Gut microbiota-mediated poly(ε-caprolactone) microplastic degradation exacerbates metabolic dysregulation.

As common biodegradable plastics (BPs), poly(ε-caprolactone) (PCL) was used in food packaging, pharmaceuticals, biomedicine, and tissue engineering, which can be easily broken down by environmental microorganisms into microplastics (MPs), leading to their exposure and accumulation in the human body. However, the adverse health effect resulting from exposure to PCL MPs remain largely unknown. Therefore, this study comprehensively investigated the impact of PCL MPs on lipid metabolism, intestinal barrier, and gut microbiota. The results indicated that PCL MPs can promote lipid synthesis while inhibit lipid oxidation and secretion in mice and exacerbate metabolic syndrome (MS) induced by high-fat diet (HFD). Simultaneously, the intestinal microenvironment was also disrupted, primarily reflected in the increased Firmicutes/Bacteroidetes (F/B) ratio, decreased the relative abundance of Actinomycetota and Verrucomicrobia, and downregulated the expression of tight junction proteins and mucin. Notably, the PCL-degrading strain Brevibacillus formosus P9 isolated from the gut microbiota (GM) may critically drive metabolic disruption through mediating PCL degradation. This study provided an experimental paradigm elucidating GM-mediated amplification of MPs detrimental effects, and highlighted the urgent need to address the potential physiological risks associated with the widespread development and application of BPs.