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61,005 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
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 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
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.
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.
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.
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.
[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.
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.
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.
Spatial Lipid MetabolicRemodeling from Placenta toMultiple Suborgans during the Gestational Micro- or Nanoplastics Exposure
Using pregnant mice exposed to polystyrene micro- and nanoplastics from gestation day 1–18, researchers used MALDI mass spectrometry imaging to construct a comprehensive spatial map of lipid metabolism changes across placenta and multiple maternal and fetal organs, revealing widespread lipid metabolic remodeling.
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.
Spatial Lipid Metabolic Remodeling from Placenta to Multiple Suborgans during the Gestational Micro- or Nanoplastics Exposure
Using pregnant mice exposed to polystyrene micro- and nanoplastics from gestation day 1–18, researchers used MALDI mass spectrometry imaging to construct a comprehensive spatial map of lipid metabolism changes across placenta and multiple maternal and fetal organs, revealing widespread lipid metabolic remodeling.
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.
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.
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.
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.
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.
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.
Integrated transcriptomics and metabolomics reveal the mechanism of polystyrene nanoplastics toxicity to mice
Researchers used gene expression and metabolic profiling to understand how polystyrene nanoplastics harm mice at the molecular level, finding disrupted energy metabolism, fat processing, and amino acid pathways in the liver. These molecular changes suggest that nanoplastic exposure could contribute to metabolic disorders, with effects becoming more severe at higher doses.
Adipose tissue as target of environmental toxicants: focus on mitochondrial dysfunction and oxidative inflammation in metabolic dysfunction-associated steatotic liver disease
This review examines how environmental toxicants, including micro and nanoplastics, target fat tissue and contribute to metabolic diseases like obesity, diabetes, and fatty liver disease. These pollutants disrupt mitochondria (the energy-producing parts of cells) and trigger a cycle of oxidative stress and inflammation that damages both fat tissue and the liver. The findings suggest that microplastic exposure could be one of several environmental factors contributing to the rising rates of metabolic disease worldwide.
Dataset for the manuscript "Lipidomic analysis of single and combined effects of polyethylene microplastics and polychlorinated biphenyls on human hepatoma cells"
This dataset provides untargeted lipidomics data from human hepatoma cells exposed to polyethylene microplastics, polychlorinated biphenyl congeners, and their combinations. The data support research showing that microplastics and PCBs can individually and jointly alter lipid profiles in human liver cells, offering insights into how these contaminants may affect cellular lipid metabolism.
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.