Gut microbiota dysbiosis correlates with a low-dose PCB126-induced dyslipidemia and non-alcoholic fatty liver disease
Gut microbiota dysbiosis correlates with a low-dose PCB126-induced dyslipidemia and non-alcoholic fatty liver disease
复制标题
肠道菌群失调与低剂量 PCB126 诱导的血脂异常和非酒精性脂肪肝相关
DOI:
10.1016/j.scitotenv.2018.10.387
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发表时间:
2019-02-25
影响因子:
9.8
通讯作者:
Dong, Sijun
中科院分区:
文献类型:
--
作者:
Chi, Yulang;Lin, Yi;Dong, Sijun
There is growing evidence that polychlorinated biphenyl 126 (PCB126) not only has adverse effects on host health but also has the ability to shift gut microbiota, which is recently recognized as a crucial factor determining numerous physiological processes. However, the interplay between the gut microbiota and host health remains largely unknown. Herein, adult female C57BL/6 mice were orally exposed to environmentally relevant low-dose of PCB126, at 50 mu g/kg body weight once per week for 6 weeks. This study aims to illuminate how PCB126 influences gut microbiota variations and host disorders and to further identify the correlation between the gut microbiota and metabolic markers of host disorders. Obtained results demonstrated that the PCB126 administration induced gut microbiota dysbiosis in mice, with changes both in the gut microbiota constitution and structure. PCB126 administration also simultaneously altered the physiological status of serum and liver, as evaluated by dyslipidemia, liver lipid accumulation and injury, and non-alcoholic fatty liver disease. Importantly, Spearman's correlation analysis suggested that several specific bacterial taxawere positively and significantly related to metabolic markers of the mentioned disorders. Moreover, based on the co-occurrence network map, some of the bacterial taxa may synergistically regulate host physiology. This work provides new insight into the mechanism underlying the interaction between the gut microbiota and host disorders. It is expected that gut microbiota modulation should be another novel way used for the prevention and treatment of PCB126-triggered diseases. (c) 2018 Elsevier B.V. All rights reserved.