Long term ingestion of dietary ALEs induces metabolic disorders in mice by inducing gut dysbiosis and inhibiting AMPK/SIRT1 pathway  

作　　者：Yaya Wang Tianchang Zhang Linqing Nie Yan Zhang Junping Wang Shuo Wang 

机构地区：[1]Tianjin Key Laboratory of Food Science and Health,School of Medicine,Nankai University,Tianjin 300071,China [2]State Key Laboratory of Food Nutrition and Safety,Key Laboratory of Food Nutrition and Safety,Ministry of Education of China,College of Food Science and Engineering,Tianjin University of Science and Technology,Tianjin 300457,China

出　　处：《Food Science and Human Wellness》2025年第2期439-449,共11页食品科学与人类健康(英文)

基　　金：supported by grants from the National Natural Science Foundation of China(32030083)。

摘　　要：Advanced lipoxidation end products(ALEs)are formed by modifying proteins with lipid oxidation products.ALEs formed in the body have been linked to diabetes and hepatic disease.However,it is not known whether ALEs formed in heat-processed foods can induce metabolic diseases.Our results indicate that dietary ALEs induce lipid accumulation in the liver of mice at an early stage and continuous feeding of ALEs induces inflammation,oxidative stress and hepatic insulin resistance.The core reason for these adverse reactions is the damage to the intestinal barrier caused by ALEs.Due to the damage to the intestinal barrier,there is an increase in lipopolysaccharides(LPS)in the liver that induces hepatic lipid accumulation by modulating hepatic lipid metabolism.Furthermore,ALEs plays a major role in the regulation of metabolic diseases by directly or indirectly inhibiting AMP activated protein kinase(AMPK)/Sirtuin 1(SIRT1)signaling through LPS.

关 键 词：Dietary advanced lipoxidation end products Metabolic disorders AMPK/SITR1 signaling pathway Gut dysbiosis Intestinal barrier 

分 类 号：R57[医药卫生—消化系统]