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儿童肥胖及相关疾病中的内分泌干扰物:早期关键暴露窗口

Endocrine Disruptors in Child Obesity and Related Disorders: Early Critical Windows of Exposure.

作者信息

Celik Mensure Nur, Yesildemir Ozge

机构信息

Department of Nutrition and Dietetics, Faculty of Health Sciences, Ondokuz Mayıs University, Samsun, Turkey.

Department of Nutrition and Dietetics, Faculty of Health Sciences, Bursa Uludag University, Bursa, Turkey.

出版信息

Curr Nutr Rep. 2025 Jan 8;14(1):14. doi: 10.1007/s13668-024-00604-1.

DOI:10.1007/s13668-024-00604-1
PMID:39775248
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11706864/
Abstract

Endocrine disruptors (EDs) can mimic or interfere with hormones in the body, leading to non-communicable diseases, such as obesity, diabetes, and metabolic syndrome. Susceptibility to EDs increases during prenatal and postnatal life, a critical time window. This review aims to summarize the latest evidence on the relation of early life exposure to some EDs with obesity and the other metabolic disorders.  RECENT FINDINGS: There is increasing evidence that early life exposure to EDs may impair adipogenesis by increasing the number and size of adipocytes, thereby increasing susceptibility to obesity in childhood. It is stated that exposure to EDs during the prenatal and postnatal period may raise the risk of type 2 diabetes in adulthood by disrupting glucose, lipid, and insulin homeostasis in the offspring. They can also accelerate the development of type 1 diabetes through various mechanisms, like immunomodulation, gut microbiota, and vitamin D pathways. There is a growing understanding that ED exposure during critical stages of life could play an important role in the development of obesity and metabolic disorders. We suggest setting national goals, global standards, and policies to reduce environmental exposure to pregnant and lactating women, and babies, considered sensitive populations.

摘要

内分泌干扰物(EDs)能够模拟或干扰体内激素,引发肥胖、糖尿病和代谢综合征等非传染性疾病。在产前和产后这一关键时间窗口,对EDs的易感性会增加。本综述旨在总结关于生命早期接触某些EDs与肥胖及其他代谢紊乱之间关系的最新证据。近期发现:越来越多的证据表明,生命早期接触EDs可能通过增加脂肪细胞的数量和大小来损害脂肪生成,从而增加儿童期肥胖的易感性。据指出,产前和产后接触EDs可能通过破坏后代的葡萄糖、脂质和胰岛素稳态,提高成年后患2型糖尿病的风险。它们还可通过免疫调节、肠道微生物群和维生素D途径等多种机制加速1型糖尿病的发展。人们越来越认识到,生命关键阶段接触EDs可能在肥胖和代谢紊乱的发展中起重要作用。我们建议制定国家目标、全球标准和政策,以减少对孕妇、哺乳期妇女和婴儿等敏感人群的环境暴露。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cd68/11706864/2aa8c1426569/13668_2024_604_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cd68/11706864/443015028a56/13668_2024_604_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cd68/11706864/2aa8c1426569/13668_2024_604_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cd68/11706864/443015028a56/13668_2024_604_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cd68/11706864/2aa8c1426569/13668_2024_604_Fig2_HTML.jpg

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本文引用的文献

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The association between prenatal exposure to bisphenol A and offspring obesity: A systematic review.孕期暴露于双酚 A 与后代肥胖的关系:系统综述。
Environ Pollut. 2024 Mar 1;344:123391. doi: 10.1016/j.envpol.2024.123391. Epub 2024 Jan 17.
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The Role of Endocrine Disruptors Bisphenols and Phthalates in Obesity: Current Evidence, Perspectives and Controversies.内分泌干扰物双酚 A 和邻苯二甲酸酯在肥胖中的作用:当前的证据、观点和争议。
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Di-(2-ethylhexyl) phthalate increases plasma glucose and induces lipid metabolic disorders via FoxO1 in adult mice.邻苯二甲酸二(2-乙基己基)酯通过 FoxO1 增加成年小鼠的血浆葡萄糖并诱导脂代谢紊乱。
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