二十二碳六烯酸（DHA）和二十碳五烯酸（EPA）对高脂肪诱导胰岛素抵抗小鼠的抗肥胖作用。
Anti-obesity effects of DHA and EPA in high fat-induced insulin resistant mice.
机构信息
Department of Nutrition and Food Hygiene, Guangdong Provincial Key Laboratory of Tropical Disease Research, School of Public Health, Southern Medical University, Guangzhou 510515, Guangdong, P. R. China.
出版信息
Food Funct. 2021 Feb 21;12(4):1614-1625. doi: 10.1039/d0fo02448a. Epub 2021 Jan 21.
Docosahexaenoic acid (DHA, 22:6) and eicosapentaenoic acid (EPA, 20:5) have been reported to improve metabolic disorders, but their differential effects on anti-obesity under insulin resistance (IR) are still unclear. We fed IR mice with high-fat diet with added 1%, 2%, 4% (w/w) DHA or EPA for 12 weeks. Changes in weight, food intake, white adipose tissue (WAT), liver and blood lipids were assessed. GPR120 and PPARγ of WAT were evaluated to explore the related molecular mechanisms of DHA and EPA for anti-obesity in IR mice. 1%DHA and 1%EPA inhibit adipogenesis by down-regulating GPR120; 4%DHA stimulates browning of WAT and improves IR and inflammatory infiltration by up-regulating PPARγ; 4%EPA exerts its anti-obesity effect by mechanisms independent of PPARγ and GPR120 signaling.
二十二碳六烯酸（DHA，22:6）和二十碳五烯酸（EPA，20:5）已被报道可改善代谢紊乱，但它们在胰岛素抵抗（IR）下对肥胖的不同作用尚不清楚。我们用高脂肪饮食喂养 IR 小鼠，添加 1%、2%、4%（w/w）的 DHA 或 EPA 喂养 12 周。评估体重、食物摄入、白色脂肪组织（WAT）、肝脏和血液脂质的变化。评估 WAT 中的 GPR120 和 PPARγ，以探讨 DHA 和 EPA 在 IR 小鼠抗肥胖中的相关分子机制。1%DHA 和 1%EPA 通过下调 GPR120 抑制脂肪生成；4%DHA 通过上调 PPARγ 刺激 WAT 褐变和改善 IR 和炎症浸润；4%EPA 通过与 PPARγ 和 GPR120 信号无关的机制发挥其抗肥胖作用。
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