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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。

英文摘要:

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).Conclusion:The MI could significantly promote the glucose consumption of the insulin-resistant HepG2 cell to improve the insulin resistance.

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