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Visfatin对SW872脂肪细胞胰岛素信号分子蛋白表达的影响 被引量:1

Effect of Visfatin on Protein Expression of Insulin Signaling Molecules in SW872 Adipocytes
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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.
出处 《武汉大学学报(医学版)》 CAS 北大核心 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)]
关键词 VISFATIN SW872脂肪细胞 胰岛素抵抗 Visfatin Signal Molecules SW872 Adipocytes Secretion Protein ExpressionInsulin Resistance
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