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Microbiota-mediated metabolic perturbations in the gut and brain of mice after microplastic exposure
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In a mouse study, oral exposure to polystyrene microplastics of two sizes altered the gut bacteria community and caused metabolic changes in both the intestines and the brain. The disrupted gut bacteria appeared to drive changes in bile acid, energy, and other metabolic pathways. These findings support the idea that microplastics in food and water could affect brain health indirectly by first disrupting the gut microbiome and its chemical signals.
Microplastics (MPs), emerging environmental toxicants, have drawn attention because of their wide distribution in the environment. Exposure to MPs induces gut microbiota dysbiosis, intestinal barrier dysfunction, metabolic perturbations, and neurotoxicity in different rodents. However, the relationship between MPs, gut microbiota, and the metabolome of the gut and brain in mice remains unclear. In this study, female C57BL/6 mice were orally gavaged with vehicle, 200 nm MP, and 800 nm MP three times per week for four weeks. Cecal contents were collected for gut microbiota analysis using 16S rRNA gene sequencing. Intestinal and brain tissues from mice were used to determine metabolic profiles using liquid chromatography-mass spectrometry (LC-MS). The results showed that MP altered microbiota composition, accompanied by metabolic perturbations in the mouse gut and brain. Specifically, Firmicutes and Bacteroidetes were suggested to be important phyla for MP exposure, partially dominating further metabolite alterations. Simultaneously, MP-induced metabolic profiles were associated with energy homeostasis and bile acid, nucleotide, and carnitine metabolic pathways. The results of the mediation analysis further revealed an MP-microbiota-metabolite relationship. Our results indicate that MPs can induce gut dysbiosis and disturb metabolic dysfunction in the mouse brain and/or intestine. Integrative omics approaches have the potential to monitor MP-induced molecular responses in various organs and systematically elucidate the complex mechanisms of human health effects.
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Researchers fed mice two sizes of polystyrene microplastics for five weeks and observed significant disruption of gut bacteria and changes in liver fat metabolism. The microplastics decreased mucus production in the gut and shifted the balance of key bacterial populations at multiple taxonomic levels. The study suggests that microplastic ingestion can trigger gut microbiota imbalance in mammals, which may in turn affect metabolic health.
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In a mouse study, oral exposure to high concentrations of polystyrene microplastics caused fatty liver disease and abnormal blood lipid levels even without prior gut leakiness. The microplastics triggered intestinal inflammation through immune cells, disrupted gut bacteria, and altered how the body processes nutrients. These results suggest that swallowing microplastics could contribute to metabolic problems and liver disease in humans.
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This review summarizes existing research on how tiny plastic particles called microplastics may affect the gut and brain. It looks at how these particles might change gut bacteria and affect behavior, and calls for more research using animal studies to understand the underlying causes.
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Mice exposed to environmentally realistic levels of polystyrene microplastics for 30 days developed damaged intestinal barriers, liver injury, and disrupted bile acid metabolism. The study revealed a gut-liver feedback loop where microplastics alter gut bacteria, which changes bile acid production, which in turn causes further liver damage, suggesting a mechanism by which everyday microplastic exposure could harm digestive health.
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