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Dietary Fat and Fiber Divergently Control Intestinal Nanoplastic Bioaccumulation through Gut Motility and Barrier Pathways
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Mice were fed a control, high-fat or high-fiber diet and given labeled polystyrene nanoplastics for eight weeks. Compared with controls, the high-fat diet raised nanoplastic levels in the colon 2.83-fold, and the high-fiber diet lowered them to 34%. The difference tracked with gut motility and barrier integrity.
The ingestion of nanoplastics (NPs) poses a growing environmental health threat, yet how intrinsic host factors modulate their intestinal fate remains poorly defined. This study tests the hypothesis that dietary patterns govern NP bioaccumulation by differentially regulating gut motility and barrier integrity. Mice were fed a control (CD), high-fat (HFD), or high-fiber diet (HFib) and exposed to 0, 5, or 25 mg/kg/day of deuterium-labeled polystyrene NPs for 8 weeks. Dietary composition profoundly altered colonic NP accumulation: compared to CD-fed mice, an HFD exacerbated the burden by 2.83-fold (328.6 ± 23.5 μg/g dry weight), whereas a HFib attenuated it to 34% (38.9 ± 7.6 μg/g). This differential accumulation was linked to barrier damage and motility suppression, most severe under HFD. Multiomics analysis revealed that HFD promoted gut dysbiosis and deficiency of short-chain fatty acids, particularly butanoic acid. This metabolic deficit was associated with disrupted enteric nervous system signaling, notably suppressed serotonergic pathways. Integrative path modeling delineated two mechanistic landscapes: a barrier-centric pathogenic cascade driven by HFD and a microbiota-led protective network sustained by HFib. Our findings establish host nutrition as a potent modifier of NP intestinal fate and accumulation, highlighting dietary fiber as a plausible nutritional strategy to enhance intestinal resilience.
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Mice fed a higher-fiber diet retained less of a swallowed nanoplastic dose than mice on a standard diet, and had less intestinal damage and lower nanoplastic levels in the liver. In separate lab tests, the fiber bound to the nanoplastic particles.
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Researchers found that the impact of microplastics on gut barrier integrity differs significantly depending on diet, with mice fed high-fat diets showing different responses than those on normal diets. The gut microbiome and its metabolites, particularly the short-chain fatty acid butyrate, appear to play a critical role in mediating these effects. The study highlights the importance of considering dietary patterns when evaluating how microplastics affect digestive health.
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Researchers investigated how different food components affect the toxicity of polystyrene nanoplastics as they pass through a simulated human digestive system. They found that fat molecules helped stabilize and disperse the nanoplastics during digestion, increasing their uptake by intestinal cells and worsening cellular damage. The study suggests that the type of food consumed alongside nanoplastic-contaminated items could significantly influence how much harm the particles cause in the gut.
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This review gathers evidence on micro- and nanoplastics in the human gut, covering barrier disruption, particle uptake and changes in gut microbiota. Smaller particles cross into the body more readily. Human evidence is limited and methods are not standardized. The authors also discuss diet, including packaged food, fiber, antioxidants and probiotics, as a factor in exposure and effects.
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