基因组
代谢组学
鹅去氧胆酸
胆汁酸
芳香烃受体
新陈代谢
微生物代谢
肠道菌群
法尼甾体X受体
代谢途径
生物
生物信息学
化学
核受体
细菌
生物化学
基因
遗传学
转录因子
作者
Chenyan Hu,Mengyuan Liu,Teng Wan,Lizhu Tang,Baili Sun,Bingsheng Zhou,Jacky W. Y. Lam,Paul K.S. Lam,Lianguo Chen
标识
DOI:10.1021/acs.est.0c06884
摘要
To determine how the aryl hydrocarbon receptor (AhR) signaling acts along the gut–liver axis, we employed an integrated metagenomic and metabolomic approach to comprehensively profile the microbial and metabolic networks. Adult zebrafish were exposed to a model agonist of the AhR: polychlorinated biphenyl (PCB) 126. The metagenomic analysis showed that PCB126 suppressed microbial activities related to primary bile acid metabolism in male intestines. Accordingly, a suite of primary bile acids consistently showed higher concentrations, suggesting that bacterial conversion of primary bile acids was blocked. PCB126 also disturbed bacterial metabolism of bile acids in female intestines, as revealed by higher concentrations of primary bile acids (e.g., chenodeoxycholic acid) and activation of the nuclear farnesoid X receptor signaling. In addition, PCB126 exposure impaired the metabolism of various essential vitamins (e.g., retinol, vitamin B6, and folate). Degradation of vitamin B6 by bacterial enzymes was inhibited in male intestines, resulting in its intestinal accumulation. However, PCB126 suppressed the bacterial metabolism of vitamins in female intestines, causing systematic deficiency of essential vitamins. Overall, we found that PCB126 exposure dysregulated gut microbial activities, consequently interrupting bile acid and vitamin metabolism along the gut–liver axis. The findings provided an insight of the AhR action in microbe-host metabolic communication related to PCBs.
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