生物
毒死蜱
肠道菌群
肥胖
胰岛素抵抗
微生物生态学
杀虫剂
医学微生物学
肠道细菌
微生物学
细菌
生态学
内分泌学
免疫学
遗传学
作者
Yiran Liang,Jing Zhan,Donghui Liu,Mai Luo,Jiajun Han,Xueke Liu,Chang Liu,Zheng Cheng,Zhiqiang Zhou,Peng Wang
出处
期刊:Microbiome
[Springer Nature]
日期:2019-02-11
卷期号:7 (1)
被引量:180
标识
DOI:10.1186/s40168-019-0635-4
摘要
Disruption of the gut microbiota homeostasis may induce low-grade inflammation leading to obesity-associated diseases. A major protective mechanism is to use the multi-layered mucus structures to keep a safe distance between gut epithelial cells and microbiota. To investigate whether pesticides would induce insulin resistance/obesity through interfering with mucus-bacterial interactions, we conducted a study to determine how long-term exposure to chlorpyrifos affected C57Bl/6 and CD-1 (ICR) mice fed high- or normal-fat diets. To further investigate the effects of chlorpyrifos-altered microbiota, antibiotic treatment and microbiota transplantation experiments were conducted.The results showed that chlorpyrifos caused broken integrity of the gut barrier, leading to increased lipopolysaccharide entry into the body and finally low-grade inflammation, while genetic background and diet pattern have limited influence on the chlorpyrifos-induced results. Moreover, the mice given chlorpyrifos-altered microbiota had gained more fat and lower insulin sensitivity.Our results suggest that widespread use of pesticides may contribute to the worldwide epidemic of inflammation-related diseases.
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