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61,005 resultsShowing papers similar to Polystyrene bead ingestion promotes adiposity and cardiometabolic disease in mice
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.
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.
Long-term polystyrene nanoplastic exposure disrupt hepatic lipid metabolism and cause atherosclerosis in ApoE-/- mice
Long-term exposure to tiny polystyrene nanoplastics caused atherosclerosis (hardening of the arteries) in mice by disrupting fat metabolism in the liver and triggering inflammation and oxidative stress. This is one of the first studies to directly link nanoplastic exposure to cardiovascular disease development, raising concerns about heart health risks from the nanoplastics found in our food and environment.
Long-term exposure to polystyrene microplastics promotes HFD-induced obesity in mice through exacerbating microbiota dysbiosis
Researchers found that long-term polystyrene microplastic exposure worsened high-fat-diet-induced obesity in mice by exacerbating gut microbiota dysbiosis, suggesting microplastic ingestion may amplify metabolic disease risk through disruption of the gut microbiome.
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.
Polystyrene microplastic exposure induces insulin resistance in mice via dysbacteriosis and pro-inflammation
Researchers found that exposing mice to polystyrene microplastics induced insulin resistance regardless of whether the animals were on a normal or high-fat diet. The study identified disruption of gut bacteria and increased intestinal inflammation as key mechanisms driving the metabolic changes. These findings suggest that microplastic exposure may contribute to metabolic health issues by altering the gut microbiome and triggering chronic inflammation.
Tissue accumulation of microplastics in mice and biomarker responses suggest widespread health risks of exposure
Researchers fed mice polystyrene microplastics of two sizes and tracked where the particles accumulated in the body, finding them in the liver, kidneys, and gut with distribution patterns depending on particle size. Biochemical analysis revealed that microplastic exposure disrupted energy and fat metabolism, caused oxidative stress, and altered markers of neurotoxicity in the blood. The study provides evidence that microplastics can accumulate in mammalian tissues and may pose widespread health risks.
Polystyrene microplastics trigger adiposity in mice by remodeling gut microbiota and boosting fatty acid synthesis
Researchers discovered that polystyrene microplastics at relatively low concentrations caused weight gain and excess fat accumulation in mice by reshaping their gut bacteria. The altered gut microbiome boosted fatty acid production, increased appetite, and lowered physical activity in the exposed mice. This finding is significant because it suggests everyday levels of microplastic exposure could contribute to obesity through changes in gut bacteria and metabolism.
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.
Polystyrene bead ingestion promotes atherosclerosis plaque progression via BMP signaling in mice
Researchers found that mice fed polystyrene microplastics for 12 weeks developed worsened atherosclerosis, the buildup of fatty plaques in blood vessels. The microplastics triggered oxidative stress and activated a signaling pathway (BMP) that caused blood vessel cells to change their identity, accelerating plaque formation. The study provides evidence that microplastic ingestion could contribute to cardiovascular problems by promoting inflammation and disrupting the normal function of blood vessel walls.
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.
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.
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.
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.
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.
Reproductive and metabolic toxic effects of polystyrene microplastics in adult female Wistar rats: a mechanistic study
Researchers gave female rats polystyrene microplastics orally for 45 days and found disruptions to both metabolic and reproductive hormone levels, including increased cholesterol, insulin resistance, and altered sex hormones. The microplastics also caused liver fibrosis and elevated inflammatory markers. The study suggests that chronic microplastic exposure may contribute to metabolic and endocrine disruption in mammals.
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.
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.
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.
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.
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.
Evaluation of Polystyrene Nanoplastics Induced Cardiotoxicity Under Different Dietary Patterns in Mice
Researchers exposed mice fed different dietary patterns to polystyrene nanoplastics and assessed cardiac toxicity. The study found that dietary habits significantly modulated nanoplastic-induced heart damage, demonstrating that diet is an important variable in evaluating the health risks of foodborne plastic contaminants.
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.
Gut Check: Microbiota and Obesity in Mice Exposed to Polystyrene Microspheres
Researchers found that gut microbiota appeared to play a mediating role in the obesity outcomes observed in mice fed manufactured polystyrene microspheres, suggesting that microplastic-induced alterations to the gut microbiome may be a mechanism linking microplastic exposure to metabolic dysfunction and weight gain.