeficiency:MarkedlyreducedHDL-CandapoA-IlevelsRapidcatabolismofapoA-IandapoA-I