We can't find the internet
Attempting to reconnect
Something went wrong!
Hang in there while we get back on track
Polystyrene nanoplastics induce lipophagy via the AMPK/ULK1 pathway and block lipophagic flux leading to lipid accumulation in hepatocytes
AI summary Read the abstract
Polystyrene nanoplastics caused fat to accumulate in human liver cells by disrupting the normal fat-breakdown process called lipophagy. The nanoplastics triggered the cells to start digesting fat droplets but then blocked the final cleanup step by damaging the cell's recycling centers (lysosomes), leaving excess fat trapped inside. This newly identified mechanism helps explain how nanoplastic exposure could contribute to fatty liver disease.
Micro- and nanoplastic pollution has emerged as a significant global concern due to their extensive presence in the environment and potential adverse effects on human health. Nanoplastics can enter the human circulatory system and accumulate in the liver, disrupting hepatic metabolism and causing hepatotoxicity. However, the precise mechanism remains uncertain. Lipophagy is an alternative mechanism of lipid metabolism involving autophagy. This study aims to explore how polystyrene nanoplastics (PSNPs) influence lipid metabolism in hepatocytes via lipophagy. Initially, it was found that PSNPs were internalized by human hepatocytes, resulting in decreased cell viability. PSNPs were found to induce the accumulation of lipid droplets (LDs), with autophagy inhibition exacerbating this accumulation. Then, PSNPs were proved to activate lipophagy by recruiting LDs into autophagosomes and block the lipophagic flux by impairing lysosomal function, inhibiting LD degradation. Ultimately, PSNPs were shown to activate lipophagy through the AMPK/ULK1 pathway, and knocking down AMPK exacerbated lipid accumulation in hepatocytes. Overall, these results indicated that PSNPs triggered lipophagy via the AMPK/ULK1 pathway and blocked lipophagic flux, leading to lipid accumulation in hepatocytes. Thus, this study identifies a novel mechanism underlying nanoplastic-induced lipid accumulation, providing a foundation for the toxicity study and risk assessments of nanoplastics.
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.
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.
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.
Lipid metabolic dysregulation: A novel developmental toxicity pathway of aged nanoplastics via inhibition of lipophagy in zebrafish
AI summary Read the abstract
Researchers showed that UV-aged polystyrene nanoplastics cause more severe developmental toxicity in zebrafish larvae than pristine particles by blocking lipophagy — the cellular process of breaking down stored fat via lysosomes — leading to abnormal lipid accumulation and disrupted early development.
Polystyrene nanoplastics induce glycolipid metabolism disorder via NF-κB and MAPK signaling pathway in mice
AI summary Read the abstract
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.
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.