中文摘要：

目的探讨线粒体解耦联机制在NYGGF4基因致胰岛素抵抗（IR）中的作用。方法以3T3-L1前体脂肪细胞为工具,建立NYGGF4基因稳定过表达细胞株,以空载质粒转染的细胞为对照,将前体脂肪细胞诱导分化为成熟脂肪细胞,采用液闪仪检测成熟脂肪细胞对[3H]-2-脱氧葡萄糖的摄取率,采用荧光定量反转录-PCR技术检测成熟脂肪细胞中解耦联蛋白（UCP）2 mRNA、UCP4mRNA表达。采用线粒体特异性染料MitoTracker Red预染成熟脂肪细胞,激光共聚焦显微镜下观察线粒体膜电位,进一步应用流式细胞仪对荧光强度进行定量分析。结果 1.NYGGF4基因过表达脂肪细胞胰岛素刺激状态下的葡萄糖摄取率显著低于对照空载脂肪细胞,NYGGF4基因可显著降低成熟脂肪细胞胰岛素刺激下的葡萄糖摄取率;2.NYGGF4过表达脂肪细胞线粒体UCP2 mRNA、UCP4 mRNA表达显著高于对照空载脂肪细胞;3.NYGGF4过表达脂肪细胞线粒体膜电位低于空载脂肪细胞,但定量分析差异无统计学意义。结论 NYGGF4基因可以上调脂肪细胞线粒体UCP2 mRNA、UCP4 mRNA表达,线粒体解耦联异常可能参与NYGGF4致脂肪细胞线粒体功能障碍及IR的机制。

英文摘要：

Objective To explore the roles of uncoupling proteins（UCP） in insulin resistance induced by NYGGF4 gene in adipocytes.Methods 3T3-L1 preadipocytes were stably transfected with either an empty expression vector or a NYGGF4 expression vector.2-Deoxy-glucose uptake in adipocytes was assayed by liquid-scintillation counting.The levels of UCP2 mRNA and UCP4 mRNA expression were determined by real-time quantitative reverse transcription-PCR.MitoTracker Red was used to evaluate the mitochondrial membrane potential using a confocal laser scanning microscope and flow cytometry.Results 1.The insulin-stimulated glucose uptake in NYGGF4-overexpressing adipocytes was significantly lower than that in vector-transfected cells.2.The levels of UCP2 mRNA and UCP4 mRNA were drama-tically increased in NYGGF4-overexpressing adipocytes.3.The NYGGF4-overexpressing adipocytes were weakly stained with MitoTracker as compared to vector-transfected cells.However,this change was not statistically signifcant.Conclusions NYGGF4 can upregulate the expression of UCP2 mRNA and UCP4 mRNA in adipocytes.The abnormality of uncoupling proteins expression may be involved in the mitochondrial dysfunction and insulin resistance induced by NYGGF4 in adipocytes.