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目的:建立L6细胞胰岛素抵抗模型,筛选出最佳诱导条件,并探讨其作用机制。方法:用MTT法确定棕榈酸、胰岛素对L6细胞增殖的影响;用葡萄糖检测试剂盒检测葡萄糖含量,确定不同浓度的棕榈酸、胰岛素对L6细胞葡萄糖消耗的影响;通过Western Blot法检测IRS-1、PI3K、P-AKT、AKT、GLUT4的蛋白表达。结果:0.4 mmol·L~(-1)棕榈酸诱导12 h、5×10~(-7)mol·L~(-1)胰岛素诱导24 h以上,对L6细胞生长无影响且出现明显胰岛素抵抗,移除刺激后24 h内能够抑制胰岛素刺激状态下的糖转运;棕榈酸降低了IRS-1、PI3K、P-AKT、GLUT4在L6细胞上的表达。结论:高浓度棕榈酸能够通过抑制IRS-1等靶蛋白表达诱导L6细胞产生胰岛素抵抗。
Objective: To establish L6 cell insulin resistance model and screen out the best induction conditions and to explore its mechanism. Methods: The effects of palmitic acid and insulin on the proliferation of L6 cells were determined by MTT method. The glucose content was detected by glucose test kit to determine the effects of different concentrations of palmitic acid and insulin on the glucose consumption of L6 cells. The expression of IRS-1 , PI3K, P-AKT, AKT, GLUT4 protein expression. Results: After treated with 0.4 mmol·L -1 palmitate for 12 h, 5 × 10 -7 mol·L -1 insulin induced more than 24 h, and had no effect on the growth of L6 cells with obvious insulin resistance , Which could inhibit the insulin-stimulated glucose transport within 24 h after the stimulation. Palmitate decreased the expression of IRS-1, PI3K, P-AKT and GLUT4 on L6 cells. Conclusion: High concentrations of palmitic acid can induce L6 cells to produce insulin resistance by inhibiting the expression of target protein such as IRS-1.