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Polystyrene Microplastics and Bisphenol A Exposure Worsen Intestinal Injury in Diabetic Mice by Disrupting Gut Microbiota and Metabolites
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Researchers exposed diabetic mice to polystyrene microplastics and bisphenol A, then examined intestinal effects using metabolomics and gut microbiome sequencing. The study found that both pollutants worsened intestinal injury in diabetic mice by disrupting gut barrier proteins, altering beneficial metabolites like long-chain fatty acids, and shifting gut microbial composition toward less favorable species.
Environmental pollutants can induce multiorgan damage, with the digestive tract particularly susceptible. Diabetic enteropathy is a significant complication of type 2 diabetes mellitus (T2D). However, the relationship between environmental pollutant exposure and T2D-associated intestinal injury has not been previously explored. In this study, T2D mice were subjected to polystyrene microplastics (PS-MPs, 100 μg/day, 3 weeks) and bisphenol A (BPA, 100 μg/kg/day, 2 weeks). Metabolomics and 16S rRNA sequencing were used to detect changes in colonic metabolites and gut microbial composition. Caco-2 cells were utilized to investigate the functions of the altered metabolites. Compared to the T2D group, mice exposed to PS-MPs and BPA exhibited shorter colon length and reduced levels of gut barrier proteins ZO-1 and Occludin. Metabolomics analysis revealed that PS-MPs primarily affected colonic long-chain fatty acids (LCFAs) and adenosine metabolism, while BPA disrupted α-ketoisovaleric acid (KIVA) and pyruvic acid (PyrA) homeostasis. Moreover, PS-MPs exposure altered the abundance of Duncaniella and Olsenella, while BPA primarily affected Phocaeicola, Olsenella, and Variovorax. In vitro experiments showed that palmitoleic acid (C16:1), γ-linolenic acid (C18:3), adenosine (Ado), and KIVA promoted the expression of ZO-1 in Caco-2 cells. Our findings provide valuable insights into the impact of environmental pollutants on intestinal injury in T2D, underscoring the importance of environmental contaminant management, particularly in susceptible populations.
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