We can't find the internet
Attempting to reconnect
Something went wrong!
Hang in there while we get back on track
Polystyrene nanoplastics induce hepatic steatosis by disrupting autophagic degradation of NCoR1 and suppressing PPARα-mediated fatty acid oxidation
AI summary Read the abstract
This study characterized microplastic contamination in Himalayan lakes, documenting plastic particle abundance and polymer types in high-altitude freshwater ecosystems. The findings reveal that even remote mountain environments are affected by microplastic pollution, likely transported via atmospheric deposition.
Micro- and nanoplastic (MNP) pollution is a global public health concern, with inevitable ingestion by humans. The liver functions as a primary target organ, and studies have confirmed the presence of microplastics in human hepatic tissues. However, the hepatotoxic effects resulting from such exposure remain poorly characterized. Although polystyrene nanoplastics (PSNPs) have been implicated in disrupting hepatic lipid homeostasis and inducing steatosis, the underlying molecular mechanisms remain elusive. In this study, C57BL/6J mice were gavaged with PSNPs to establish an in vivo exposure model. Histopathological analysis demonstrated that exposure to PSNPs, in conjunction with a high-fat diet (HFD), facilitated the development of a hepatic steatotic phenotype. Multi-omics analysis revealed significant suppression of the PPARα signaling pathway, mechanistically linked to impaired fatty acid β-oxidation. Further experiments demonstrated that PSNPs inhibited the autophagic degradation of NCoR1. Concurrently, PSNP exposure activated the mTOR/S6K2 signaling pathway, promoting NCoR1 phosphorylation and nuclear translocation, thereby suppressing PPARα-regulated expression of genes involved in fatty acid β-oxidation, ultimately leading to hepatic lipid accumulation. Overall, this study elucidates the molecular mechanism by which PSNPs induce hepatic steatosis through NCoR1 dysregulation, providing a theoretical foundation for nanoplastic-related hepatotoxicity research and advancing health risk assessment related to MNP pollution.
More Papers Like This
Polystyrene microplastics induce hepatic lipid metabolism and energy disorder by upregulating the NR4A1-AMPK signaling pathway
AI summary Read the abstract
Researchers found that polystyrene microplastics accumulate in the liver and disrupt fat and energy metabolism by activating a specific molecular pathway called NR4A1-AMPK. This activation triggers a self-cleaning process called autophagy that reduces fat production in liver cells, while also increasing harmful reactive oxygen species. The findings suggest that long-term microplastic exposure could lead to ongoing liver damage through this metabolic disruption.
Polystyrene nanoplastics potentiate the development of hepatic fibrosis in high fat diet fed mice
AI summary Read the abstract
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.
Low‐Dose Polystyrene Nanoplastics Alleviate High‐Fat Diet‐Induced Hepatic Injury via AMPK / mTOR ‐Mediated Lipophagy Activation
AI summary Read the abstract
Researchers fed rats a high-fat diet alongside low-dose polystyrene nanoplastics for 90 days and found the nanoplastics unexpectedly reduced liver fat accumulation and inflammation by activating AMPK-mediated lipophagy, revealing a context-dependent interaction where low-dose plastic exposure can trigger a stress-adaptation response that partially counteracts diet-induced hepatic injury.
Untargeted metabolomics and transcriptomics joint analysis of the effects of polystyrene nanoplastics on lipid metabolism in the mouse liver
AI summary Read the abstract
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.
Polystyrene Nanoplastics Exacerbate HFD-induced MASLD by Reducing Cathepsin Activity and Triggering Large Vacuole Formation via Impaired Lysosomal Acidification
AI summary Read the abstract
Researchers found that polystyrene nanoplastics, when combined with a high-fat diet in mice, significantly worsened fatty liver disease symptoms compared to either factor alone. The nanoplastics impaired the function of lysosomes, the cell's recycling centers, by preventing proper acidification and reducing enzyme activity. The study suggests that nanoplastic exposure could amplify diet-related liver problems by interfering with how cells process and break down fats.
Research digests by email
When a large batch of papers lands in the Atlas, we read through it and send a short write-up of what stood out.