地塞米松体外诱导胰岛素抵抗细胞模型的建立  

Insulin Resistance Model Induced Dexamethasone in Vitro Cell

作　　者：谢洁[1] 杨瑞仪[1] 

机构地区：[1]广州中医药大学热带医学研究所,广州510405

出　　处：《科技通报》2015年第10期31-33,共3页Bulletin of Science and Technology

基　　金：国家自然科学基金资助项目(No 81202968)

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。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) in-duced liver cell HepG2 and matured HepG2, C2C12 cells, with glucose oxidase method to detect the cell to glucose con-sumption situation. Results:1 mu mol/L DEX effect can inhibit cell 24 h and 48 h glucose consumption, remove DEX, in-sulin resistance stability of the cell model within 48 h. In HepG2 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 con-sumption. Conclusion:DEX can induce 3 t3-L1, HepG2, C2C12 cells produce insulin resistance, the cell model is sim-ple and stable.

关 键 词：地塞米松 胰岛素抵抗 HEPG2 3T3-L1 C2C12 

分 类 号：R457[医药卫生—治疗学]