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20 resultsShowing papers similar to Molecular LandscapeRemodeling Unravels the Cross-Linksof Microplastics-Induced Lipidomic Fluctuations,Nutrient Disorders and Energy Disarrangements
ClearMolecular LandscapeRemodeling Unravels the Cross-Linksof Microplastics-Induced Lipidomic Fluctuations,Nutrient Disorders and Energy Disarrangements
Proteomic and lipidomic profiling of mouse livers after polypropylene microplastic exposure revealed crosstalk between hepatic lipid fluctuations, nutrient metabolism disorders, and energy pathway disarrangements, providing mechanistic insight into microplastic-induced liver toxicity.
Molecular LandscapeRemodeling Unravels the Cross-Linksof Microplastics-Induced Lipidomic Fluctuations,Nutrient Disorders and Energy Disarrangements
This study examined how polypropylene microplastics accumulate in and damage the mouse liver, using integrated lipidomics and transcriptomics to map the molecular landscape of microplastic-induced lipid disruption and metabolic dysfunction.
Molecular LandscapeRemodeling Unravels the Cross-Linksof Microplastics-Induced Lipidomic Fluctuations,Nutrient Disorders and Energy Disarrangements
Researchers used combined lipidomic and transcriptomic analysis to demonstrate that polypropylene microplastics accumulated in mouse liver and disrupted key metabolic pathways including lipid biosynthesis, cholesterol metabolism, and energy homeostasis.
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.
Molecular LandscapeRemodeling Unravels the Cross-Linksof Microplastics-Induced Lipidomic Fluctuations,Nutrient Disorders and Energy Disarrangements
Researchers examined polypropylene microplastic retention in mouse liver using lipidomics and transcriptomics, finding that chronic exposure disrupted lipid metabolism, cholesterol turnover, and antioxidant defense, with high-dose treatment causing regional liver fibrosis.
Molecular LandscapeRemodeling Unravels the Cross-Linksof Microplastics-Induced Lipidomic Fluctuations,Nutrient Disorders and Energy Disarrangements
This study assessed the liver toxicity of polypropylene microplastics in mice using combined lipidomics and transcriptomics, identifying disrupted lipid metabolism, altered cholesterol handling, and fibrotic tissue remodeling as key pathological outcomes.
Lipidomics and transcriptomics insight into impacts of microplastics exposure on hepatic lipid metabolism in mice
Researchers used lipidomics and transcriptomics to examine how polystyrene microplastic exposure affects liver lipid metabolism in mice over eight weeks. The study found that while body weight and serum lipid levels were not significantly affected, microplastics caused impaired glucose metabolism and specific changes in hepatic lipid profiles, revealing subtle but measurable disruptions to liver function.
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.
Integrated multi-omics of gut-liver axis to dissect the mechanism underlying hepatotoxicity induced by sub-chronic tire wear particles exposure in mice
Researchers gavaged female mice with tire wear particles (a major microplastic source) at three doses and performed integrated gut-liver multi-omics analysis, finding that sub-chronic exposure disrupted lipid metabolism, promoted liver inflammation, and altered gut microbial communities in a dose-dependent manner.
[The effect and mechanism of exposure to polystyrene nanoplastics on lipid metabolism in mice liver].
Researchers exposed mice to 20 nm polystyrene nanoplastics and investigated the effects on hepatic lipid metabolism using multi-omics approaches. Nanoplastic exposure disrupted lipid metabolic pathways in the liver, causing significant changes in lipid accumulation and related gene expression, suggesting a mechanism by which nanoplastic ingestion may contribute to metabolic disorders.
Impacts of polypropylene microplastics on lipid profiles of mouse liver uncovered by lipidomics analysis and Raman spectroscopy
Researchers found that polypropylene microplastics accumulated in mouse liver tissue and caused significant changes to lipid metabolism, even without obvious outward health symptoms. Advanced analysis revealed altered fat profiles and lipid droplet buildup in the liver. This study suggests that microplastic exposure could quietly disrupt liver fat processing, which is relevant to understanding long-term metabolic health effects in mammals.
