ArticleClinical epigenetics2025
Childhood obesity and DNA methylation in an epigenome-wide association study: findings from the Hokkaido Birth Cohort.
Article in Clinical epigenetics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundChildhood obesity is a pressing public health and pediatric issue. Recently, epigenome-wide association study (EWAS) has received increasing research attention and revealed the association between cord blood methylation and pediatric health problems. However, the relationship between cord blood DNA methylation and childhood obesity remains incompletely understood. This study aimed to assess cord blood DNA methylation and its association with childhood obesity using an EWAS.
resultsThe present study included 12-year-old children with obesity and control participants from the Hokkaido Study on Environment and Children's Health (the Hokkaido cohort), a prospective birth cohort study. The Hokkaido cohort study collected participants' cord blood samples at birth, which were evaluated using an EWAS. We conducted robust linear regression analysis for the differentially methylated positions (DMPs). Thereafter, we also conducted differentially methylated region (DMR) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses. As a result, our analysis involved 500 children, comprising 218 individuals with obesity and 282 controls with no obesity. After quality control, 428 high-quality samples remained (192 children with obesity and 236 controls). Although our DMP analysis did not produce statistically significant results with adjusted p-values with Bonferroni correction and local false discovery rate (FDR) correction, our DMP analysis identified potential candidate genes with a global FDR correction of < 0.05. Three differentially methylated cytosine-phosphate-guanine candidate sites (cg27093962 in dynein regulatory complex 1 [DRC1], cg25187049 in Potassium Voltage-Gated Channel Subfamily B Member 2 [KCNB2], and cg07817806 in Uromodulin [UMOD]) were found to be potentially associated with childhood obesity. Among them, KCNB2 and UMOD are implicated in metabolic and inflammatory pathways relevant to obesity. While DMR analysis did not produce statistically significant results, KEGG analysis revealed potential pathways associated with childhood obesity.
conclusionThe present study suggests three candidate DMPs and pathways that may explain the association between DNA methylation at birth and obesity at 12 years of age.
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