CAJ | 학술논문

目的：探讨津力达对高脂诱导的胰岛素抵抗ApoE-/-小鼠骨骼肌胆固醇相关基因的影响。方法10只♂C57BL/6J小鼠设为正常组(NF)；50只♂ ApoE-/-小鼠高脂喂养16周后分为模型组( HF)、罗格列酮组( LGLT)、津力达低剂量组( JLDL,0．95 g · kg-1· d-1)、津力达中剂量组( JLDM,1．9 g·kg-1· d-1)、津力达高剂量组( JLDH,3．8 g ·kg-1·d-1),开始灌胃给药,连续8周。采用油红O染色观察小鼠骨骼肌的脂肪蓄积情况；采用实时荧光定量反转录PCR( RT-PCR)和蛋白质印迹法( Western blot)测定小鼠骨骼肌胰岛素受体(INSR)、胰岛素受体底物-1(IRS-1)、低密度脂蛋白受体( LDLR)、胆固醇敏感器( SCAP) mRNA 和蛋白表达。结果与NF组相比,HF组小鼠空腹血糖( FBG)、胆固醇(TC)、甘油三酯(TG)和低密度脂蛋白胆固醇(LDL-C)均明显升高,高密度脂蛋白(HDL-C)明显降低(P<0．05)；与HF组相比,津力达组能够不同程度降低小鼠的FBG、TC、TG和LDL-C,升高HDL-C(P<0．05)；津力达(Jinlida,JLD)能够下调空腹血清胰岛素( FINS )水平,提高胰岛素敏感指数(ISI)(P<0．05)；津力达能够明显改善小鼠的骨骼肌脂肪蓄积；与NF组比较,HF组骨骼肌INSR、IRS-1、LDLR mRNA和蛋白水平均明显下降( P<0．05), SCAP mRNA和蛋白水平明显升高(P<0．05)；与HF组比较,津力达各组能够不同程度地上调INSR、IRS-1、LDLR mRNA和蛋白水平( P<0．05),下调SCAP mRNA和蛋白水平( P<0．05)。结论津力达能够通过调节骨骼肌胆固醇相关基因表达,改善高脂诱导的ApoE-/-小鼠的胰岛素抵抗。
목적：탐토진력체대고지유도적이도소저항ApoE-/-소서골격기담고순상관기인적영향。방법10지♂C57BL/6J소서설위정상조(NF)；50지♂ ApoE-/-소서고지위양16주후분위모형조( HF)、라격렬동조( LGLT)、진력체저제량조( JLDL,0．95 g · kg-1· d-1)、진력체중제량조( JLDM,1．9 g·kg-1· d-1)、진력체고제량조( JLDH,3．8 g ·kg-1·d-1),개시관위급약,련속8주。채용유홍O염색관찰소서골격기적지방축적정황；채용실시형광정량반전록PCR( RT-PCR)화단백질인적법( Western blot)측정소서골격기이도소수체(INSR)、이도소수체저물-1(IRS-1)、저밀도지단백수체( LDLR)、담고순민감기( SCAP) mRNA 화단백표체。결과여NF조상비,HF조소서공복혈당( FBG)、담고순(TC)、감유삼지(TG)화저밀도지단백담고순(LDL-C)균명현승고,고밀도지단백(HDL-C)명현강저(P<0．05)；여HF조상비,진력체조능구불동정도강저소서적FBG、TC、TG화LDL-C,승고HDL-C(P<0．05)；진력체(Jinlida,JLD)능구하조공복혈청이도소( FINS )수평,제고이도소민감지수(ISI)(P<0．05)；진력체능구명현개선소서적골격기지방축적；여NF조비교,HF조골격기INSR、IRS-1、LDLR mRNA화단백수평균명현하강( P<0．05), SCAP mRNA화단백수평명현승고(P<0．05)；여HF조비교,진력체각조능구불동정도지상조INSR、IRS-1、LDLR mRNA화단백수평( P<0．05),하조SCAP mRNA화단백수평( P<0．05)。결론진력체능구통과조절골격기담고순상관기인표체,개선고지유도적ApoE-/-소서적이도소저항。
Aim To investigate the effect of Jinlida on cholesterol-related genes in skeletal muscle in fat-in-duced insulin resistance ApoE-/ - mice. Methods Ten male C57 BL/6 J mice were selected as normal group ( NF );50 male ApoE-/ - mice with a high-fat feeding after 16 weeks ( HF) were divided into model group, rosiglitazone ( LGLT ) , Jinlida low dose group ( JLDL, 0. 95 g · kg-1 · d-1 ) , Jinlida medium dose group ( JLDM, 1. 9 g·kg-1 ·d-1 ) , Jinlida high dose group (JLDH, 3. 8 g·kg-1·d-1), which were per-formed intragastric administration for 8 weeks. Oil red O staining of mouse skeletal muscle was used for fat ac-cumulation. Insulin receptor ( INSR) , insulin receptor body substrate-1 ( IRS-1 ) , low-density lipoprotein re-ceptor ( LDLR ) , cholesterol sensor ( SCAP ) mRNA and protein expression in mouse skeletal muscle were measured by quantitative reverse transcription PCR ( RT-PCR ) and Western blot. Results Compared with NF group, fasting blood glucose ( FBG) , choles-terol ( TC ) , triglyceride ( TG ) and low density lipo-protein cholesterol ( LDL-C ) of HF mice were signifi-cantly elevated, while high-density lipoprotein ( HDL-C ) significantly decreased ( P < 0. 05 ) . Compared with HF group, Jinlida group could reduce to varying degrees FBG, TC, TG and LDL-C in mice, and in-crease HDL-C ( P <0. 05 ) . Jinlida could downgrade fasting serum insulin ( FINS ) level, and improve the insulin sensitive index ( ISI ) ( P < 0. 05 ) . Jinlida could obviously improve skeletal muscle fat accumula-tion of mice. Compared with NF group, skeletal mus-cle INSR, IRS-1, LDLR mRNA and protein levels of HF group were significantly decreased ( P <0. 05 ) , while SCAP mRNA and protein level increased signifi-cantly (P<0. 05). Compared with HF group, Jinlida could increase to varying degrees INSR, IRS-1, LDLR mRNA and protein levels ( P < 0. 05 ) , and lower SCAP mRNA and protein levels ( P<0. 05 ) . Conclu-sion Jinlida can alleviate fat-induced insulin resist-ance in ApoE-/ - mice through regulation of cholester-ol-related gene expression.