中文摘要：

目的：探讨饱和脂肪酸是否造成骨骼肌细胞胰岛素抵抗，并检测核糖体s6蛋白激酶（S6K）是否参与此机制。方法：将棕榈酸偶联到无脂肪酸的牛血清白蛋白（BSA）上，制备成浓度为5mmol／L的棕榈酸储存液，备用。棕榈酸组用0．5mmol／L的棕榈酸孵育16h；溶剂组用含相同浓度的无脂肪酸的牛血清白蛋白（BSA）孵育16h；对照组没有任何处理。用偶联抗体的吸光度分析法测定细胞膜上GLUT4myc的含量，免疫印迹检测胰岛素信号分子胰岛素受体底物（IRS1）、蛋白激酶B（Akt）和S6K的磷酸化水平。结果：与对照组和溶剂组相比，棕榈酸组胰岛素刺激的GLUT4myc转位降低（P〈0．05）；Akt的磷酸化水平降低，S6K的磷酸化水平没有变化，IRS1 S636／639的磷酸化水平也没有改变。结论：棕榈酸可导致骨骼肌细胞胰岛素抵抗，其机制可能不涉及S6K。

英文摘要：

Objective： To study if saturated fatty acids cause insulin resistance in skeletal muscle cells, and detect whether ribosomal S6 kinase （S6K） is involved in this mechanism. Methods： Palmitic acid coupled to fatty acid-free bovine albumin （BSA） was prepared in a concentration of 5 mmol/L of storage solution. For palmitic acid group, C2C12GLUT4myc skeletal muscle cells were incubated with 0.5 mmol / L palmitic acid for 16 h; for solvent group, the cells were incubated with the same concentration of BSA for 16 h; for the control group, there was no any treatment. The amount of GLUT4myc on the cell surface was measured by an antibody-coupled absorbance assay. Phosphorylation of the insulin signaling molecules, such as insulin receptor substrate （IRSI）, protein kinase B （Akt） and S6K were detected by Western blotting. Results： Compared to the control group and solvent group, insulin-stimulated GLUT4myc translocation decreased in pahnitic acid group （ P〈0.05）; and the level of phosphorylation of Akt decreased, there was no change in the level of S6K phosphorylation, the level of IRS1 S636/639 phosphorylation did not change, either. Conclusion： Pahnitic acid can directly cause insulin resistance in skeletal muscle cells, and its mechanism may not involve S6K.