MiRNA-27a对3T3-L1细胞胰岛素抵抗的作用及机制  

Effect and Mechanism of MiRNA-27a on Insulin Resistance in 3T3-L1 Cells

作　　者：谢军[1] 蔡克银[1] 

机构地区：[1]中国人民解放军广州军区武汉总医院干部病房二科,湖北武汉430070

出　　处：《华南国防医学杂志》2014年第2期97-99,112,共4页Military Medical Journal of South China

摘　　要：目的研究miRNA-27a对3T3-L1细胞葡萄糖摄取的影响,并初步探讨其作用机制。方法通过肿瘤坏死因子α(tumor necrosis factor alpha,TNF-α)诱导建立3T3-L1脂肪细胞胰岛素抵抗的细胞模型,观察miRNA-27a对3T3-L1细胞葡萄糖摄取的影响,酶联免疫吸附(enzyme-linked immunosorbent assay,ELISA)检测细胞培养上清中白细胞介素6(interleukin 6,IL-6)的变化,Western blot检测细胞内总Akt和磷酸化Akt的变化。结果 miRNA-27a明显抑制3T3-L1细胞对胰岛素诱导的葡萄糖的摄取,miRNA-27a可促进炎症因子IL-6的产生并抑制Akt的磷酸化。结论 miRNA-27a可促进脂肪细胞产生胰岛素抵抗,其作用可能通过抑制胰岛素信号通路PI3K/Akt实现。Objective To research the influence of miRNA-27a on glucose uptake of 3T3-L1 adipocyte and the probability mechanisms. Methods 3T3-L1 cell model with insulin resistance was established by tumor necrosis factor al- pha （TNF-α） induction. The influence of miRNA-27a on glucose uptake of 3T3-L1 adipocyte was observed. Changes of in- terleukin 6 （IL-6） levels were tested by enzyme-linked immunosorbent assay （ELISA）. Changes of total Akt and Akt phosphorylation were tested by Western blot. Results MiRNA-27a significantly inhibited the glucose uptake of 3T3-L1 adipocyte,and promoted IL-6 secretion and inhibited phosphorylation of Akt. Conclusion miRNA-27a can promote insulin resistance of adipocyte possibly by inhibiting PI3K/Akt signal pathway.

关 键 词：miRNA-27a 胰岛素抵抗3T3-L1脂肪细胞 PBK AKT信号通路 

分 类 号：R587.1[医药卫生—内分泌]