Gut Flora Mediated Mouse Metabolic Health Risk Caused by Dietary Exposure of Acetamiprid and Tebuconazole

Abstract Background:Dietary pesticide residue is an important dietary inducement of metabolic syndrome. Results:Chronic inflammation, insulin resistance, obesity, and non-alcoholic fatty liver disease were induced to tested mice through long-term and low-level of acetamiprid and tebuconazole. On the basis of these phenotypes, the mouse gut flora with metabolites, host circulation metabolic profiling, and their interrelations were investigated, and host metabolic pathways were detected. Results showed that pesticide exposure differently altered the abundance of gut microbial species, such as high ratio of Firmicutes/Bacteroidetes and increased high lipopolysaccharide-production species. Correlation analysis between gut flora and its metabolic profiling further explained these changes and their associations. Under these influences, metabolic profiling of host serum and liver was performed, and metabolic disorders were characterized. The relationships between serum and gut flora were determined via their significantly different metabolites. Alterations to the metabolic pathways of liver were clarified to deeply explore the influences on host physiology. Host metabolic disorders were evidently released by fructooligosaccharide and fecal microbiota transplantation intervention, directly proving that gut flora is a vital medium in metabolic health risk caused by pesticide exposure.Conclusion:Dietary long-term and low-level pesticides threated metabolic health via affecting intestinal flora. Metabolism of intestinal flora and host were all stressed by the exposure, and their alterations were in close proximity. Dietary interventions mitigated metabolic diseases via improving disorder of intestinal flora. This work supplied theoretical bases and intervention approaches to body metabolic problems caused by pesticides exposure on the basis of gut flora.