Visfatin对SW872脂肪细胞胰岛素信号分子蛋白表达的影响  

Effect of Visfatin on Protein Expression of Insulin Signaling Molecules in SW872 Adipocytes

作　　者：马新瑜[1] 卢慧玲[2] 李瑞珍[3] 温宇[2] 姚辉[3] 杨禄红[3] 秦原[3] 黄小力[3] 林汉华[2] 

机构地区：[1]武汉市儿童医院放射科,湖北武汉430016 [2]华中科技大学同济医学院附属同济医院儿科,湖北武汉430030 [3]武汉市儿童医院内分泌科,湖北武汉430016

出　　处：《武汉大学学报（医学版）》2013年第6期810-813,853,共5页Medical Journal of Wuhan University

基　　金：国家自然科学基金资助项目(编号:81270949);湖北省自然科学基金资助项目(编号:2010CDB08802);武汉市卫生局基金资助项目[编号:武卫〔2012〕70号;WX12D12)]

摘　　要：目的:观察visfatin对胰岛素抵抗状态下的SW872成熟脂肪细胞胰岛素信号分子胰岛素受体底物-1(IRS-1)、胰岛素受体底物-2(IRS-2)和磷脂酰肌醇3-激酶(PI3K)蛋白表达的影响。方法:体外培养SW872前脂肪细胞,诱导细胞分化成熟,建立胰岛素抵抗模型,用含有100nmol/L visfatin的无血清培养液孵育1h后收获细胞,采用Western印迹法检测visfatin刺激前后信号分子IRS-1、IRS-2和PI3K的蛋白表达水平。结果:在正常状态下(正常组内比较),visfatin促进脂肪细胞IRS-1、IRS-2和PI3K的蛋白表达,分别增加了51.65%(P<0.01)、44.74%(P<0.01)和61.38%(P<0.01)。在胰岛素抵抗状态下,visfatin刺激组的IRS-1、IRS-2和PI3K的蛋白表达水平,分别比基础状态组增加了26.98%(P<0.05)、35.59%(P<0.05)、27.61%(P<0.01)。结论:在胰岛素抵抗状态下,visfatin通过调节脂肪细胞胰岛素信号分子IRS-1、IRS-2和PI3K蛋白表达而发挥促进葡萄糖转运、改善胰岛素抵抗的生物学作用。To evaluate the effects of visfatin on the protein expression of insulin signal mole- cules including insulin receptor substrate-1 （IRS-1）, insulin receptor substrate-2 （IRS-2） and phosphatidylinositol 3-kinase （PI3K） on the states of insulin resistant in SW872 Adipocytes. Methods： Pre-adipocytes of the line SW872 were cultured and induced to differentiate into ma- tured SW872 adipocytes. Then the cells were treated with oleate at concentration of 1.0 mmol/L for 94 h to induce insulin resistance. And the cells were cultured with Visfatin at concentration of100 nmol/L for 1 h, and then the cell proteins were extracted. Western blot assay was used to detect the protein expression of IRS-1, IRS-2, and PI3K. Results： In the normal states, com- pared with the control group, 100 nmol/L visfatin promoted the protein expression of IRS-1, IRS-2, and PI3K in SW872 adipocytes significantly. The levels of IRS-1, IRS-2, and PI3K were increased respectively by 51.65% （P〈0.01）, 44.74% （P〈0.01）, and 61.38% （P〈0.01）. In the insulin resistant states, after the stimulating by visfatin, the protein expression of IRS-1, IRS-2 and PI3K were increased by 26.98%（P%0.05）, 35.59% （P〈0.05）, and 27.61%（P〈 0.01）. Conclusion： Visfatin might promote the glucose transport and play a physiological role in the insulin resistance in SW872 adipocytes by modulating the signaling molecules of IRS-1, IRS- 2, and PI3K.

关 键 词：VISFATIN SW872脂肪细胞 胰岛素抵抗 

分 类 号：R587.1[医药卫生—内分泌]