脂肪变性
新陈代谢
肠道菌群
脂肪肝
碳水化合物代谢
生物化学
胆汁酸
透视图(图形)
化学
脂肪酸代谢
脂肪酸
生物
内科学
内分泌学
医学
疾病
人工智能
计算机科学
作者
Xueyan Gu,Huihui Yang,Wu Liu,Zhenliang Fu,Shibiao Zhou,Zehui Zhang,Yu Liu,Miao Zhang,Shuai Liu,Wuting Lu,Qiyu Wang
标识
DOI:10.1016/j.jhazmat.2024.136104
摘要
Altered gut microbiota is a pathogenic mechanism of 6:2 Cl-PFESA (F-53B)-induced hepatic steatosis, indicated by correlations between gut microbiota and lipid indices. However, the detailed mechanism remains unknown. In this study, adult zebrafish were exposed to 0.25, 5 and 100 μg/L F-53B for 28 days to explore how microbiota regulate hepatic lipid metabolism from the perspective of glucose and fatty acid metabolism. Results showed glucose and fatty acids were transported from blood into liver after 100 μg/L F-53B exposure, in which glucose was further transformed into acetyl-CoA and fatty acid. The accumulated fatty acids were then converted into triglycerides (TGs), inducing hepatic steatosis. Changes in the abundances of certain gut microbiota contributed to the above processes, which was verified by the fact that the levels of g_Crenobacter, g_Shewanella, and g_Vibrio restored to control levels after Lactobacillus rhamnosus GG intervention, and the levels of their related lipid indicators recovered partially towards the control levels. 0.25 and 5 μg/L F-53B had no effect on the hepatic lipid profile due to the few changed TG synthesis related indicators. Our findings provide novel insights into lipid metabolic disorders caused by F-53B exposure, highlighting the health risks linked to gut microbial dysbiosis.
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