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61,005 resultsShowing papers similar to The effect and a mechanistic evaluation of polystyrene nanoplastics on a mouse model of type 2 diabetes
ClearEffects 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.
Micro- and nanoplastic impact on insulin resistance and related metabolic disorder in rodents: A systematic review
This systematic review examined whether micro- and nanoplastics contribute to insulin resistance in animal studies. The findings suggest that polystyrene plastic particles can disrupt how the body processes sugar and responds to insulin, pointing to a possible link between plastic exposure and metabolic disorders like type 2 diabetes.
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.
Adverse Effects of Nanoplastics Administration on the Metabolic Profile and Glucose Control in Mice
This systematic review examines how nanoplastic exposure in mice affects metabolism and blood sugar control. The findings suggest that ingesting nanoplastics may disrupt metabolic processes and glucose regulation in mammals, raising concerns about potential links between everyday plastic exposure and metabolic health conditions like diabetes 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.
Polystyrene nanoplastics with different functional groups and charges have different impacts on type 2 diabetes
A study found that polystyrene nanoplastics can induce symptoms similar to type 2 diabetes, and the severity depends on the surface charge of the particles. Positively charged (amino-modified) nanoplastics caused the most serious blood sugar regulation problems by interfering with insulin signaling, suggesting that as plastics age and their surface chemistry changes, their health risks may increase.
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.
Airborne Nanoplastics Exposure Inducing Irreversible Glucose Increase and Complete Hepatic Insulin Resistance
Mice exposed to airborne nanoplastics developed irreversible increases in blood sugar and complete insulin resistance in the liver, a hallmark of type 2 diabetes. The nanoplastics triggered widespread inflammation and disrupted key metabolic pathways at concentrations similar to what people might actually breathe in polluted areas. This is one of the first studies to show that inhaling tiny plastic particles could directly contribute to metabolic diseases like diabetes.
Integrated transcriptomics and metabolomics reveal the mechanism of polystyrene nanoplastics toxicity to mice
Researchers used gene expression and metabolic profiling to understand how polystyrene nanoplastics harm mice at the molecular level, finding disrupted energy metabolism, fat processing, and amino acid pathways in the liver. These molecular changes suggest that nanoplastic exposure could contribute to metabolic disorders, with effects becoming more severe at higher doses.
Exploring the micro- and nanoplastics–diabetes nexus: Shattered barriers, toxic links, and methodological horizons
This review examines growing evidence that micro- and nanoplastics may contribute to diabetes by disrupting blood sugar regulation, insulin signaling, and fat metabolism through oxidative stress and inflammation. Animal studies show that plastic particles can damage the pancreas, liver, and gut in ways that mirror the development of diabetes, though human studies are still limited. The review calls for more research into whether everyday microplastic exposure could be a hidden factor in the global rise of metabolic diseases.
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.
Short term exposure to polystyrene nanoplastics in mice evokes self-regulation of glycolipid metabolism
Researchers exposed mice to polystyrene nanoplastics and UV-aged nanoplastics via oral gavage for seven days to evaluate short-term metabolic effects. The study found that even brief nanoplastic exposure triggered self-regulatory responses in hepatic glucose and lipid metabolism, suggesting that the body may mount compensatory metabolic adjustments in response to short-term nanoplastic intake.
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.
Polystyrene 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.
Cerebral to Systemic Representations of Alzheimer’s Pathogenesis Stimulated by Polystyrene Nanoplastics
Researchers found that environmentally realistic levels of polystyrene nanoplastics worsened Alzheimer's disease symptoms in mice, triggering brain inflammation, neuron death, and cognitive decline. The nanoplastics also disrupted metabolism and caused organ damage beyond the brain, including liver and kidney effects. This study provides some of the first evidence that nanoplastic exposure could accelerate brain diseases like Alzheimer's, especially as nanoplastics have been found in human brain tissue.
[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.
A comparative study in healthy and diabetic mice followed the exposure of polystyrene microplastics: Differential lipid metabolism and inflammation reaction
Researchers compared the effects of polystyrene microplastic exposure in healthy versus diabetic mice, finding that diabetic mice experienced significantly greater liver damage, abnormal lipid metabolism, and inflammation. The study suggests that individuals with chronic conditions like diabetes may be more sensitive to microplastic pollution due to their already altered metabolic balance.
Polystyrene microplastics disturb maternal glucose homeostasis and induce adverse pregnancy outcomes
Pregnant mice exposed to polystyrene microplastics developed abnormal blood sugar levels and experienced poor pregnancy outcomes, including placental damage and restricted fetal growth. The study found that microplastics disrupted glucose metabolism through inflammation and a cellular stress response, suggesting that microplastic exposure during pregnancy could contribute to complications similar to gestational diabetes.
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.
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.
Cytotoxic and dysmetabolic impact of polystyrene nanoplastics, a new potential atherosclerotic cardiovascular risk factor, on a steatosis model of HepG2 cells
Researchers exposed cell cultures to polystyrene nanoplastics and found significant cytotoxic effects and metabolic disruption including mitochondrial dysfunction and altered glucose metabolism, suggesting nanoplastics may act as a novel class of metabolic disruptors.
Maternal polystyrene nanoplastics exposure during pregnancy induces obesity development in adult offspring through disrupting lipid homeostasis
Researchers found that maternal inhalation exposure to polystyrene nanoplastics during pregnancy induced obesity development in adult offspring of mice, suggesting in utero exposure to airborne nanoplastics programs metabolic dysfunction. The study linked prenatal nanoplastic exposure to increased adiposity and metabolic changes persisting into adulthood.
Polystyrene nanoplastics-induced altered glycolipid metabolism in the liver: A comparative study between pregnant and non-pregnant mice
Researchers compared glycolipid metabolism effects of polystyrene nanoplastics in pregnant versus non-pregnant mice, finding that pregnancy amplified hepatic lipid disruption, with both low and high doses impairing fat metabolism and altering glucose regulation more severely during gestation.
Systematic toxicity evaluation of polystyrene nanoplastics on mice and molecular mechanism investigation about their internalization into Caco-2 cells
Researchers fed mice polystyrene nanoplastics (about 100 nm) for 28 days and found the particles accumulated in multiple organs including the spleen, lungs, kidneys, intestines, testes, and brain. The nanoplastics caused cell death, inflammation, and tissue damage in these organs, as well as disrupted fat metabolism and blood cell counts. This study demonstrates that ingested nanoplastics can spread throughout the body and cause widespread harm, raising concerns about long-term human exposure.