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Polystyrene nanoplastics promote adipogenesis by stimulating nuclear translocation of PPARγ
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Researchers showed that polystyrene nanoplastics promote fat cell formation in mice and mouse preadipocytes by driving the master fat-cell regulator PPAR-gamma (peroxisome proliferator-activated receptor gamma) into the cell nucleus, where it activates genes that accelerate lipid accumulation and fat tissue expansion.
As an emerging contaminant, nanoplastics (NPs) are widespread in the food chain and environment, raising concerns about their potential toxicity. However, their effects on lipid metabolic homeostasis and the underlying mechanisms remain unclear. This study used polystyrene nanoplastics (PS-NPs), common in food packaging, to examine their impact on adipogenic differentiation and lipid synthesis. Our research results indicated that after 10 days of oral exposure, PS-NPs significantly accumulated in the adipose tissue of mice. Within the exposure concentration range of 1-100 μg/mL, PS-NPs significantly increased the expression of genes related to adipogenesis, accelerated mitotic clonal expansion (MCE) during early differentiation, and enhanced triglyceride (TG) accumulation in mouse 3T3-L1 preadipocytes, leading to adipogenic differentiation and lipogenesis. These effects were positively correlated with the exposure concentration. Protein quantification and immunofluorescence revealed that PS-NPs promoted the nuclear translocation of peroxisome proliferator-activated receptor γ (PPARγ). Molecular dynamics simulations confirmed that PS-NPs bind to the nuclear localization signal (NLS) region of PPARγ. These findings suggested a new molecular mechanism in which PS-NPs influence PPARγ's subcellular localization through NPs-protein interactions, triggering adipogenic programs. This study provides valuable insights for the safety assessment and toxicology of nanoplastics.
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Polystyrene nanoplastics dysregulate lipid metabolism in murine macrophages in vitro
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Researchers investigated the effects of polystyrene nanoplastics on immune cell metabolism and found that macrophages exposed to nanoplastics transformed into lipid-laden foam cells. The study suggests that nanoplastic exposure dysregulates lipid metabolism in immune cells, with implications for understanding how these particles may interact with the immune system at the cellular level.
Dietary exposure to polystyrene nanoplastics impairs fasting-induced lipolysis in adipose tissue from high-fat diet fed mice
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Researchers demonstrated that fluorescent polystyrene nanoplastics accumulate in the white adipose tissue of mice and can traffic across adipocyte cells. The study found that dietary exposure to nanoplastics impaired fasting-induced fat breakdown in mice fed a high-fat diet, suggesting that nanoplastics may interfere with lipid metabolism and potentially play a role in obesity progression.
Cellular Uptake and Nuclear Accumulation of Polystyrene Nanoplastics in 3T3 Fibroblasts and Hepatocytes of Rattus norvegicus
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Scientists found that tiny plastic particles called nanoplastics can get inside liver and connective tissue cells from rats, and even sneak into the cell's nucleus, where DNA is stored. Cells exposed to these plastics showed signs of stress and damage, including swelling and higher rates of cell death, suggesting these ultra-small plastic particles may be more harmful than previously thought. While this study used animal cells rather than human cells, it raises important questions about what everyday exposure to nanoplastics (found in food packaging, water, and other sources) might mean for our own cellular health.
Polystyrene nanoplastics target lysosomes interfering with lipid metabolism through the PPAR system and affecting macrophage functionalization
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Researchers examined how polystyrene nanoplastics affect lysosomal function and lipid metabolism in macrophages through the PPAR signaling system. The study suggests that nanoplastics can interfere with cellular lipid processing by targeting lysosomes, which may affect immune cell function.
Untargeted metabolomics and transcriptomics joint analysis of the effects of polystyrene nanoplastics on lipid metabolism in the mouse liver
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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.
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