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61,005 resultsShowing papers similar to Polystyrene microplastics impair brown and beige adipocyte function via the gut microbiota-adipose tissue crosstalk in high-fat diet mice
ClearPolystyrene nanoplastics inhibit beige fat function and exacerbate metabolic disorder in high-fat diet-fed mice
Researchers found that polystyrene nanoplastics worsened metabolic problems in mice fed a high-fat diet by shutting down the function of beige fat cells, which normally help burn energy. The nanoplastics accumulated in fat tissue and suppressed a key protein needed for heat generation, leading to increased fat storage, liver damage, and impaired blood sugar control. This study suggests that nanoplastic exposure could contribute to obesity and metabolic disease in humans, especially those already eating an unhealthy diet.
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.
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.
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.
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.
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.
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.
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.
Impact of Microplastic Exposure on Blood Glucose Levels and Gut Microbiota: Differential Effects under Normal or High-Fat Diet Conditions
Mice exposed to polystyrene microplastics showed changes in blood sugar levels and gut bacteria, with the effects being worse when combined with a high-fat diet. The microplastics disrupted the balance of beneficial gut bacteria and increased markers associated with type 2 diabetes. This study suggests that microplastic exposure could contribute to blood sugar problems in people, especially those who already eat an unhealthy diet.
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.
Impacts of polystyrene microplastic on the gut barrier, microbiota and metabolism of mice
Researchers exposed mice to polystyrene microplastics for six weeks and found that the particles accumulated in the gut, reduced protective mucus secretion, and damaged the intestinal barrier. The microplastics also significantly altered the composition of gut bacteria, decreasing beneficial species and increasing harmful ones. The study suggests that microplastic ingestion could disrupt gut health in mammals by simultaneously impairing the physical barrier and reshaping the microbiome.
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.
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.
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.
Polystyrene microplastics exposure increases the disruption of intestinal barrier integrity and gut microbiota homeostasis during obesity and aging
Researchers found that polystyrene microplastic exposure worsened intestinal barrier dysfunction in mice on high-fat diets, with the combination of obesity and microplastic exposure producing greater gut permeability and inflammation than either factor alone, suggesting compounding risks in metabolically vulnerable individuals.
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.
Microbiota-mediated metabolic perturbations in the gut and brain of mice after microplastic exposure
In a mouse study, oral exposure to polystyrene microplastics of two sizes altered the gut bacteria community and caused metabolic changes in both the intestines and the brain. The disrupted gut bacteria appeared to drive changes in bile acid, energy, and other metabolic pathways. These findings support the idea that microplastics in food and water could affect brain health indirectly by first disrupting the gut microbiome and its chemical signals.
Metabolic Reprogramming in Gut Microbiota Exposed to Polystyrene Microplastics
This pilot study exposed common gut bacteria to polystyrene microplastics in the lab and found that the plastics reduced bacterial growth in a dose-dependent manner and disrupted key metabolic pathways. When gut bacteria from mice were tested, microplastic exposure shifted the microbial community balance, reducing beneficial species. These results suggest that microplastics ingested through food and water could alter the gut microbiome, which plays an important role in digestion, immunity, and overall health.
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.
Polystyrene bead ingestion promotes adiposity and cardiometabolic disease in mice
Researchers fed mice polystyrene microplastic beads and found that ingestion promoted fat accumulation and markers of cardiometabolic disease, including changes in cholesterol levels and inflammatory markers. The microplastics appeared to disrupt metabolic processes related to fat storage and energy regulation. The study suggests that dietary microplastic exposure may contribute to obesity and cardiovascular risk factors, adding a new dimension to concerns about microplastics in the food supply.
Interactions between polystyrene-derived micro- and nanoplastics and the microbiota: a systematic review of multi-omics mouse studies
Researchers systematically reviewed 15 mouse studies and found that exposure to polystyrene micro- and nanoplastics consistently disrupted gut bacteria — reducing beneficial species like Lactobacillus and increasing harmful ones — while also altering metabolic pathways throughout the body. Nanoplastics caused more severe microbiome disruption than larger microplastics, highlighting a serious health concern for humans.
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.
Mixtures of polystyrene micro and nanoplastics affects fat and glucose metabolism in 3T3-L1 adipocytes and zebrafish larvae
Exposure to a mixture of micro- and nanoplastics increased fat production and impaired the body's ability to use insulin and process sugar in both cell and zebrafish experiments. The plastic mixture triggered inflammation, boosted fat-storing genes, and suppressed insulin signaling pathways. These findings suggest that microplastic exposure could contribute to obesity and type 2 diabetes.
Dual impact of microplastic exposure in a mouse model: Impaired uterine receptivity and altered maternal-offspring metabolism
Researchers exposed female mice to polystyrene microplastics and found that the particles impaired uterine receptivity, which is critical for embryo implantation, and altered metabolic profiles in both the mothers and their offspring. The microplastics disrupted gene expression related to uterine function and caused metabolic changes across multiple organs. The findings suggest that microplastic exposure could have reproductive and metabolic consequences that extend to the next generation.