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61,005 resultsShowing papers similar to 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
ClearDisruption 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.
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.
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.
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.
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.
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.
Dose-dependent alteration in hepatic and cerebral glucose metabolism following exposure to polystyrene microplastic in Wistar rats
Researchers exposed Wistar rats to polystyrene microplastics and observed dose-dependent changes in glucose metabolism in both the liver and brain. The study suggests that microplastic exposure may disrupt normal metabolic processes, with higher doses leading to more pronounced alterations in hepatic and cerebral glucose handling.
Supporting information.
Researchers found that nine weeks of oral polystyrene microplastic administration disrupted hepatic lipid, glucose, and amino acid metabolism in leptin-knockout obese mice while also altering fecal microbiota composition, suggesting that microplastic exposure compounds metabolic dysfunction in obesity.
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.
Polystyrene microplastics induce gut microbiota dysbiosis and hepatic lipid metabolism disorder in mice
Researchers fed mice two sizes of polystyrene microplastics for five weeks and observed significant disruption of gut bacteria and changes in liver fat metabolism. The microplastics decreased mucus production in the gut and shifted the balance of key bacterial populations at multiple taxonomic levels. The study suggests that microplastic ingestion can trigger gut microbiota imbalance in mammals, which may in turn affect metabolic health.
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.
Polystyrene microplastic exposure disturbs hepatic glycolipid metabolism at the physiological, biochemical, and transcriptomic levels in adult zebrafish
Researchers exposed adult zebrafish to polystyrene microplastics for 21 days and examined effects on liver metabolism at multiple biological levels. The study found that microplastic exposure caused significant decreases in body weight and disrupted glycolipid metabolism, with reduced levels of key metabolic enzymes and gene expression changes in the liver. Transcriptomic analysis confirmed widespread downregulation of genes related to fatty acid, amino acid, and carbon metabolism.
Disturbed Gut-Liver axis indicating oral exposure to polystyrene microplastic potentially increases the risk of insulin resistance
Researchers found that oral exposure to polystyrene microplastics in mice disrupted the gut-liver axis, causing intestinal inflammation and liver metabolic dysfunction that together increased the risk of insulin resistance. The study showed that microplastics damaged the intestinal barrier, allowing harmful substances to reach the liver and trigger metabolic disturbances. These findings suggest a potential pathway by which microplastic ingestion could contribute to metabolic health problems.
[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.
Effects of oral administration of polystyrene nanoplastics on plasma glucose metabolism in mice
Researchers fed polystyrene nanoplastics to mice and tracked their accumulation in organs including the liver, kidneys, and pancreas. They found that the nanoplastics disrupted liver function, altered lipid metabolism, and affected blood glucose regulation. The study suggests that nanoplastic ingestion may interfere with metabolic processes, raising concerns about potential endocrine-related health effects.
Subchronic oral exposure to polystyrene microplastics affects hepatic lipid metabolism, inflammation, and oxidative balance in gilthead seabream (Sparus aurata)
Gilthead seabream fed polystyrene microplastics for 21 days developed signs of liver damage including fat buildup, inflammation, and oxidative stress -- changes similar to early-stage fatty liver disease. Since fish liver responds to microplastics in ways comparable to mammalian livers, these findings raise concerns about what chronic microplastic exposure might do to liver health in humans and other animals.
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.
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.
Polystyrene microplastics induce hepatotoxicity and disrupt lipid metabolism in the liver organoids
Using lab-grown human liver organoids, researchers showed that polystyrene microplastics caused liver cell damage even at concentrations found in the environment. The microplastics disrupted fat metabolism, increased harmful reactive oxygen species, and triggered inflammation in the liver tissue. This study provides early evidence that microplastic exposure could contribute to liver problems like fatty liver disease in humans.
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.
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.
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.
Microplastics (Polystyrene) Exposure Induces Metabolic Changes in the Liver of Rare Minnow (Gobiocypris rarus)
Researchers exposed rare minnow fish to polystyrene microplastics and observed significant metabolic changes in the liver after four weeks. The microplastics caused cellular and tissue alterations along with shifts in metabolic pathways related to energy production and lipid metabolism. The study suggests that chronic microplastic exposure can disrupt normal liver function in freshwater fish even at sublethal concentrations.