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61,005 resultsShowing papers similar to Untargeted metabolomics and transcriptomics joint analysis of the effects of polystyrene nanoplastics on lipid metabolism in the mouse liver
Clear[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.
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.
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.
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.
Polystyrene nanoplastics induce glycolipid metabolism disorder via NF-κB and MAPK signaling pathway in mice
Researchers fed mice polystyrene nanoplastics and found that the particles disrupted the animals' ability to regulate blood sugar and fat metabolism. The nanoplastics triggered oxidative stress and inflammation in the liver, activating signaling pathways that led to insulin resistance and abnormal fat accumulation. The study provides evidence that nanoplastic exposure may contribute to metabolic disorders through specific molecular mechanisms involving the NF-kB and MAPK pathways.
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.
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.
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
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.
Polystyrene nanoplastics potentiate the development of hepatic fibrosis in high fat diet fed mice
Researchers found that polystyrene nanoplastics worsened liver damage in mice fed a high-fat diet by increasing oxidative stress, inflammation, and the infiltration of immune cells in liver tissue. The nanoplastic exposure accelerated the progression from fatty liver to hepatic fibrosis in the diet-induced model. The study suggests that nanoplastic exposure may compound the health risks associated with metabolic conditions affecting the liver.
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.
Tissue Distribution of Polystyrene or Mixed Polymer Microspheres and Metabolomic Analysis after Oral Exposure in Mice.
Mice orally exposed to polystyrene or mixed polymer microspheres showed plastic particle distribution across multiple tissues including the liver, kidney, and spleen, with metabolomic analysis revealing distinct alterations in lipid, amino acid, and energy metabolism pathways.
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.
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.
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.
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.
Oral exposure to high concentrations of polystyrene microplastics alters the intestinal environment and metabolic outcomes in mice
In a mouse study, oral exposure to high concentrations of polystyrene microplastics caused fatty liver disease and abnormal blood lipid levels even without prior gut leakiness. The microplastics triggered intestinal inflammation through immune cells, disrupted gut bacteria, and altered how the body processes nutrients. These results suggest that swallowing microplastics could contribute to metabolic problems and liver disease in humans.
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.
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.
Dietary exposure to polystyrene nanoplastics impairs fasting-induced lipolysis in adipose tissue from high-fat diet fed mice
Researchers demonstrated that fluorescent polystyrene nanoplastics accumulate in the white adipose tissue of mice and can traffic across adipocyte cells. The study found that dietary exposure to nanoplastics impaired fasting-induced fat breakdown in mice fed a high-fat diet, suggesting that nanoplastics may interfere with lipid metabolism and potentially play a role in obesity progression.
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.
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.
The cardiovascular toxicity of polystyrene microplastics in rats: based on untargeted metabolomics analysis
A rat study using metabolomics analysis found that long-term exposure to high concentrations of polystyrene microplastics led to abnormal fat metabolism and cardiovascular damage. The harm appeared to be driven by oxidative stress and inflammation, suggesting that chronic microplastic exposure could contribute to heart and blood vessel disease.
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.