POPs调控肝内脂肪酸从头合成相关分子的研究进展

Research progress on regulation of persistent organic pollutants in molecules related to de novo synthesis of hepatic fatty acid

肝脏是重要的代谢器官,主要通过调控循环脂肪酸的摄取,肝内脂肪酸从头合成,脂肪酸氧化和极低密度脂蛋白输出4个关键途径维持脂肪酸的相对稳定。持久性有机污染物(POPs)因其亲脂性和高毒性,常蓄积于肝脏并诱发肝脏毒性。POPs暴露与肝脏疾病密切相关,多可导致脂肪酸的合成与分解失衡。肝内脂肪酸从头合成作为脂肪酸代谢的重要环节,对于维持肝脏代谢稳定至关重要。因此,研究POPs对肝内脂肪酸从头合成过程的调控,有助于进一步认识和解析POPs的肝毒性机制。该文基于肝内脂肪酸从头合成途径来探讨POPs暴露对肝脏脂肪酸代谢的影响,重点阐述了POPs对肝内脂肪酸从头合成过程相关分子的调控机制。

The liver is an important metabolic organ that maintains the relative stability of fatty acids through 4 key pathways:regulation of circulating fatty acid uptake,intrahepatic de novo synthesis,fatty acid oxidation and very low density lipoprotein output.The persistent organic pollutants(POPs),because of their lipophilic nature and high toxicity,often accumulate in the liver and induce hepatotoxicity.The POPs exposure is closely associated with liver disease and can lead to imbalances in the synthesis and catabolism of fatty acids.The de novo synthesis of fatty acids in the liver is an important link of fatty acid metabolism and is essential for maintaining stable liver metabolism.Therefore,studying the regulation of de novo lipogenesis by POPs helps to further understand and analyze the hepatotoxic mechanisms of POPs.This paper investigates the effects of POPs exposure on hepatic fatty acid metabolism based on the pathway of intrahepatic de novo lipogenesis,with a focus on the molecular mechanisms of POPs in the regulation of hepatic fatty acid de novo synthesis.