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61,005 resultsShowing papers similar to Proinflammatory properties and lipid disturbance of polystyrene microplastics in the livers of mice with acute colitis
ClearOral 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.
Polystyrene microplastics exacerbate experimental colitis in mice tightly associated with the occurrence of hepatic inflammation
Researchers found that polystyrene microplastics worsened experimentally induced colitis in mice, causing greater intestinal inflammation, reduced mucus secretion, and increased gut permeability. The study also revealed that microplastic exposure in mice with colitis increased the risk of secondary liver inflammation, suggesting that individuals with pre-existing gut conditions may be more vulnerable to 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.
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.
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.
Oral Exposure to Polystyrene Microplastics of Mice on a Normal or High-Fat Diet and Intestinal and Metabolic Outcomes
Researchers found that polystyrene microplastics caused metabolic problems like diabetes and fatty liver disease in mice, but only when combined with a high-fat diet. The high-fat diet appeared to damage the gut lining enough to allow microplastics to deposit in the intestinal wall, triggering inflammation that altered nutrient absorption. This suggests that people with poor diets may be more vulnerable to the harmful effects of microplastic exposure.
Low-dose polystyrene microplastics exposure increases susceptibility to obesity-induced MASLD via disrupting intestinal barrier integrity and gut microbiota homeostasis
A mouse study found that even low doses of polystyrene microplastics made fatty liver disease significantly worse when combined with a high-fat diet, creating a "double hit" effect. The microplastics damaged the gut lining, disrupted beneficial gut bacteria, and triggered inflammation that spread to the liver, and these harmful effects were difficult to reverse even after two weeks of stopping exposure.
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 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.
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.
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.
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 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 Microplastics Exacerbate Systemic Inflammation in High-Fat Diet-Induced Obesity
Researchers found that polystyrene microplastics significantly worsened inflammation and metabolic problems in obese mice fed a high-fat diet. The microplastics were found throughout the body including the brain, where they activated immune cells in the hypothalamus, a region that controls appetite and metabolism. This study suggests that microplastic exposure could be an overlooked factor contributing to the worsening of obesity-related health problems like insulin resistance and chronic inflammation.
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.
Chronic Waterborne Exposure to Polystyrene Microplastics Induces Kupffer Cell Polarization Imbalance and Hepatic Lipid Accumulation
Researchers found that long-term exposure to polystyrene microplastics in drinking water caused significant fat accumulation in the livers of mice over 9 to 12 weeks. The microplastics triggered an imbalance in immune cells in the liver called Kupffer cells, shifting them toward a pro-inflammatory state. The study identifies a specific signaling pathway through which microplastics may disrupt fat metabolism and contribute to liver problems.
Long-Term Exposure to Environmentally Relevant Doses of Large Polystyrene Microplastics Disturbs Lipid Homeostasis via Bowel Function Interference
Researchers exposed mice to environmentally relevant doses of large polystyrene microplastics in their diet for 21 weeks and found significant disruptions to fat metabolism and gut bacterial communities. The microplastics interfered with bowel function, which in turn altered how the body processes and stores lipids. The study provides evidence that even low-level, long-term microplastic exposure through food may affect metabolic health in mammals.
Long-Term Exposure to Polystyrene Microspheres and High-Fat Diet-Induced Obesity in Mice: Evaluating a Role for Microbiota Dysbiosis.
A long-term mouse study examined how chronic exposure to polystyrene microspheres interacts with a high-fat diet to affect obesity-related outcomes, finding that microplastics worsened metabolic disruption and fat accumulation compared to diet alone. The results raise concern that microplastic exposure may be an environmental factor contributing to the global obesity epidemic.
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.
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.
Prolonged oral ingestion of microplastics induced inflammation in the liver tissues of C57BL/6J mice through polarization of macrophages and increased infiltration of natural killer cells
Researchers found that prolonged oral ingestion of polystyrene microplastics caused liver inflammation in mice by polarizing macrophages and increasing natural killer cell infiltration, revealing how microplastics disrupt the liver immune microenvironment.
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.
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.
[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.