肌肉肌醇对HepG2胰岛素抵抗模型葡萄糖消耗量影响的细胞实验研究(英文)  

In Vitro study of Effect of MI on the Insulin-resistant HepG2 Cell Model

作　　者：高丽鹤 宋扬[1] 刘翠萍[1] 付敏[1] 王鹏[1] 

机构地区：[1]青岛大学医学院营养研究所,山东青岛266021

出　　处：《现代生物医学进展》2016年第12期2245-2248,共4页Progress in Modern Biomedicine

基　　金：国家自然科学基金项目(81373001)~~

摘　　要：目的:研究肌肉肌醇(myo-inositol,MI)对胰岛素抵抗细胞(IR-HepG2)细胞外葡萄糖消耗量的影响。方法:采用CCK-8法观察MI、高糖对HepG2细胞活力的影响,通过高糖持续作用,胰岛素刺激诱导HepG2细胞建立胰岛素抵抗细胞模型,葡萄糖氧化酶法(GOD-POD法)鉴定模型是否成立,并用GOD-POD法检测正常HepG2细胞和MI对HepG2胰岛素抵抗细胞葡萄糖消耗量的变化。结果:在对HepG2细胞活性没有影响的情况下,MI增加了胰岛素抵抗模型的葡萄糖消耗量。与模型对照组相比,葡萄糖氧化酶法结果显示,MI可显著增加胰岛素抵抗模型葡糖糖的消耗量(P<0.01)。结论:MI可明显增加IR-HepG2细胞模型葡萄糖的消耗量,对IR-HepG2细胞模型胰岛素抵抗有显著的改善作用。Objective： To explore effect of myo-inositol（MI） on improving glucose consumption of insulin-resistant HepG2（IR-HepG2） cell model. Methods： IR-HepG2 cell model was established by high glucose and insulin stimulation. Successful authentication of model was determined by glucose oxidase method（GOD-POD）. Effect of high glucose, MI on activity of HepG2 cells was detected by CCK-8 assay. Glucose consumption of normal HepG2 cell and IR-HepG2 cell were determined by GOD-POD. Results：MI treatment groups had no valid influence on HepG2 cell, while they could increase glucose consumption of IR-HepG2 cell. GOD-POD analysis found that compared with model control group, consumption of D-glucose was significantly higher in MI treatment groups（P〈0.01）. Conclusions： The MI could significantly promote the glucose consumption of the insulin-resistant HepG2 cell to improve the insulin resistance.

关 键 词：肌肉肌醇 胰岛素抵抗 HEPG2细胞 葡萄糖消耗量 

分 类 号：R151[医药卫生—营养与食品卫生学] R-33[医药卫生—公共卫生与预防医学]