线粒体融合蛋白2改善高脂诱导的骨骼肌细胞胰岛素抵抗机制的研究

目的 探讨线粒体融合蛋白2 （Mfn2）是否通过减轻氧化应激改善大鼠骨骼肌细胞IR.方法 建立高脂诱导骨骼肌细胞IR模型（PA组）,以Mfn2基因重组腺病毒转染细胞（PMfn2组）,观察细胞内葡萄糖摄取率、超氧化物歧化酶总活力（T-SOD）、过氧化氢酶（CAT）、活性氧簇（ROS）及MDA的改变. 结果 （1）与正常对照（NC）组相比,高脂（PA）组葡萄糖摄取率降低（P＜0.01）,T-SOD及CAT活性降低,ROS、MDA含量增加（P＜0.05）;（2）与PA组相比,Mfn2基因重组腺病毒转染（PMfn2）组T-SOD及CAT活力均增加（P＜0.05）;ROS水平、MDA含量降低（P＜0.05）;GSH-Px活力无明显改变. 结论 上调高脂干预后骨骼肌细胞的Mfn2水平可减轻细胞氧化应激,改善IR.

The mechanism for mitofusin 2 improving insulin resistance induced by high fat diet in skeletal muscle cells

Objective To study the mechanism for Mitofusin 2 improving insulin resistance in skeletal muscle cells induced by high fat diet.Methods High fat-induced insulin resistance rat model was established （PA group） and the skeletal muscle cells were studied.Mfn2 genetic recombination adenovirus were used for transfecting cells （PMfn2 group）.And changes of intracellular glucose uptake rate,the total activity of superoxide dismutase （T-SOD）,catalase （CAT）,reactive oxygen species （ROS） and MDA were examined.Results （1） The glucose uptake rate and T-SOD and CAT activities were lower in PA group than in NC group （P〈0.01）,and the contents of ROS and MDA were higher in PA group than in NC group （P〈0.05） ; （2） As compared with the PA group,PMfn2 group showed that T-SOD and CAT activities were increased （P〈0.05）,ROS levels and MDA content were decreased （P〈 0.05）,and GSH-Px activity had no significant change.Conclusion Increasing the Mfn2 level of skeletal muscle cells by intervention of high fat diet can reduce cellular oxidative stress,and improve insulin resistance.