Alfano Rossella, Robinson Oliver, Handakas Evangelos, Nawrot Tim S, Vineis Paolo, Plusquin Michelle
Department of Epidemiology and Biostatistics, The School of Public Health, Imperial College London, London, UK.
Medical Research Council-Health Protection Agency Centre for Environment and Health, Imperial College London, London, UK.
Obes Rev. 2022 Jan;23 Suppl 1:e13389. doi: 10.1111/obr.13389. Epub 2021 Nov 23.
The tremendous increase in childhood obesity prevalence over the last few decades cannot merely be explained by genetics and evolutionary changes in the genome, implying that gene-environment interactions, such as epigenetic modifications, likely play a major role. This systematic review aims to summarize the evidence of the association between epigenetics and childhood obesity. A literature search was performed via PubMed and Scopus engines using a combination of terms related to epigenetics and pediatric obesity. Articles studying the association between epigenetic mechanisms (including DNA methylation and hydroxymethylation, non-coding RNAs, and chromatin and histones modification) and obesity and/or overweight (or any related anthropometric parameters) in children (0-18 years) were included. The risk of bias was assessed with a modified Newcastle-Ottawa scale for non-randomized studies. One hundred twenty-one studies explored epigenetic changes related to childhood obesity. DNA methylation was the most widely investigated mechanism (N = 101 studies), followed by non-coding RNAs (N = 19 studies) with evidence suggestive of an association with childhood obesity for DNA methylation of specific genes and microRNAs (miRNAs). One study, focusing on histones modification, was identified. Heterogeneity of findings may have hindered more insights into the epigenetic changes related to childhood obesity. Gaps and challenges that future research should face are herein described.
在过去几十年里，儿童肥胖患病率急剧上升，这不能仅仅用遗传学和基因组的进化变化来解释，这意味着基因与环境的相互作用，如表观遗传修饰，可能起着主要作用。本系统综述旨在总结表观遗传学与儿童肥胖之间关联的证据。通过PubMed和Scopus引擎进行文献检索，使用与表观遗传学和儿童肥胖相关的术语组合。纳入研究表观遗传机制（包括DNA甲基化和羟甲基化、非编码RNA以及染色质和组蛋白修饰）与儿童（0至18岁）肥胖和/或超重（或任何相关人体测量参数）之间关联的文章。使用改良的纽卡斯尔-渥太华量表对非随机研究的偏倚风险进行评估。121项研究探讨了与儿童肥胖相关的表观遗传变化。DNA甲基化是研究最广泛的机制（N = 101项研究），其次是非编码RNA（N = 19项研究），有证据表明特定基因和微小RNA（miRNA）的DNA甲基化与儿童肥胖有关。确定了一项关注组蛋白修饰的研究。研究结果的异质性可能阻碍了对与儿童肥胖相关的表观遗传变化的进一步深入了解。本文描述了未来研究应面对的差距和挑战。
