LITAF基因对脂肪酸诱导HPA-v细胞胰岛素抵抗的影响

Effect of LITAF Gene on Fatty-Acid Induced Insulin Resistance in HPA-v Cells

目的:通过RNA干扰技术特异性抑制LITAF基因,观察HPA-v人前脂肪细胞胰岛素信号通路的变化情况。方法:将HPA-v人前脂肪细胞和THP-1源巨噬细胞共培养,分为3组,分别为阴性对照组(Scramble组)、siRNA组和正常对照组(NC组),通过qRT-PCR,Western blot法检测LITAF,IRS-2,p-PKC,PI3-K及GLUT2的表达。结果:在软脂酸的刺激下Scramble组LITAF的表达较高于LITAF siRNA和IVC组;IRS-2,p-PKC,PI3-K及GLUT2在LITAF RNAi组较NC组和Scramble组明显提高(P<0.05)。结论:LITAF参与了软脂酸引起的脂肪细胞胰岛素抵抗,而脂肪酸作用于巨噬细胞的受体TLR4同样也是LITAF通路的细胞膜受体,软脂酸减弱了对胰岛素信号通路分子的抑制作用,因此LITAF参与胰岛素抵抗对糖尿病的发病起了至关重要的作用。

Objective： To observe the changes of insulin signaling pathway in HPA-v pre-adipocytes cells by inhibiting LITAF gene using RNA intereference.Methods： THP-1 macrophages cells and HPA-v pre-adipocytes cells were co-cultured in vitro.qRT-PCR and Western-blot analysis was used to observe the expression of LITAF,IRS-2,p-PKC,PI3K,and GLUT2.Results： Palmitic acid significantly increased the expression of LITAF in scramble group compared to LITAF RNAi group and NC group.IRS-2,p-PKC,PI3-K and GLUT2 expression was significantly increased in LITAF RNAi compared to NC and Scramble group（all P0.05）.Conclusion： LITAF is involved in fatty acid induced insulin resistance.Fatty acid induces TLR4 receptors of macrophages through LITAF pathway.PA weakens the inhibition on insulin signaling pathway.Therefore,LITAF plays an important role in the pathogenesis of insulin resistance in diabetes.