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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。
Objective: To observe the effect of visfatin on the insulin signaling molecule insulin receptor substrate-1 (IRS-1), insulin receptor substrate-2 (IRS-2) and phosphatidylinositol 3-kinase (PI3K) protein expression. Methods: SW872 preadipocytes were cultured in vitro to induce cell differentiation and maturation. The model of insulin resistance was established. The cells were harvested with serum-free medium containing 100 nmol / L visfatin for 1 h. Western blotting was used to detect the expression of IRS-1, IRS-2 and PI3K protein expression levels. Results: Visfatin increased the protein expression of IRS-1, IRS-2 and PI3K in adipocytes by 51.65% (P <0.01), 44.74% (P <0.01) and 61.38 % (P <0.01). In insulin resistant group, the protein expression levels of IRS-1, IRS-2 and PI3K in visfatin group were increased by 26.98% (P <0.05), 35.59% (P <0.05) and 27.61% P <0.01). CONCLUSIONS: In the condition of insulin resistance, visfatin plays a biological role in promoting glucose transport and improving insulin resistance by regulating the expression of insulin signaling molecules IRS-1, IRS-2 and PI3K in adipocytes.