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61,005 resultsShowing papers similar to Disruption of hepatic metabolism in Lep KO mice.
ClearImpact 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.
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.
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.
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.
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.
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 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.
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.
Chronic environmental exposure to polystyrene microplastics increases the risk of nonalcoholic fatty liver disease
A mouse study found that long-term exposure to polystyrene microplastics increased the risk of developing non-alcoholic fatty liver disease. The microplastics accumulated in the liver and disrupted fat metabolism, causing inflammation and liver damage, which is concerning because most previous studies only looked at short-term exposure effects.
Polystyrene microplastics induce hepatic lipid metabolism and energy disorder by upregulating the NR4A1-AMPK signaling pathway
Researchers found that polystyrene microplastics accumulate in the liver and disrupt fat and energy metabolism by activating a specific molecular pathway called NR4A1-AMPK. This activation triggers a self-cleaning process called autophagy that reduces fat production in liver cells, while also increasing harmful reactive oxygen species. The findings suggest that long-term microplastic exposure could lead to ongoing liver damage through this metabolic disruption.
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.
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.
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.
Obesogenic polystyrene microplastic exposures disrupt the gut-liver-adipose axis
Mice that drank water containing polystyrene microplastics for 13 weeks developed signs of obesity and metabolic dysfunction, with disruptions across the gut, liver, and fat tissue. The microplastics caused intestinal bacteria changes, liver inflammation, and altered fat storage, affecting the entire gut-liver-fat tissue communication system. These findings suggest that chronic microplastic ingestion through contaminated water and food could contribute to obesity and metabolic disease in humans.
Adverse Effect of Polystyrene Nanoplastics in Impairing Glucose Metabolism in Liver Injury
Polystyrene nanoplastics disrupted glucose metabolism in liver cells by interfering with insulin signaling pathways and mitochondrial function, suggesting that nanoplastic exposure could contribute to metabolic disorders including insulin resistance.
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.
Oral exposure to polyethylene microplastics induces inflammatory and metabolic changes and promotes fibrosis in mouse liver.
Mice fed polyethylene microplastics in their food for 6 to 9 weeks developed liver inflammation, metabolic disruption, oxidative stress, and increased cell growth in the liver. The microplastics also worsened liver scarring (fibrosis) when tested in mice with pre-existing liver damage. This is the first study to show that ingesting polyethylene, the most common type of plastic, can directly damage the mammalian liver and could worsen existing liver conditions.
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.
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.
[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.
PS-MPs Induced Inflammation and Phosphorylation of Inflammatory Signalling Pathways in Liver
Polystyrene microplastics (0.1 µm) induced inflammatory responses and activated multiple inflammatory signalling pathways in mouse and human liver cell lines after 28 days of exposure. The study identified specific phosphorylation cascades through which PS MPs trigger hepatic inflammation, linking microplastic exposure to liver damage mechanisms.