【摘要】 目的:探讨在体外建立方便可靠的肝胰岛素抵抗细胞模型、脂肪细胞胰岛素抵抗模型和肌细胞胰岛素抵抗模型的方法。方法:3T3-L1小鼠前脂肪细胞、C2C12小鼠成肌细胞分别诱导分化为成熟的脂肪细胞和肌细胞。采用地塞米松(EDX)诱导人肝细胞Hep G2以及分化成熟的Hep G2、C2C12细胞,以葡萄糖氧化酶法检测细胞对葡萄糖的消耗情况。结果:1μmol/L DEX作用24 h和48 h均能抑制细胞葡萄糖消耗,撤掉DEX,胰岛素抵抗细胞模型在48 h内维持稳定。对于Hep G2和C2C12细胞,DEX造模48 h优于24 h;但对于3T3-L1细胞,DEX造模24 h和48 h对细胞葡萄糖消耗影响无显著性差异。结论:DEX可诱导3T3-L1、Hep G2、C2C12细胞产生胰岛素抵抗,这种细胞模型简便稳定。更多还原

【Abstract】 Objective:To investigate the establish a convenient and reliable hepatic insulin resistance in vitro cell model,the fat cells insulin resistance model and the method of muscle insulin resistance model. Methods: 3 t3- L1 before the fat cells in mice, mice C2C12 myoblast differentiation into mature fat cells and muscle cells. Using dexamethasone(EDX) induced liver cell Hep G2 and matured Hep G2, C2C12 cells, with glucose oxidase method to detect the cell to glucose consumption situation. Results: 1 mu mol/L DEX effect can inhibit cell 24 h and 48 h glucose consumption, remove DEX, insulin resistance stability of the cell model within 48 h. In Hep G2 and C2C12 cells, 24 h, 48 h DEX made model is superior to the But for the 3 t3 cells- L1, DEX building 24 h and 48 h there was no significant difference effect on cell glucose consumption. Conclusion: DEX can induce 3 t3- L1, Hep G2, C2C12 cells produce insulin resistance, the cell model is simple and stable.更多还原