Jaskulak Marta, Zimowska Malwina, Rolbiecka Marta, Zorena Katarzyna
Department of Immunobiology and Environmental Microbiology, Department of Health Sciences, Medical University of Gdansk, Poland.
Department of Immunobiology and Environmental Microbiology, Department of Health Sciences, Medical University of Gdansk, Poland.
Ecotoxicol Environ Saf. 2025 Jul 1;299:118401. doi: 10.1016/j.ecoenv.2025.118401. Epub 2025 May 23.
The prevalence of obesity has reached epidemic proportions worldwide, posing a significant public health concern due to its association with various chronic diseases and healthcare costs. In addition to traditional risk factors such as diet and physical activity, emerging evidence suggests that environmental pollutants, termed obesogens, may contribute to the obesity epidemic. Obesogens are endocrine-disrupting chemicals (EDCs) that can alter lipid homeostasis, promote adipogenesis, and disrupt metabolic regulation, leading to increased adiposity and obesity risk. This review explores available data from human studies published in the last decade, along with the mechanisms underlying obesogenic action, including their effects on adipocyte differentiation, adipose tissue development, and metabolic regulation. Overall, 75 studies were analyzed. Early-life exposure during critical developmental windows has been shown to increase obesity risk later in life, potentially through epigenetic modifications and transgenerational effects. Epidemiological studies provide evidence of associations between prenatal or early-life exposure and increased obesity risk in offspring. Additionally, study found more consistent associations between exposure to some EDCs (including phthalates, parabens, and bisphenols) and obesity or metabolic outcomes in children and women, while results for other chemicals (i.e. PFAS and organochlorine pesticides) were more heterogeneous, especially in adolescents and adults. Key findings indicate consistent associations between phthalate exposure and obesity in children, with mixed results for adults. Future research should focus on elucidating the full spectrum of obesogens, their mechanisms of action, and their implications for obesity risk across generations. This knowledge will inform preventive strategies and public health interventions aimed at addressing the obesity epidemic and its associated health burden.
肥胖症的患病率在全球已达到流行程度,因其与各种慢性疾病及医疗成本相关联,故而成为重大的公共卫生问题。除了饮食和身体活动等传统风险因素外,新出现的证据表明,被称为致肥胖物的环境污染物可能促使了肥胖症的流行。致肥胖物是内分泌干扰化学物质(EDCs),它们能够改变脂质稳态、促进脂肪生成并扰乱代谢调节,导致肥胖增加和肥胖风险上升。本综述探讨了过去十年发表的人体研究中的现有数据,以及致肥胖作用的潜在机制,包括它们对脂肪细胞分化、脂肪组织发育和代谢调节的影响。总共分析了75项研究。关键发育窗口期的早期暴露已被证明会增加日后患肥胖症的风险,这可能是通过表观遗传修饰和跨代效应实现的。流行病学研究为产前或早期暴露与后代肥胖风险增加之间的关联提供了证据。此外,研究发现某些内分泌干扰化学物质(包括邻苯二甲酸盐、对羟基苯甲酸酯和双酚)与儿童及女性的肥胖或代谢结果之间的关联更为一致,而其他化学物质(如全氟辛烷磺酸和有机氯农药)的结果则更为多样,尤其是在青少年和成年人中。主要研究结果表明,邻苯二甲酸盐暴露与儿童肥胖之间存在一致的关联,而成年人的结果则好坏参半。未来的研究应侧重于阐明致肥胖物的全貌、它们的作用机制以及它们对几代人肥胖风险的影响。这些知识将为旨在应对肥胖症流行及其相关健康负担的预防策略和公共卫生干预措施提供依据。