We can't find the internet
Attempting to reconnect
Something went wrong!
Hang in there while we get back on track
Microplastics cause hepatotoxicity in diabetic mice by disrupting glucolipid metabolism via PP2A/AMPK/HNF4A and promoting fibrosis via the Wnt/β‐catenin pathway
AI summary Read the abstract
Researchers found that microplastic exposure caused liver damage in diabetic mice by disrupting the way the liver processes sugars and fats through specific cellular signaling pathways. The microplastics also promoted liver scarring through activation of a fibrosis-related pathway. The study suggests that individuals with existing metabolic conditions like diabetes may be particularly vulnerable to the harmful effects of microplastic accumulation in the body.
In recent years, microplastics (MPs) have gained significant attention as a persistent environmental pollutant resulting from the decomposition of plastics, leading to their accumulation in the human body. The liver, particularly of individuals with type 2 diabetes mellitus (T2DM), is known to be more susceptible to the adverse effects of environmental pollutants. Therefore, to investigate the potential impact of MPs on the liver of diabetic mice and elucidate the underlying toxicological mechanisms, we exposed db/db mice to 0.5 μm MPs for 3 months. Our results revealed that MPs exposure resulted in several harmful effects, including decreased body weight, disruption of liver structure and function, elevated blood glucose levels, impaired glucose tolerance, and increased glycogen accumulation in the hepatic tissue of the mice. Furthermore, MPs exposure was found to promote hepatic gluconeogenesis by perturbing the PP2A/AMPK/HNF4A signaling pathway. In addition, MPs disrupt redox balance, leading to oxidative damage in the liver. This exposure also disrupted hepatic lipid metabolism, stimulating lipid synthesis while inhibiting catabolism, ultimately resulting in the development of fatty liver. Moreover, MPs were found to induce liver fibrosis by activating the Wnt/β-catenin signaling pathway. Furthermore, MPs influenced adaptive thermogenesis in brown fat by modulating the expression of uncoupling protein 1 (UCP1) and genes associated with mitochondrial oxidative respiration thermogenesis in brown fat. In conclusion, our study demonstrates that MPs induce oxidative damage in the liver, disturb glucose and lipid metabolism, promote hepatic fibrosis, and influence adaptive thermogenesis in brown fat in diabetic mice. These findings underscore the potential adverse effects of MPs on liver health in individuals with T2DM and highlight the importance of further research in this area.
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 microplastics and hepatic fibrosis-related indices in type 2 diabetes: a cross-sectional analysis with experimental validation
AI summary Read the abstract
Researchers found that polystyrene microplastics detected in blood were the polymer most consistently linked to elevated liver fibrosis markers in type 2 diabetic patients, and confirmed in diabetic mice that PS-MPs worsen hepatic steatosis and fibrosis by activating the NLRP3 inflammasome and TGF-β1/Smad signaling pathways.
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.
Long-term exposure to polystyrene microplastics induces hepatotoxicity by altering lipid signatures in C57BL/6J mice
AI summary Read the abstract
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.
Microplastics increase the hepato-pathophysiological complications and decrease the therapeutic efficacy of Metformin in T2-DM rats
AI summary Read the abstract
In diabetic rats, exposure to microplastics worsened liver damage and actually made the diabetes drug metformin less effective at controlling blood sugar and protecting the liver. This matters because it suggests that everyday plastic contamination could quietly undermine treatment for the millions of people managing type 2 diabetes, though more research is needed to confirm this happens in humans.
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.