CAJ | 학술논문

目的：研究胰岛素对骨骼肌细胞固醇调节原件结合蛋白1c（SREBP‐1c）的调节作用。方法将诱导分化完成的大鼠骨骼肌L6肌管细胞分为对照组、胰岛素组、磷酸酰基醇3激酶抑制剂wortmannin＋胰岛素组、单磷酸腺苷依赖的蛋白激酶（AM PK ）抑制剂compound C＋胰岛素组、高脂对照组、高脂＋胰岛素组、高脂＋wortmannin＋胰岛素组和高脂＋compound C＋胰岛素组。Western blot检测SREBP‐1c、苏氨酸蛋白激酶（Akt）‐哺乳动物雷帕霉素靶蛋白（mTOR）、AMPK‐mTOR通路相关蛋白的表达。结果与对照组相比，胰岛素组SREBP‐1c、p‐Akt、p‐AMPK、p‐mTOR蛋白表达升高（P＜0．05）；与胰岛素组相比，wortmannin＋胰岛素组SREBP‐1c表达降低（P＜0．05）；与高脂对照组相比，高脂＋胰岛素组 SREBP‐1c、p‐mTOR 蛋白表达降低，p‐Akt、p‐AMPK 蛋白表达升高（P＜0．05）；与高脂＋胰岛素组相比，高脂＋compound C＋胰岛素组SREBP‐1c表达升高（P＜0．05）。结论骨骼肌细胞生理状态下，胰岛素对SREBP‐1c的上调作用可能主要通过Akt‐mTOR通路；胰岛素抵抗状态下，胰岛素治疗对SREBP‐1c的下调作用可能主要通过AMPK‐mTOR通路。
목적：연구이도소대골격기세포고순조절원건결합단백1c（SREBP‐1c）적조절작용。방법장유도분화완성적대서골격기L6기관세포분위대조조、이도소조、린산선기순3격매억제제wortmannin＋이도소조、단린산선감의뢰적단백격매（AM PK ）억제제compound C＋이도소조、고지대조조、고지＋이도소조、고지＋wortmannin＋이도소조화고지＋compound C＋이도소조。Western blot검측SREBP‐1c、소안산단백격매（Akt）‐포유동물뢰파매소파단백（mTOR）、AMPK‐mTOR통로상관단백적표체。결과여대조조상비，이도소조SREBP‐1c、p‐Akt、p‐AMPK、p‐mTOR단백표체승고（P＜0．05）；여이도소조상비，wortmannin＋이도소조SREBP‐1c표체강저（P＜0．05）；여고지대조조상비，고지＋이도소조 SREBP‐1c、p‐mTOR 단백표체강저，p‐Akt、p‐AMPK 단백표체승고（P＜0．05）；여고지＋이도소조상비，고지＋compound C＋이도소조SREBP‐1c표체승고（P＜0．05）。결론골격기세포생리상태하，이도소대SREBP‐1c적상조작용가능주요통과Akt‐mTOR통로；이도소저항상태하，이도소치료대SREBP‐1c적하조작용가능주요통과AMPK‐mTOR통로。
Objective To study the regulatory effects of insulin on sterol regulatory element binding protein‐1c (SREBP‐1c ) in skeletal muscle cells .Methods Rat L6 muscle cells were differentiated into myotubes ,which were divided into eight groups of A1(not given drug as controls) , A2(treated with insulin ) ,A3 (treated with insulin plus wortmannin ) ,A4 (treated with insulin plus compound C) ,B1(given palmitic acid) ,B2(treated with insulin under given palmitic acid ) ,B3(treated with insulin plus wortmannin under given palmitic acid ) and B4(treated with insulin plus compound C under given palmitic acid) .The protein levels of SREBP‐1c ,threonine protein kinase(Akt)‐mTOR and adenosine phosphate dependent protein kinase (AMPK )‐mTOR pathways were assayed by Western blot .Results Compared with group A1 ,the protein levels of SREBP‐1c ,p‐Akt and p‐AMPK were increased in group A2(P<0 .05) .Compared with group A2 ,SREBP‐1c was decreased in group A3 (P<0 .05) .Compared with group B1 ,the protein levels of SREBP‐1c and p‐mTOR were decreased , while those of p‐Akt and p‐AMPK were increased in group B2(P<0 .05) .Compared with group B2 , SREBP‐1c was increased in group B4 ( P<0 .05 ) .Conclusion Under physiological condition of skeletal muscle ,the effect of insulin on the upregulation of SREBP‐1c may work mainly through Akt‐mTOR pathway .Under insulin resistance condition ,the effect of insulin on the downregulation of SREBP‐1c may work mainly through AMPK‐mTOR pathway .