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61,005 resultsShowing papers similar to Impacts of polypropylene microplastics on lipid profiles of mouse liver uncovered by lipidomics analysis and Raman spectroscopy
ClearLipidomics 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.
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 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.
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 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.
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.
Molecular 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.
Polypropylene microplastics triggered mouse kidney lipidome reprogramming combined with ROS stress as revealed by lipidomics and Raman biospectra
Researchers exposed mice to polypropylene microplastics and found significant disruptions to kidney fat metabolism, with altered levels of triglycerides and phospholipids alongside increased oxidative stress. Advanced imaging confirmed changes at the cellular level, including damage to kidney filtration structures. The study suggests that microplastic exposure can reprogram lipid metabolism in the kidneys, potentially contributing to kidney injury through combined fat and oxidative stress pathways.
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.
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.
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.
[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.
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.
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.
Impact of the Oral Administration of Polystyrene Microplastics on Hepatic Lipid, Glucose, and Amino Acid Metabolism in C57BL/6Korl and C57BL/6-Lepem1hwl/Korl Mice
Researchers investigated the effects of orally administered polystyrene microplastics on liver metabolism in normal and obese mice over eight weeks. They found that microplastic exposure altered lipid, glucose, and amino acid metabolism pathways in the liver and adipose tissues. The study suggests that microplastic ingestion may disrupt hepatic metabolic functions, with potentially different impacts depending on baseline metabolic health status.
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.
Proinflammatory properties and lipid disturbance of polystyrene microplastics in the livers of mice with acute colitis
Researchers studied the effects of polystyrene microplastics on the livers of mice fed a high-fat diet and found that the particles triggered significant inflammatory responses and disrupted lipid metabolism. The microplastics worsened fat accumulation in the liver and activated inflammatory signaling pathways. The findings suggest that microplastic exposure combined with a high-fat diet may amplify liver damage and metabolic disturbances.
Disruption of hepatic metabolism in Lep KO mice.
Researchers found that polystyrene microplastics administered orally for nine weeks accumulated in liver tissue of leptin-knockout obese mice and induced histopathological liver alterations, including disruption of hepatic lipid, glucose, and amino acid metabolism.
Microplastics and Metabolism: Physiological Responses in Mice Following Ingestion
Researchers found that mice orally exposed to microplastic microspheres showed changes in lipid metabolism and other metabolic pathways, with particles detected in tissues throughout the body. The effects were more pronounced when mice were exposed to mixed microplastic types compared to polystyrene alone, suggesting that real-world mixtures of microplastics may have broader physiological impacts.
Quantitative monitoring of microplastics and lipid metabolism in live zebrafish via hyperspectral stimulated Raman scattering microscopy
Researchers used spectral focusing hyperspectral stimulated Raman scattering (SRS) microscopy to longitudinally monitor microplastic uptake, size-dependent organ accumulation, and lipid metabolic changes in live zebrafish during development. They found that microplastic exposure disrupted hepatic lipid metabolism and energy homeostasis, with the SRS imaging approach enabling real-time, label-free tracking of microplastics and associated biochemical changes in living organisms.
Liver Metabolic Dysregulation Induced by Polypropylene Nano- and Microplastics in Nile Tilapia Using Internal Extractive Electrospray Ionization Mass Spectrometry
Researchers exposed Nile tilapia fish to polypropylene nano- and microplastics and analyzed changes in liver metabolism using advanced mass spectrometry. They identified 46 metabolites that were significantly altered, including phospholipids, amino acids, and energy-related compounds, indicating disrupted liver function. The study suggests that polypropylene plastic particles can cause measurable metabolic disturbances in fish even without obvious visible harm.
Large polystyrene microplastics results in hepatic lipotoxicity in mice
Researchers found that long-term exposure to large polystyrene microplastics (40-100 micrometers) caused hepatic lipid metabolism disruption and lipotoxicity in mice, demonstrating that even large microplastics that do not accumulate in tissues can still cause significant liver damage.
Toxicity Study and Quantitative Evaluation of Polyethylene Microplastics in ICR Mice
Researchers fed polyethylene microplastics to mice over 28 days to study their toxicity, and used Raman spectroscopy to track where the particles ended up. They detected microplastics in the lungs, stomach, intestines, and blood serum, with repeated oral exposure leading to inflammation in lung tissue. The findings provide evidence that ingested microplastics can travel beyond the gut and accumulate in other organs.