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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) 被引量:2

In Vitro study of Effect of MI on the Insulin-resistant HepG2 Cell Model
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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.
出处 《现代生物医学进展》 CAS 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)~~
关键词 肌肉肌醇 胰岛素抵抗 HEPG2细胞 葡萄糖消耗量 MI Insulin resistance(IR) HepG2 cells Glucose consumption
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