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61,005 resultsShowing papers similar to Therapeutic Effect of Prolyl Endopeptidase Inhibitor in High-fat Diet-induced Metabolic Dysfunction-associated Fatty Liver Disease
ClearAdipose tissue as target of environmental toxicants: focus on mitochondrial dysfunction and oxidative inflammation in metabolic dysfunction-associated steatotic liver disease
This review examines how environmental toxicants, including micro and nanoplastics, target fat tissue and contribute to metabolic diseases like obesity, diabetes, and fatty liver disease. These pollutants disrupt mitochondria (the energy-producing parts of cells) and trigger a cycle of oxidative stress and inflammation that damages both fat tissue and the liver. The findings suggest that microplastic exposure could be one of several environmental factors contributing to the rising rates of metabolic disease worldwide.
Chronic Nanoplastic Exposure Promotes the Development and Progression of Metabolic Dysfunction‐Associated Steatotic Liver Disease
This study found that chronic exposure to nanoplastics promotes the development and worsening of metabolic dysfunction-associated steatotic liver disease (formerly known as fatty liver disease). Nanoplastics appear to increase vulnerability to liver disease progression. The finding is concerning because fatty liver disease is already widespread, and everyday nanoplastic exposure through food and water could be making it worse.
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.
Microplastics in metabolic dysfunction-associated steatotic liver disease: An emerging threat to liver health
This review examined emerging evidence linking microplastic exposure to the development and progression of metabolic dysfunction-associated steatotic liver disease (MASLD, formerly NAFLD). The authors found that microplastics detected in liver tissue can exacerbate hepatic inflammation, lipid accumulation, and oxidative stress through multiple mechanisms, adding a novel environmental risk factor to MASLD pathogenesis.
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.
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.
Examining the Pathogenesis of MAFLD and the Medicinal Properties of Natural Products from a Metabolic Perspective
This review examines the causes and potential treatments for metabolic-associated fatty liver disease (MAFLD), which affects about two-fifths of the global population. While focused on natural product remedies rather than microplastics, the metabolic pathways discussed, including lipid metabolism disruption and oxidative stress, are the same mechanisms through which microplastics have been shown to damage liver cells. Understanding these pathways helps explain how microplastic exposure could contribute to liver disease.
Molecular LandscapeRemodeling Unravels the Cross-Linksof Microplastics-Induced Lipidomic Fluctuations,Nutrient Disorders and Energy Disarrangements
This study examined how polypropylene microplastics accumulate in and damage the mouse liver, using integrated lipidomics and transcriptomics to map the molecular landscape of microplastic-induced lipid disruption and metabolic dysfunction.
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.
Single-cell transcriptome analysis of liver immune microenvironment changes induced by microplastics in mice with non-alcoholic fatty liver
Using advanced single-cell analysis, researchers showed that microplastics worsened non-alcoholic fatty liver disease in mice fed a high-fat diet by changing how immune cells behaved in the liver. Microplastic exposure amplified inflammatory responses and altered the communication between different liver cell types. This study is important because it reveals specific immune mechanisms by which microplastics could worsen liver disease, a condition already affecting roughly one in four adults worldwide.
[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.
Nanoplastic propels diet-induced NAFL to NASH via ER-mitochondrial tether-controlled redox switch
Researchers investigated how nanoplastic exposure may accelerate the progression of diet-induced fatty liver conditions in animal models. The study found that nanoplastics disrupted the connections between the endoplasmic reticulum and mitochondria, triggering oxidative stress responses that worsened liver inflammation and damage.
Non-parenchymal cells: key targets for modulating chronic liver diseases
This review examines how specialized non-parenchymal cells in the liver drive chronic liver diseases like fatty liver disease, fibrosis, and cirrhosis through inflammation and scarring. While not directly about microplastics, these are the same cell types and disease pathways that microplastics and nanoplastics have been shown to activate when they accumulate in liver tissue. Understanding these mechanisms helps explain how environmental pollutants like microplastics could contribute to the growing burden of chronic liver disease.
Molecular LandscapeRemodeling Unravels the Cross-Linksof Microplastics-Induced Lipidomic Fluctuations,Nutrient Disorders and Energy Disarrangements
Mouse liver studies with polypropylene microplastics revealed interconnected disruptions in lipid metabolism, nutrient processing, and energy balance, with proteomic and transcriptomic data highlighting the complexity of hepatic responses to chronic microplastic exposure.
Overview of the hazardous impacts of metabolism-disrupting chemicals on the progression of fatty liver diseases.
This review examined how metabolism-disrupting chemicals (MDCs)—including bisphenol A and phthalates from plastics—promote the development and progression of metabolic dysfunction-associated steatotic liver disease (MASLD, formerly NAFLD). MDC exposure was found to impair liver lipid homeostasis and contribute to the global rise in fatty liver disease.
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.
The nexus of environmental endocrine-disrupting chemical exposure and metabolic dysfunction-associated steatotic liver disease: An emerging public health challenge
This review examines evidence that chronic low-dose exposure to endocrine-disrupting chemicals, including micro- and nanoplastics, may be an underappreciated factor driving the global rise of metabolic liver disease. Researchers found that these pollutants can promote liver fat accumulation, inflammation, and scarring by disrupting hormone signaling, gut health, and mitochondrial function. The study suggests that environmental chemical exposures should be considered alongside diet and lifestyle when assessing liver disease risk.
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.
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.
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.
Exposure to submicroplastics promotes the progression of nonalcoholic fatty liver disease in ApoE-deficient mice
Researchers found that exposing mice to submicron-sized polystyrene plastics in their drinking water for 12 weeks accelerated the progression of nonalcoholic fatty liver disease. The tiny plastic particles accumulated in the liver, worsened fat buildup, increased inflammation, and disrupted cholesterol metabolism. This study suggests that people who already have risk factors for liver disease may be especially vulnerable to health effects from microplastic exposure.
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.
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.
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.