津力达对高脂诱导的胰岛素抵抗ApoE—/—小鼠骨骼肌脂质转运酶类的表达变化(1)
[摘要]目的：探究津力达对高脂诱导的胰岛素抵抗ApoE-/-小鼠骨骼肌脂质转运酶类相关基因的表达变化。方法：8只雄性C57BL/6J小鼠设为正常组(NF);40只雄性ApoE-/-小鼠喂养16周后分为模型组(HF)、罗格列酮组(LGLT)、津力达低剂量组(JLDL)、津力达中剂量组(JLDM)、津力达高剂量组(JLDH)，开始灌胃给药，连续8周。采用组织游离脂肪酸、BCA蛋白浓度法测定骨骼肌FFA含量;实时荧光定量反转录PCR(RT-PCR)和蛋白质印迹法(Westernblot)测定小鼠骨骼肌脂肪酸转位酶(FAT/CD36)、肉毒碱棕榈酰基转移酶1(CPT1)、过氧化物酶体增殖物激活受体α(PPARα)mRNA和蛋白表达。结果：津力达能够不同程度降低小鼠的空腹血糖(FBG)、胆固醇(TC)、甘油三酯(TG)和游离脂肪酸(FFA);下调空腹胰岛素(FIns)水平，提高胰岛素敏感指数(ISI);津力达能够不同程度的上调小鼠CPT1，PPARαmRNA和蛋白表达，下调FAT/CD36的mRNA和蛋白水平。结论：津力达能够通过调节骨骼肌脂质转运酶类的表达变化，改善高脂诱导的ApoE-/-小鼠的胰岛素抵抗。
, 百拇医药
[关键词]津力达;ApoE-/-小鼠;胰岛素抵抗;骨骼肌脂质转运酶
EffectofJinlidaonchangesinexpressionofskeletalmusclelipidtransport
enzymesinfat-inducedinsulinresistanceApoE-/-mice
JINXin/1，ZHANGHui-xin1，2*，ZHANGYan-fen2，3，CUIWen-wen/1，BIYao/1，HEQi-long/1，ZHOUSheng-shan/1
(1.HeilongjiangUniversityofChineseMedicine，Harbin150040，China;
, 百拇医药
2.YilingMedicalResearchInstituteofHebeiProvince，KeyLaboratoryofStateAdministrationofTraditionalChinese
Medicine(Cardio-CerebralVascularNetworkDisease)，Shijiazhuang050035，China;
3.KeyLaboratoryofNetworkDiseaseofHebeiProvince，Shijiazhuang050035，China)
[Abstract]Objective：TostudytheeffectofJinlidaonchangesinexpressionofskeletalmusclelipidtransportenzymesinfat-inducedinsulinresistanceApoE-/-mice.Method：EightmaleC57BL/6Jmicewereselectedinthenormalgroup(NF)，40maleApoE-/-micewerefedfor16weeks，dividedintothemodelgroup(HF)，therosiglitazonegroup(LGLT)，theJinlidalow-dosegroup(JLDL)，theJinlidamedium-dosegroup(JLDM)，theJinlidahigh-dosegroup(JLDH)andthenorallygivendrugsfor8weeks.Theorganizationfreefattyacids，BCAproteinconcentrationdeterminationmethodswereusedtodeterminetheskeletalmuscleFFAcontent.TheReal-timefluorescentquantitativereversetranscriptionPCR(RT-PCR)andWesternblotmethodwereadoptedtodeterminemRNAandproteinexpressionsofmicefattyacidstranspositionenzyme(FAT/CD36)，carnitinepalmacyltransferase1(CPT1)，peroxideproliferators-activatedreceptorα(PPARα).Result：Jinlidacoulddecreasefastingbloodglucose(FBG)，cholesterol(TC)，triglyceride(TG)，freefattyacid(FFA)andfastinginsulin(FIns)andraiseinsulinsensitiveindex(ISI)inmicetovaryingdegrees.Itcouldalsoup-regulatemRNAandproteinexpressionsofCPT1andPPARα，anddown-regulatemRNAandproteinlevelsofFAT/CD36.Conclusion：Jinlidacanimprovefat-inducedinsulinresistanceApoE-/-inmicebyadjustingthechangesinexpressionofskeletalmusclelipidtransportenzymes.
[Keywords]Jinlida;ApoE-/-mice;insulinresistance;skeletalmusclelipidtransportenzyme, 百拇医药(金鑫 张会欣 张彦芬 崔雯雯 秘尧 何其龙 周升山)
, 百拇医药
[关键词]津力达;ApoE-/-小鼠;胰岛素抵抗;骨骼肌脂质转运酶
EffectofJinlidaonchangesinexpressionofskeletalmusclelipidtransport
enzymesinfat-inducedinsulinresistanceApoE-/-mice
JINXin/1，ZHANGHui-xin1，2*，ZHANGYan-fen2，3，CUIWen-wen/1，BIYao/1，HEQi-long/1，ZHOUSheng-shan/1
(1.HeilongjiangUniversityofChineseMedicine，Harbin150040，China;
, 百拇医药
2.YilingMedicalResearchInstituteofHebeiProvince，KeyLaboratoryofStateAdministrationofTraditionalChinese
Medicine(Cardio-CerebralVascularNetworkDisease)，Shijiazhuang050035，China;
3.KeyLaboratoryofNetworkDiseaseofHebeiProvince，Shijiazhuang050035，China)
[Abstract]Objective：TostudytheeffectofJinlidaonchangesinexpressionofskeletalmusclelipidtransportenzymesinfat-inducedinsulinresistanceApoE-/-mice.Method：EightmaleC57BL/6Jmicewereselectedinthenormalgroup(NF)，40maleApoE-/-micewerefedfor16weeks，dividedintothemodelgroup(HF)，therosiglitazonegroup(LGLT)，theJinlidalow-dosegroup(JLDL)，theJinlidamedium-dosegroup(JLDM)，theJinlidahigh-dosegroup(JLDH)andthenorallygivendrugsfor8weeks.Theorganizationfreefattyacids，BCAproteinconcentrationdeterminationmethodswereusedtodeterminetheskeletalmuscleFFAcontent.TheReal-timefluorescentquantitativereversetranscriptionPCR(RT-PCR)andWesternblotmethodwereadoptedtodeterminemRNAandproteinexpressionsofmicefattyacidstranspositionenzyme(FAT/CD36)，carnitinepalmacyltransferase1(CPT1)，peroxideproliferators-activatedreceptorα(PPARα).Result：Jinlidacoulddecreasefastingbloodglucose(FBG)，cholesterol(TC)，triglyceride(TG)，freefattyacid(FFA)andfastinginsulin(FIns)andraiseinsulinsensitiveindex(ISI)inmicetovaryingdegrees.Itcouldalsoup-regulatemRNAandproteinexpressionsofCPT1andPPARα，anddown-regulatemRNAandproteinlevelsofFAT/CD36.Conclusion：Jinlidacanimprovefat-inducedinsulinresistanceApoE-/-inmicebyadjustingthechangesinexpressionofskeletalmusclelipidtransportenzymes.
[Keywords]Jinlida;ApoE-/-mice;insulinresistance;skeletalmusclelipidtransportenzyme, 百拇医药(金鑫 张会欣 张彦芬 崔雯雯 秘尧 何其龙 周升山)