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61,005 resultsShowing papers similar to Nano‐plastics disrupt systemic metabolism by remodeling the bile acid–microbiota axis and driving hepatic–intestinal dysfunction
ClearIn Vivo Tissue Distribution of Microplastics and the Systemic Metabolic Changes After Gastrointestinal Exposure in Mice
Mice exposed to microplastics via the gastrointestinal route showed systemic distribution of particles to multiple organs and measurable changes in metabolic pathways, providing early in vivo evidence of systemic impacts from plastic ingestion.
In Vivo Tissue Distribution of Microplastics and Systemic Metabolomic Alterations After Gastrointestinal Exposure
Researchers fed mice a mixture of common microplastics and then tracked where the particles ended up in the body and how they affected metabolism. They found that ingested microplastics crossed the gut barrier and accumulated in the liver, kidneys, and other tissues, causing measurable changes in metabolic pathways. The study provides evidence that microplastic exposure through the digestive system can lead to widespread tissue distribution and systemic metabolic disruption in mammals.
Comparative Analysis of Metabolic Dysfunctions Associated with Pristine and Aged Polyethylene Microplastic Exposure via the Liver-Gut Axis in Mice
Mice fed both new and weathered polyethylene microplastics developed disrupted fat metabolism, liver oxidative stress, and shifts in gut bacteria, with weathered (aged) particles causing more severe effects. This study suggests that the microplastics people encounter in the real world, which have been degraded by sunlight and time, may be more harmful than the pristine particles typically used in lab studies.
Dysbiosis of gut microbiota in C57BL/6-Lepem1hwl/Korl mice during microplastics-caused hepatic metabolism disruption
Researchers administered polypropylene microplastics orally to obese mice for 9 weeks and found disruption of hepatic lipid, glucose, and amino acid metabolism alongside structural changes in gut microbiota, with microplastic-treated mice showing decreased hepatic lipid accumulation and altered abundance of specific bacterial genera.
Comparative Analysisof Metabolic Dysfunctions Associatedwith Pristine and Aged Polyethylene Microplastic Exposure via theLiver-Gut Axis in Mice
Researchers fed mice low doses of pristine and aged polyethylene microplastics for several weeks and analyzed changes in blood metabolites, liver proteins, and gut bacteria. Both forms caused lipid metabolism disruptions and reduced beneficial gut bacteria, with aged microplastics showing greater toxicity linked to changes in fatty acid processing enzymes.
Chronic exposure to polyethylene terephthalate microplastics induces gut microbiota dysbiosis and disordered hepatic lipid metabolism in mice
Researchers found that mice exposed to PET microplastics (the type commonly found in plastic bottles) over 17 weeks developed liver damage, including fat buildup, oxidative stress, and cell death. The study revealed that the damage was driven by changes in gut bacteria that altered lipid metabolism, and when researchers depleted the gut bacteria, the liver damage was reduced. This suggests the gut microbiome plays a key role in how microplastics cause harm to internal organs.
Environmentally Relevant Concentrations of Microplastic Exposure Cause Cholestasis and Bile Acid Metabolism Dysregulation through a Gut-Liver Loop in Mice
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.
In vivo exposure of mixed microplastic particles in mice and its impacts on the murine gut microbiome and metabolome
Mice were orally exposed to a mixed polystyrene, polyethylene, and PLGA microplastic suspension for several weeks and gut microbiome composition and metabolomics were analyzed. Mixed microplastic exposure shifted the gut microbiome toward dysbiotic profiles in both male and female mice, with accompanying metabolome changes related to lipid and amino acid metabolism.
Continuous oral exposure to micro- and nanoplastics induced gut microbiota dysbiosis, intestinal barrier and immune dysfunction in adult mice
Researchers fed mice micro- and nanoplastics at environmentally relevant levels and found significant gut damage, including disrupted gut bacteria, weakened intestinal barriers, and reduced immune function. The ratio of beneficial to harmful gut bacteria shifted, and immune cells in the gut decreased. Importantly, the duration of exposure and the size of plastic particles mattered more than the amount consumed, suggesting even low-level long-term exposure could harm gut health.
Multiomics Reveals Nonphagocytosable Microplastics Induce Colon Inflammatory Injury via Bile Acid-Gut Microbiota Interactions and Barrier Dysfunction
Researchers used multi-omics analysis to understand how large microplastics that cannot be absorbed by intestinal cells still cause colon inflammation in mice. They found that long-term oral exposure to polystyrene microplastics disrupted bile acid metabolism and gut barrier function, leading to the accumulation of specific bile acids that triggered cell death in colon tissue. The study reveals a novel mechanism linking microplastic exposure to intestinal inflammation through bile acid-gut microbiota interactions.
Gut dysbiosis exacerbates inflammatory liver injury induced by environmentally relevant concentrations of nanoplastics via the gut-liver axis
This mouse study found that swallowing nanoplastics at levels found in the environment disrupted gut bacteria and damaged the intestinal barrier, allowing toxins to leak into the bloodstream and cause liver inflammation. When researchers transplanted gut bacteria from nanoplastic-exposed mice into healthy mice, those mice also developed liver damage. This demonstrates that nanoplastics may harm the liver indirectly by first disrupting the gut, a finding relevant to understanding how everyday plastic exposure could affect human health.
