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Environmental pollutant-mediated disruption of gut microbial metabolism of the prebiotic inulin
- Hoffman, Jessie B., Flythe, Michael D., Hennig, Bernhard
- Anaerobe 2019 v.55 pp. 96-102
- cardiovascular diseases, cell membranes, dietary carbohydrate, digestive system, feces, fermentation, glucose, high performance liquid chromatography, intestinal microorganisms, inulin, lipid metabolism, metabolic diseases, mice, pollutants, polychlorinated biphenyls, potassium, prebiotics, propionic acid, risk, risk reduction, short chain fatty acids, succinic acid, viability
- Exposure to environmental pollutants is associated with a greater risk for metabolic diseases including cardiovascular disease. Pollutant exposure can also alter gut microbial populations that may contribute to metabolic effects and progression of inflammatory diseases. Short-chain fatty acids (SCFAs), produced from gut fermentation of dietary carbohydrates, such as inulin, exert numerous effects on host energy metabolism and are linked to a reduced risk of diseases. The hypothesis was that exposure to dioxin-like pollutants modulate gut microbial viability and/or fermentation processes. An inulin-utilizing isolate was collected from murine feces, characterized and used in subsequent experiments. Exposure to polychlorinated biphenyl, PCB 126 impeded bacterial viability of the isolate at concentrations of 20 and 200 μM. PCB 126 exposure also resulted in a significant loss of intracellular potassium following exposure, indicating cell membrane disruption of the isolate. Furthermore, total fecal microbe samples from mice were harvested, resuspended and incubated for 24 h in anaerobic media containing inulin with or without PCB 126. HPLC analysis of supernatants revealed that PCB 126 exposure reduced succinic acid production, but increased propionate production, both of which can influence host glucose and lipid metabolism. Overall, the presented evidence supports the idea that pollutant exposure may contribute to alterations in host metabolism through gut microbiota-dependent mechanisms, specifically through bacterial fermentation processes or membrane disruption.