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目的通过研究t10,c12-共轭亚油酸(t10,c12-CLA)对高游离脂肪酸环境中骨骼肌细胞脂肪酸代谢的影响,探讨t10,c12-CLA改善脂代谢的作用机制。方法体外培养成熟的C2C12骨骼肌细胞,通过施加软脂酸在体外模拟高游离脂肪酸环境,再给予不同浓度的t10,c12-CLA(20、30和40μmol/L),通过荧光免疫法利用激光共聚焦显微镜观察t10,c12-CLA对细胞脂肪酸转运蛋白(FAT/CD36)的影响,应用Western blot法检测t10,c12-CLA对C2C12细胞脂肪酸代谢相关酶及AMP激活的蛋白激酶(AMPK)的作用。结果t10,c12-CLA剂量依赖性的增加了高游离脂肪酸环境中细胞对脂肪酸的摄取,抑制了乙酰辅酶A羧化酶(ACC)的活性,增加了肉碱酰基转移酶-1(CPT-1)的表达,并且激活了AMPK。结论t10,c12-CLA可通过激活AMPK增强细胞对脂肪酸的氧化代谢。
Objective To investigate the effects of t10, c12-CLA (conjugated linoleic acid) on the fatty acid metabolism of skeletal muscle cells in high free fatty acids and to explore the mechanism of t10 and c12-CLA on lipid metabolism. Methods Mature C2C12 skeletal muscle cells were cultured in vitro. Palmitic acid was used to simulate high free fatty acid in vitro. Different concentrations of t10, c12-CLA (20, 30 and 40 μmol / L) The effects of t10 and c12-CLA on the fatty acid transporter (FAT / CD36) were observed with a confocal microscope. The effect of t10 and c12-CLA on the fatty acid metabolism related enzymes and AMP-activated protein kinase (AMPK) in C2C12 cells was detected by Western blot. Results t10 and c12-CLA dose-dependently increased the uptake of fatty acids by cells in high free fatty acids, inhibited the activity of acetyl-CoA carboxylase (ACC) and increased the activity of carnitine acyltransferase-1 (CPT-1 ), And activate AMPK. Conclusion t10 and c12-CLA can enhance the cellular oxidative metabolism of fatty acids by activating AMPK.