Adjusting ω-3/ω-6 polyunsaturated fatty acids (PUFAs) ratio in high-fat diet is one potential mean to improve metabolic syndrome; however, underlying mechanisms remain unclear. Four groups of mice were fed 60% kcal diets with saturated fatty acids, three different ω-3/ω-6 PUFAs ratios (low, middle and high) for 12 weeks, respectively. Body weight, atherosclerosis marker, insulin signal index and level of lipid accumulation in liver were significantly lowered in High group compared with saturated fatty acids group and Low group at week 12. Expressions of p-mTOR and raptor were inhibited by high ω-3 PUFAs. Importantly, ω-3 PUFAs intake up-regulated mitochondrial electron transport chain and tricarboxylic acid cycle pathway through metabolomics analysis in liver. Mitochondrial complexes activities were raised, fumaric acid was reduced and oxidative stress was alleviated in High group. We conclude that consuming long-term high-fat diet with same calories but high ω-3/ω-6 PUFAs ratio relieves metabolic syndrome by regulating mTORC1 pathway to enhance mitochondrial function.

调整高脂饮食中ω-3/ω-6多不饱和脂肪酸（PUFA）的比例是改善代谢综合征的一种潜在手段。但是，基本机制仍不清楚。四组小鼠分别接受60％大卡饮食，饱和脂肪酸，三种不同的ω-3/ω-6PUFA比（低，中和高）喂养12周。与饱和脂肪酸组和低剂量组相比，高剂量组在第12周时的体重，动脉粥样硬化标志物，胰岛素信号指数和肝脏中的脂质蓄积水平显着降低。ω-3 PUFAs抑制了p-mTOR和猛禽的表达。重要的是，通过肝脏代谢组学分析，ω-3PUFAs上调了线粒体电子传输链和三羧酸循环途径。线粒体复合物的活性提高了，高组降低了富马酸，减轻了氧化应激。我们得出结论，食用具有相同卡路里但高ω-3/ω-6PUFAs比例的长期高脂饮食可通过调节mTORC1途径增强线粒体功能来缓解代谢综合征。