Department of Environmental and Occupational Health Sciences, Downstate Medical Center School of Public Health, State University of New York, Brooklyn, NY, USA; Columbia Center for Children's Environmental Health, Mailman School of Public Health, Columbia University, New York, NY, USA.
Environ Res. 2019 Jun;173:54-68. doi: 10.1016/j.envres.2019.03.012. Epub 2019 Mar 6.
There is significant evidence of globally ubiquitous prenatal exposures to bisphenol A (BPA). Childhood obesity as an epidemic has been a global concern for over a decade. Experimental models and epidemiological evidence suggest that BPA may act as an obesogen during adipogenesis. Results from stem cell models and birth cohort studies support the developmental origins of health and disease theory. While literature reviews have presented a variety of potential mechanisms of BPA action during adipogenesis, there remains no consensus. This review is the first to explore the proliferator-activated receptor gamma (PPARγ) mechanism in detail. This review will also examine the obesogenic effect of prenatal exposure to BPA during critical windows of vulnerability. Although vast experimental literature exists, there is limited epidemiological evidence to support the hypothesis for the obesogenic effect of BPA. The primary goal of this review is to provide researchers with a roadmap of existing research and suggestions for future directions for analyzing the relationship between prenatal BPA exposures and childhood obesity.
有大量证据表明，双酚 A（BPA）在全球范围内普遍存在于产前暴露中。儿童肥胖症作为一种流行病，已经成为十多年来的全球关注焦点。实验模型和流行病学证据表明，BPA 可能在脂肪生成过程中作为一种致肥胖物发挥作用。来自干细胞模型和出生队列研究的结果支持健康和疾病的发育起源理论。虽然文献综述提出了 BPA 在脂肪生成过程中作用的多种潜在机制，但仍未达成共识。这篇综述是第一篇详细探讨过氧化物酶体增殖物激活受体γ（PPARγ）机制的综述。这篇综述还将探讨在易损期内产前暴露于 BPA 的致肥胖作用。尽管存在大量的实验文献，但支持 BPA 致肥胖假说的流行病学证据有限。本综述的主要目的是为研究人员提供现有研究的路线图，并为分析产前 BPA 暴露与儿童肥胖之间的关系提供未来研究方向的建议。