Systemic effects of nanoplastics on multi-organ at the environmentally relevant dose: The insights in physiological, histological, and oxidative damages
Researchers gave mice nanoplastics at doses estimated to match real-world human exposure levels and found the particles crossed the intestinal barrier and accumulated in the liver and kidneys. Even at these low, environmentally relevant doses, the nanoplastics caused oxidative stress and tissue damage across multiple organs. The findings suggest that everyday nanoplastic exposure may pose broader health risks than previously assumed.
Perturbation of gut microbiota plays an important role in micro/nanoplastics-induced gut barrier dysfunction
Researchers investigated how micro- and nanoplastics disrupt gut barrier function in mice, finding that different surface chemistries caused varying levels of damage. The study suggests that these plastic particles harm the gut by altering the gut microbiome, which then leads to inflammation and weakening of the intestinal barrier that normally keeps harmful substances out of the body.
Molecular Landscape Remodeling Unravels the Cross-Links of Microplastics-Induced Lipidomic Fluctuations, Nutrient Disorders and Energy Disarrangements
Researchers fed mice polypropylene microplastics chronically and used lipidomics and transcriptomics to show that microplastics accumulated in the liver and disrupted lipid metabolism, cholesterol homeostasis, and redox balance, with high doses causing fibrotic liver changes.
Gut–Liver Axis Mediates the Combined Hepatointestinal Toxicity of Triclosan and Polystyrene Microplastics in Mice: Implications for Human Co-Exposure Risks
Mice co-exposed to the antimicrobial triclosan and polystyrene microplastics showed markedly worse intestinal and liver damage than those exposed to either contaminant alone, with gut microbiome disruption identified as a key mediating mechanism.
Oral exposure to nanoplastics altered lipid profiles in mouse intestine
Researchers exposed mice to nanoplastics orally for 14 days and found significant changes in lipid profiles within their intestinal tissue, even without visible tissue damage. The nanoplastics disrupted key fat metabolism pathways and triggered signs of abnormal cellular cleanup processes called autophagy. The study suggests that nanoplastic ingestion may alter how the gut processes fats, with potential implications for metabolic health.
Oral exposure to polyethylene microplastics of adult male mice fed a normal or western-style diet: impact on gut and gut-liver axis homeostasis
Researchers exposed adult male mice to polyethylene microplastics on normal or Western diet for 90 days, examining synergistic effects between plastic and dietary stress on gut and liver health. Microplastic exposure disrupted gut barrier integrity, altered the microbiome, and affected liver homeostasis, with some effects differing between normal and Western diet groups.
Microbiota-mediated metabolic perturbations in the gut and brain of mice after microplastic exposure
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.
Dysfunctional digestive tract highlights the metabolic hallmarks of nanoplastic-exacerbated Parkinson’s pathology
Researchers found that oral exposure to polystyrene nanoplastics worsened Parkinson's disease progression in genetically predisposed mice by damaging the gut lining, disrupting the gut microbiome, and altering hundreds of metabolites through the gut-liver axis. The findings suggest that everyday nanoplastic ingestion could accelerate neurodegeneration in people already at risk for Parkinson's disease.
Oral exposure to PLA microplastics induces time-dependent nanotoxicity via the gut-liver axis
Researchers fed mice polylactic acid (PLA) microplastics, a type derived from biodegradable plastic, and tracked health effects over time using advanced metabolic and microbiome analysis. Short-term exposure caused gut inflammation and altered gut bacteria composition, followed by metabolic disturbances in the liver and intestine. However, prolonged exposure triggered adaptive changes, suggesting the body can partially adjust to sustained microplastic presence, though the long-term implications remain uncertain.
A Western-style diet shapes the gut and liver responses to low-dose, fit-for-purpose polystyrene nanoplastics in mice
A subchronic mouse study found that low-dose polystyrene nanoplastics designed to mimic real-world particle characteristics impaired gut and liver health in a non-monotonic, diet-dependent manner, with Western-style diet amplifying the effects.
Oral exposure to polyethylene microplastics alters gut morphology, immune response, and microbiota composition in mice
Researchers fed mice polyethylene microplastics of two sizes commonly found in human stool for six weeks and examined the effects on gut health. The study found that microplastic exposure altered gut structure, disrupted immune cell function, changed gene expression related to inflammation and gut barrier integrity, and shifted the composition of gut bacteria. Mice exposed to both sizes simultaneously showed the most severe effects, suggesting that real-world exposure to mixed microplastic sizes may compound the damage.
In vivo exposure of mixed microplastic particles in mice and its impacts on the murine gut microbiome and metabolome
Researchers exposed mice to a mixture of common microplastic types to investigate effects on the gut microbiome and metabolome. The study found that ingested microplastic particles altered gut microbial composition and disrupted metabolic pathways, suggesting that realistic mixed-microplastic exposure may have broader biological effects than single-polymer studies indicate.
Molecular LandscapeRemodeling Unravels the Cross-Linksof Microplastics-Induced Lipidomic Fluctuations,Nutrient Disorders and Energy Disarrangements
Mouse liver studies with polypropylene microplastics revealed interconnected disruptions in lipid metabolism, nutrient processing, and energy balance, with proteomic and transcriptomic data highlighting the complexity of hepatic responses to chronic microplastic exposure.