Untargeted metabolomics and transcriptomics joint analysis of the effects of polystyrene nanoplastics on lipid metabolism in the mouse liver
Mice exposed to polystyrene nanoplastics for 12 weeks gained weight without eating more and showed increased cholesterol levels and fat accumulation in their livers. Gene and metabolite analysis revealed that the nanoplastics disrupted fat metabolism pathways in the liver, essentially reprogramming how the body processes and stores fat. These findings suggest that nanoplastic exposure could be a hidden factor contributing to obesity and fatty liver disease in humans.
Untargeted lipidomics uncover hepatic lipid signatures induced by long-term exposure to polystyrene microplastics in vivo
Researchers exposed rats to polystyrene microplastics over 6 and 12 months and used advanced lipid profiling to assess liver damage. They found that long-term exposure caused liver inflammation, fatty liver changes, and significant alterations in eight key lipid metabolites involved in fat processing. The study provides evidence that chronic microplastic exposure can disrupt liver lipid metabolism, raising concerns about long-term health effects.
Long-term exposure to polystyrene microplastics induces hepatotoxicity by altering lipid signatures in C57BL/6J mice
Researchers exposed mice to tiny polystyrene particles for 16 weeks and found the plastics accumulated in their livers, disrupting fat metabolism and energy production. The microplastics altered lipid profiles and interfered with key enzymes involved in cellular energy cycles. The study suggests that long-term microplastic exposure may contribute to liver damage through metabolic disruption.
Integrated transcriptomic and metabolomic analyses to decipher the regulatory mechanisms of polystyrene nanoplastic-induced metabolic disorders in hepatocytes
Using combined transcriptomic and metabolomic analysis, this study found that polystyrene nanoplastics disrupt lipid and amino acid metabolism in hepatocytes, identifying key regulatory genes and providing data relevant to assessing health risks from nanoplastic exposure.
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.
Transcriptomic and metabolomic analysis reveals hepatic lipid metabolism disruption in Japanese quail under polystyrene microplastics exposure
Researchers fed Japanese quail polystyrene microplastics at environmentally relevant concentrations for 35 days and analyzed liver effects using transcriptomics and metabolomics. Low doses caused increased food intake and weight gain with liver lipid accumulation, while high doses led to decreased intake and weight loss, suggesting a hormetic dose-response pattern. The study found that microplastic exposure disrupted hepatic lipid metabolism pathways and caused liver oxidative stress in birds.
A metabolomics perspective on the effect of environmental micro and nanoplastics on living organisms: A review
This review examines how scientists use metabolomics, the study of small molecules produced by cellular processes, to understand the toxic effects of microplastics and nanoplastics on living organisms. The research shows that these plastic particles disrupt metabolism in consistent ways across species, affecting energy production, fat processing, and amino acid pathways. These shared metabolic disruptions across different organisms suggest that microplastics could cause similar metabolic problems in humans.
Hepatic and metabolic outcomes induced by sub-chronic exposure to polystyrene microplastics in mice
Researchers studied the effects of sub-chronic polystyrene microplastic exposure on mouse livers using multiple analytical approaches. They found that microplastics accumulated in liver tissue and caused inflammation, oxidative stress, and disruption of normal metabolic processes including lipid and amino acid metabolism. The study suggests that prolonged microplastic ingestion may pose significant risks to liver health.
Nano‐plastics disrupt systemic metabolism by remodeling the bile acid–microbiota axis and driving hepatic–intestinal dysfunction
Mice were exposed to polyethylene terephthalate nanoparticles, and researchers used histopathology, metabolomics, and metagenomics to track downstream effects. Nanoplastic ingestion caused severe metabolic disruption—including weight loss, organ atrophy, and liver-intestinal dysfunction—by remodeling the bile acid–gut microbiota axis.