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2573-P: Polystyrene Microplastics Exposure Exacerbates Thyroid–Brown Adipose Tissue Axis Dysregulation to Promote Obesity and Glucose–Lipid Metabolic Disorders
Original title: 2573-P: Polystyrene Microplastics Exposure Exacerbates Thyroid–Brown Adipose Tissue Axis Dysregulation to Promote Obesity and Glucose–Lipid Metabolic Disorders
Summary
In mice, tiny amounts of microplastics made a high-fat diet even worse for metabolism—leading to more weight gain, blood sugar problems, and unhealthy cholesterol levels—by throwing off the thyroid's ability to regulate calorie-burning "brown fat." The good news: giving the mice thyroid hormone reversed these effects, suggesting a possible future treatment target, though this research was done in mice and still needs to be confirmed in humans before we know if the same risks apply to people eating unhealthy diets while exposed to everyday plastics.
Introduction and Objective: The global prevalence of obesity and diabetes has escalated dramatically in recent decades, driven by both obesogenic dietary patterns (e.g., high-fat diet, HFD) and environmental contaminants such as microplastics (MPs). However, the combined effects of chronic low-dose MPs exposure and HFD consumption on the progression of metabolic diseases remain poorly understood. This study aims to investigate the role of polystyrene microplastics (PS-MPs) in exacerbating HFD-induced metabolic dysfunction and its underlying mechanisms. Methods: Male C57BL/6J mice were randomized into four groups: normal chow diet (NCD), NCD + PS-MPs, HFD, and HFD + PS-MPs. PS-MPs (25-30 μg/kg body weight/day) was administered via oral gavage for 14-16 weeks. Metabolic parameters including body weight gain, energy expenditure, body fat composition, glucose tolerance, insulin sensitivity, and thyroid function were systematically evaluated. Results: PS-MPs exposure significantly exacerbated HFD-induced obesity and metabolic disorders, characterized by accelerated weight gain, reduced energy metabolism, impaired glucose homeostasis, and dysregulated lipid profiles. Mechanistically, in vivo and in vitro experiments confirmed that low-dose PS-MPs primarily disrupt the thyroid-brown adipose tissue (BAT) axis to mediate these adverse effects. Notably, thyroid hormone supplementation reversed the metabolic impairments, further validating the causal role of the thyroid-BAT axis in PS-MPs-induced metabolic dysfunction. Conclusion: These findings highlight the critical contribution of chronic low-dose PS-MPs exposure to the pathogenesis of obesity and diabetes, particularly in the context of pre-existing metabolic stress (e.g., HFD). The identification of the thyroid-BAT axis as a key mediator provides novel therapeutic targets for mitigating metabolic diseases associated with environmental MPs exposure. Disclosure G. Wei: None. F. Shen: None. F. Ma: None. W. Cao: None. J. Yang: None.