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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.
The health concerns of microplastics (MPs) and nanoplastics (NPs) surge, but the key indicators to evaluate the adverse risks of MPs/NPs are elusive. Recently, MPs/Ps were found to disturb glucose and lipid metabolism in rodents, suggesting that MPs/NPs may play a role in obesity progression. In this study, we firstly demonstrated that the distribution of fluorescent polystyrene nanoplastics (nPS, 60 nm) white adipose tissue (WAT) of mice. Furthermore, nPS could traffic across adipocytes in vitro and reduced lipolysis under β-adrenergic stimulation in adipocytes in vitro and ex vivo. Consistently, chronic oral exposure to nPS at the dietary exposure relevant concentrations (3 and 223 μg/kg body weight) impaired fasting-induced lipid mobilization in obese mice and subsequently contributed to larger adipocyte size in the subcutaneous WAT. In addition, the chronic exposure of nPS induced macrophage infiltration in the small intestine and increased lipid accumulation in the liver, accelerating the disruption of systemic metabolism. Collectively, our findings highlight the potential obesogenic role of nPS via diminishing lipid mobilization in WAT of obese mice and suggest that lipolysis relevant parameters may be used for evaluating the adverse effect of MPs/NPs in clinics.
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Polystyrene nanoplastics inhibit beige fat function and exacerbate metabolic disorder in high-fat diet-fed mice
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Researchers found that polystyrene nanoplastics worsened metabolic problems in mice fed a high-fat diet by shutting down the function of beige fat cells, which normally help burn energy. The nanoplastics accumulated in fat tissue and suppressed a key protein needed for heat generation, leading to increased fat storage, liver damage, and impaired blood sugar control. This study suggests that nanoplastic exposure could contribute to obesity and metabolic disease in humans, especially those already eating an unhealthy diet.
[The effect and mechanism of exposure to polystyrene nanoplastics on lipid metabolism in mice liver].
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Researchers exposed mice to 20 nm polystyrene nanoplastics and investigated the effects on hepatic lipid metabolism using multi-omics approaches. Nanoplastic exposure disrupted lipid metabolic pathways in the liver, causing significant changes in lipid accumulation and related gene expression, suggesting a mechanism by which nanoplastic ingestion may contribute to metabolic disorders.
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.
Exposure to polystyrene nanoplastics impairs lipid metabolism in human and murine macrophages in vitro
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Researchers exposed human and mouse macrophages to polystyrene nanoplastics and found that the particles disrupted lipid metabolism in these immune cells. The study observed that nanoplastic exposure altered how macrophages process and store fats, which could affect their ability to function properly. These findings suggest that nanoplastic accumulation in immune cells may interfere with normal metabolic processes at the cellular level.
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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