Beijing Advanced Innovation Center for Food Nutrition and Human Health, College of Science, China Agricultural University, No. 2, West Yuanmingyuan Road, Beijing, 100193, People's Republic of China.
College of Chemistry and Biological Engineering, University of Science and Technology Beijing, No. 30, Xueyuan Road, Beijing, 100083, People's Republic of China.
Microbiome. 2019 Feb 11;7(1):19. doi: 10.1186/s40168-019-0635-4.
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.
肠道微生物组稳态的破坏可能会引发低度炎症，导致与肥胖相关的疾病。一个主要的保护机制是利用多层黏液结构使肠上皮细胞和微生物群保持安全距离。为了研究农药是否会通过干扰黏液-细菌相互作用而导致胰岛素抵抗/肥胖，我们进行了一项研究，以确定长期接触毒死蜱如何影响高脂肪或正常脂肪饮食喂养的 C57Bl/6 和 CD-1（ICR）小鼠。为了进一步研究毒死蜱改变的微生物群的影响，我们进行了抗生素处理和微生物群移植实验。
结果表明，毒死蜱导致肠道屏障完整性受损，导致内毒素进入体内增加，最终引发低度炎症，而遗传背景和饮食模式对毒死蜱诱导的结果影响有限。此外，给予毒死蜱改变的微生物群的小鼠积累了更多的脂肪，胰岛素敏感性降低。
我们的结果表明，广泛使用农药可能导致与炎症相关的全球性疾病流行。
