This study aimed to investigate the metabolites of conjugated linoleic acid (CLA) from the perspective of metabolomics, so as to reveal the potential mechanism of CLA in lowing blood lipids. 30 male non-adult SD rats were divided into: normal diet group, high-fat diet group, and CLA group (intragastric administration of 0.5 g/kg·BW CLA). Results indicate improvements in body weight and visceral fat deposition in obese rats treated with CLA. Metabolomic analysis reveals significant changes in the arachidonic acid (ARA) pathway and its intestinal metabolite oxylipins. Key biomarkers (PGE1, PGE2, TXB2, PGF2α, and 12S-HHTrE) catalyzed by Cox and Lox are identified, influencing blood lipid reduction. Network analysis links these biomarkers to Pparγ. PCR and western blot confirm Pparγ changes in rat liver and intestine, impacting downstream lipid metabolism. This study reveals a potential mechanism: CLA mitigates obesity through the ARA-Cox/Lox-PGE2-Pparγ pathway, offering insights for treating obesity and dyslipidemia.

中文翻译：

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整合非靶向和氧脂素靶向代谢组学揭示共轭亚油酸对高脂饮食大鼠的抗肥胖和降血脂机制


本研究旨在从代谢组学的角度研究共轭亚油酸（CLA）的代谢产物，以揭示CLA降血脂的潜在机制。 30只雄性非成年SD大鼠分为：正常饮食组、高脂饮食组、CLA组（灌胃0.5 g/kg·BW CLA）。结果表明，用 CLA 治疗的肥胖大鼠的体重和内脏脂肪沉积有所改善。代谢组学分析揭示了花生四烯酸 (ARA) 途径及其肠道代谢产物氧脂素的显着变化。确定了 Cox 和 Lox 催化的影响血脂降低的关键生物标志物（PGE1、PGE2、TXB2、PGF2α 和 12S-HHTrE）。网络分析将这些生物标志物与 Pparγ 联系起来。 PCR 和蛋白质印迹证实了大鼠肝脏和肠道中 Pparγ 的变化，影响下游脂质代谢。这项研究揭示了一个潜在的机制：CLA 通过 ARA-Cox/Lox-PGE2-Pparγ 途径减轻肥胖，为治疗肥胖和血脂异常提供见解。