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Background <p>Childhood 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.</p> Results <p>The 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 &lt; 0.05. Three differentially methylated cytosine-phosphate-guanine candidate sites (cg27093962 in <i>dynein regulatory complex 1</i> [<i>DRC1]</i>, cg25187049 in <i>Potassium Voltage-Gated Channel Subfamily B Member 2</i> [<i>KCNB2]</i>, and cg07817806 in <i>Uromodulin</i> [<i>UMOD]</i>) 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.</p> Conclusion <p>The present study suggests three candidate DMPs and pathways that may explain the association between DNA methylation at birth and obesity at 12&#xa0;years of age.</p>

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Childhood obesity and DNA methylation in an epigenome-wide association study: findings from the Hokkaido Birth Cohort

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年12月1日

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  • Hiroyoshi Iwata,
  • Chihiro Miyashita,
  • Takeshi Yamaguchi,
  • Atsuko Ikeda,
  • Ryu Miura,
  • Machiko Minatoya,
  • Naomi Tamura,
  • Yu Ait Bamai,
  • Sachiko Itoh,
  • Keiko Yamazaki,
  • Rahel Mesfin Ketema,
  • Mariko Itoh,
  • Maki Tojo,
  • Rieko Yamamoto,
  • Keitaro Makino,
  • Reiko Kishi

摘要

Background

Childhood 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.

Results

The 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.

Conclusion

The 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.