Laboratory of Cell-Cell Interactions, Department of Morphology, Institute of Biological Sciences, Federal University of Minas Gerais, Minas Gerais, Brazil.
J Cell Biochem. 2020 Jun;121(5-6):3042-3057. doi: 10.1002/jcb.29544. Epub 2019 Nov 10.
Childhood obesity is a global burden affecting millions of children worldwide. It is well-known that the adiposity profile in children is critical for future occurrence of diseases. As a multifactorial disease, obesity is associated with genetic and environmental factors. Epigenetic mechanisms link the plethora of environmental clues to a given phenotype. DNA methylation is the most studied epigenetic mark and its importance in several diseases was acknowledged. In childhood obesity, specifically, the studies show a consistent association between adiposity and methylation at the gene and genome-wide scales. The relationship between DNA methylation and childhood obesity has been proved strong for some genes and pathways. However, the studies are heterogeneous in their design, methodologies, and results. The aim of this review is to discuss this heterogeneity and point out some aspects that should be considered in future studies to clarify the role of DNA methylation in childhood obesity.
儿童肥胖是一个全球性的负担，影响着全球数以百万计的儿童。众所周知，儿童的肥胖状况对未来疾病的发生至关重要。作为一种多因素疾病，肥胖与遗传和环境因素有关。表观遗传机制将大量的环境线索与特定的表型联系起来。DNA 甲基化是研究最多的表观遗传标记，其在多种疾病中的重要性已得到认可。具体来说，在儿童肥胖中，研究表明在基因和全基因组水平上，肥胖与甲基化之间存在一致的关联。DNA 甲基化与儿童肥胖之间的关系在一些基因和途径中已经得到了证实。然而，这些研究在设计、方法和结果上存在异质性。本综述的目的是讨论这种异质性，并指出在未来研究中应考虑的一些方面，以阐明 DNA 甲基化在儿童肥胖中的作用。
