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Nanoplastics disrupt hepatic lipid metabolism via the inhibition of PPARγ: a study based on digestive system exposure
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Using data from a large U.S. health survey, researchers linked bottled water consumption (a known source of nanoplastic exposure) to higher rates of nonalcoholic fatty liver disease. In mouse experiments, nanoplastics disrupted fat metabolism in the liver by blocking a key protein called PPARgamma. This suggests that nanoplastics entering the body through everyday drinking water could contribute to liver disease by interfering with how the liver processes fats.
Nanoplastics (NPs) are emerging environmental contaminants capable of crossing biological barriers and accumulating in organs such as the liver, raising growing concerns about their potential contribution to nonalcoholic fatty liver disease (NAFLD). Notably, bottled water has been recognised as a major daily source of NP exposure. However, the associations between NP exposure and NAFLD onset, as well as the mechanistic basis, remain unclear. To investigate this, we analysed data from the National Health and Nutrition Examination Survey (NHANES) 2013-2016 cycles, using daily bottled water intake to estimate NP exposure and the hepatic steatosis index (HSI) as an indicator of liver fat accumulation. Animal and cellular experiments were conducted to evaluate NP-induced hepatic alterations. Additionally, transcriptomic analysis of liver tissues was performed, and integration with DisGeNET and the Comparative Toxicogenomics Database (CTD) enabled bioinformatic analyses and identification of key regulatory pathways. Epidemiological results revealed a significant positive correlation between bottled water consumption and HSI. Experimental findings demonstrated that NP exposure induced liver vacuolisation, oxidative damage, metabolic disruption, and inflammation in both in vivo and in vitro models. Transcriptomic and database integration revealed that NP exposure suppressed the PPAR signalling pathway, particularly by downregulating PPARγ expression, with excessive ROS generation likely contributing to this inhibition. These results were summarised in an adverse outcome pathway (AOP) framework, illustrating how NP exposure may impair PPARγ signalling and promote hepatic lipid accumulation. In conclusion, this study provides evidence that environmental NP exposure may be a contributing factor to NAFLD development and highlights the potential public health impact of the intake of NPs from bottled water.
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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.
Nanoplastic Exposure at Environmental Concentrations Disrupts Hepatic Lipid Metabolism through Oxidative Stress Induction and Endoplasmic Reticulum Homeostasis Perturbation
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A study in fish found that nanoplastics at environmentally realistic concentrations accumulated in the liver and disrupted fat metabolism, causing a condition similar to fatty liver disease. Smaller nanoplastics (100 nanometers) caused more severe damage than larger microplastics by disrupting protein processing in cells and triggering oxidative stress. These findings raise concerns that nanoplastics in the environment could affect liver health in fish and potentially in humans who consume contaminated seafood.
Exposure to submicroplastics promotes the progression of nonalcoholic fatty liver disease in ApoE-deficient mice
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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.
Microplastics and nanoplastics: Emerging drivers of hepatic pathogenesis and metabolic dysfunction
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This review examines emerging evidence linking micro- and nanoplastic exposure to liver disease, including metabolic dysfunction-associated liver disease, cirrhosis, and liver cancer. Researchers found that these particles may contribute to liver damage through oxidative stress, inflammation, and disruption of metabolic pathways. The study highlights the need for further research into how environmental plastic contamination may be influencing the rising rates of liver disease worldwide.
Are Ingested or Inhaled Microplastics Involved in Nonalcoholic Fatty Liver Disease?
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This review explored the potential connection between microplastic exposure through ingestion and inhalation and nonalcoholic fatty liver disease, which has become a leading cause of chronic liver injury. The study discusses how dietary and environmental microplastic exposure could potentially influence liver health through mechanisms including inflammation and endocrine disruption, though further research is needed to establish definitive links.
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