胰島素抵抗與糖、脂代謝紊亂論文

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　　胰島素抵抗與糖、脂代謝紊亂論文【關鍵詞】胰島素抵抗;脂代謝紊亂;糖代謝紊亂在眾多心血管疾病的危險因素中胰島素抵抗(Insulinresistance,IR)處于核心地位，IR可先于糖尿病及心血管疾病多年而存在。目前將胰島素抵抗、中心性肥胖、糖耐量減低、高血壓、血脂代謝紊亂等多種疾病的組合,統(tǒng)稱為胰島素抵抗綜合征。盡管有很多遺傳因素可誘導IR產生，但目前認為IR最主要的誘因是過量的糖和脂肪。高糖和高脂均能引起肌肉和脂肪組織的IR,高脂還能導致肝臟IR的產生。高脂喂養(yǎng)動物或者靜脈輸注高脂均能破壞葡萄糖的轉運而迅速形成IR。血漿中脂類水平的升高,主要是游離脂肪酸(FFA)和甘油三酯(TG)、低密度脂蛋白膽固醇(LDL)含量增加是導致IR的重要原因〔1〕。2型糖尿病血糖過高會引起胰腺β細胞分泌胰島素減少,高血糖本身還進一步導致IR〔2〕?，F(xiàn)就IR與糖、脂代謝紊亂的關系綜述如下。1脂代謝紊亂與IR1.1FFA升高與IRFFA是引起IR的最主要非激素物質之一，可通過多種方式干擾胰島素的作用和葡萄糖代謝,能破壞胰島素敏感組織中的胰島素表達。肝臟高水平的FFA使肝糖異生和糖原分解增加,還抑制肝細胞對胰島素的滅活〔3〕，同時，F(xiàn)FA能啟動纖維蛋白原和纖溶酶原激活物抑制因子1(PAI1)在肝臟的合成〔4〕。在骨骼肌主要是抑制葡萄糖的攝取和氧化〔5〕。體內FFA長期升高還會耗竭胰島β細胞的分泌，導致其凋亡。在脂肪組織中，F(xiàn)FA抑制脂蛋白脂酶的活性.freeletabolismintheetiologyoftype2diabetes〔J〕.Diabetes,2002;51(1)：718.2RossettiL,GiaccariA,DeFronzoRA.Glucosetoxicity〔J〕.DiabetesCare,1990;13：610.3SunY,LiuS,FergusonS,etal.Phosphoenolpyruvatecarboxykinaseoverexpressionselectivelyattenuatesinsulinsignalingandhepaticinsulinsensitivityintransgenicmice〔J〕.JBiolChem,2002;277:233017.4KittFP,GeraldIS.Etilogyofinsulinresistance〔J〕.AmJMed,2006;119(5A):s106.5YuC,ChenY,ClineGechanismbyuscle〔J〕.JBiolChem,2002;277:502306. 6BarbaraM,JanjaM,AndrejJ,etal.Molecularmechanismofinsulinresistanceandassociateddiseases〔J〕.ClinChimActa,2006;375:2035.7RandlePJ,Hales,GarlandPB,etal.Theglucosefattyacidcyde.Itsroleininsulinsensitivityandthemetabolicdisturbancesofdiabetesmellitus〔J〕.Lancet,1963;1:7859.8Yoshikaentofperoxisomeproliferatorsactivatedreceptorsαorpancreatic/duodenalhomeobox〔J〕.Metabolism,2001;50:6138.9GrundySM,HansenB,SmithSC,etal,ClinicalManagementofMetabolicSyndrome.ReportoftheAmericanHeartAssociation/NationalHeart,Lung,andBloodInstitute/AmericanDiabetesAssociationConferenceonscientificissuesrelatedtomanagement〔J〕.Circulation,2004;109:5516.10FerranniniE,HaffnerSM,MitchellBD,etal.Hyperinsulinaemia:thekeyfeatureofacardiovascularandmetabolicsyndrome〔J〕.Diabetologia,1991;34:41622.11KenhE,ajorpulmonaryembolism:revieodynamicallysignificantpulmonaryembolism〔J〕.Chest,2002;121:877905.12ArcasoySM,KreitJetabolism,2000;49(12):162731.14Eschetabolicsyndrome,insulinresistanceandincreasedcardiovascular(CV)morbidityandmortalityintype2diabetes:aetiologicalfactorsinthedevelopmentofCVplications〔J〕.DiabetesMetab,2003;29(4Pt2);S1927.15AbbasiF,BroendolaC,etal.RelationshipbetCollCardiol,2002;40:93743.16HamelE,PacouretG,VincentelliD,etal.Thrombolysisorheparintherapyinmassivepulmonaryembolisma128patientmonocenterregistry〔J〕.Chest,2001;120:1205.17SohneM,ten,BullerHR.Biomarkersinpulmonaryembolism〔J〕.CurrOpinCardiol,2004;19:55862. 18KonstantinidesS,TiedeN,teGeibelA,etal.parisionofalteplaseversusheparnforresolutionofmajorpulmonaryembolism〔J〕.AMJCardiol,1998;82:96670.19McRaeSJ,GinsbergJS.Initialtreatmentofvenousthromboembolism〔J〕.Circulation,2004;110:s39.20吳正,姜月華.脂毒性和2型糖尿病關系探討〔J〕.現(xiàn)代中西醫(yī)結合雜志,2004;13(20):27934.21朱姿英,薛耀明.高甘油三酯血癥和2型糖尿病〔J〕.中國糖尿病雜志,2003;11(2):1534.22沈彥,方水林,袁靜平.控制血糖對2型糖尿病脂質代謝紊亂的影響〔J〕.浙江中西醫(yī)結合雜志,2004;14(11):6812.23GrundySM,BreanJI,etal.Definitionofmetabolicsyndrome:reportoftheNationalHeart,Lung,andBloodInstituteAmericanHeartAssociationconferenceonscientificissuesrelatedtodefinition〔J〕.ArteriosclerThrombVascBiol,2004;24(2):138.24MarshallS,BacoteV,TraxingerRR.Discoveryofametabolicpathediatingglucoseinduceddesensitizationoftheglucosetransportsystem〔J〕.JBiolChem,1991;266:4706.25VerenaKL.Highglucoseinducedtransforminggroediatedbythehexosaminepatherularmesangialcells〔J〕.JClinInvest,1998;101:160.26OkiT,YamazakiK,KuromitsuJ,etal.cDNAcloningandmappingofanovelsubtypeofglutamine:fructose6phosphateamidotransferase(GFAT2)inhumanandmouse〔J〕.Genomics,1999;57(2):227.