ArticleFrontiers in immunology2024
Oral exposure to high concentrations of polystyrene microplastics alters the intestinal environment and metabolic outcomes in mice.
Article in Frontiers in immunology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
14 citing papers in PubMed.
- Transcriptomic responses to repeated exposure of human C3A liver spheroids to polystyrene nanoplastics.Archives of toxicology · 2026Article
- Microplastics and nanoplastics in inflammatory bowel disease: Mechanistic plausibility, human evidence and future research priorities.World journal of gastrointestinal pathophysiology · 2026Review
- Microplastics in early-onset carcinogenesis.Carcinogenesis · 2026Review
- Micro- and Nanoplastics as Disruptors of Digestive and Hepatopancreatic Homeostasis: Insights into the Plastic-Gut-Liver Axis.International journal of molecular sciences · 2026Review
- Emerging evidence on micro- and nanoplastics carcinogenicity: mechanisms, models, and signaling networks.Molecular cancer · 2026Review
- In vitro evidence and integrative bioinformatics identify the SGLT2-PPARγ axis as a target against polyethylene microplastic-driven metabolic reprogramming in colorectal cancer cells.Journal of translational medicine · 2026Article
- From the Gut to the Brain: Microplastic-Associated Neurovascular Dysfunction and Implications for Stroke Risk.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Review
- Microplastics, Gut Dysbiosis, and Inflammatory Pathways in Ulcerative Colitis.Journal of inflammation research · 2026Review
- Polysaccharides-gut microbiota interaction: mechanisms regulating the hepatocellular carcinoma immune microenvironment.Frontiers in immunology · 2026Review
- Polylactic acid microplastics as metabolic disruptors: Linking gut dysbiosis to systemic toxicity by disrupting microbiota-host co-metabolism.Current research in toxicology · 2026Review
- Article
- Chronic Waterborne Exposure to Polystyrene Microplastics Induces Kupffer Cell Polarization Imbalance and Hepatic Lipid Accumulation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Invited Perspective: Should You Scrap Your Plastic Cutting Board?Environmental health perspectives · 2025Article
- Overview of the hazardous impacts of metabolism-disrupting chemicals on the progression of fatty liver diseases.Molecular & cellular toxicology · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Introduction: Oral exposure to microplastics (MPs) is a global health concern. In our previous study, MPs induced glucose intolerance and non-alcoholic fatty liver disease (NAFLD) under a high-fat diet-induced leaky gut syndrome (LGS). This study aims to evaluate the effects of high concentrations of MP on lipid metabolism under normal dietary conditions and to assess the changes in the intestinal tract resulting from MP exposure. Methods: C57BL6/J mice were fed a normal diet (ND) without polystyrene MPs (PS-MPs) or with PS-MPs (1000 µg/L or 5000 µg/L) for six weeks. Subsequently, intestinal permeability, gut microbiota, and metabolite levels in the serum, feces, and liver were determined. Results: Mice fed the ND showed no increase in intestinal permeability in either group. However, high MPs concentrations led to increased serum lipid levels and exacerbated fatty liver function. Oral exposure to MPs did not affect the number of innate lymphoid cells or short-chain fatty acids in the intestine. However, it increased the number of natural killer cells, altered the gut microbiota, induced inflammation, and modulated the expression of genes related to nutrient transport in the intestine. The severity of intestinal disturbance tended to worsen with dose. Discussion: Despite the absence of LGS, high concentrations of MPs induced dyslipidemia and NAFLD. Oral exposure to MPs triggered intestinal inflammation via natural killer cells, altered the gut microbiota, and modulated nutrient metabolism. Our study highlights the need for environmental measures to reduce oral MPs exposure in the future.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.