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Gene‐specific changes in DNA methylation in response to chronic folic acid supplementation in normal weight and obese women of child‐bearing age (817.3)
Author(s) -
Park Hea Jin,
Shade Deanna,
Hausman Dorothy,
Hohos Natalie,
Meagher Richard,
Kauwell Gail,
Smith Alicia,
Bailey Lynn
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.817.3
Subject(s) - dna methylation , cpg site , methylation , obesity , endocrinology , medicine , gene , biology , genetics , gene expression
Folate plays an important role in one‐carbon metabolism including DNA methylation. We reported a lower acute pharmacokinetic response to folic acid (FA) in obesity. Both maternal folate deficiency and obesity are associated with increased risk for neural tube defects (NTDs). However, the impact of folate or obesity on DNA methylation of NTD‐related genes remains unclear. We provided 800 ug/d of FA to healthy normal weight (NW; BMI 18.5‐24.9 kg/m 2 ;n = 12) and obese (BMI > 30 kg/m 2 ; n = 6) women (18‐35y) for 8‐wks and determined changes in DNA methylation in CD 16 + cells, isolated from blood using magnetic bead technology. DNA methylation was examined across 2107 CpG sites in 91 NTD‐ and folate pathway‐ related genes using the Infinium Human Methylation450 Bead Chip. For each CpG site, the proportion of DNA methylation that changed over the supplementation was evaluated by fitting a separate linear model. The analysis indicated changes in 57 vs. 101 CpG sites (36 vs. 47 genes) following the supplementation in NW and obese women, respectively. Among them, 68% vs. 76% of the CpG sites (26 vs 37 genes) decreased in methylation. These data suggest that DNA methylation in NTD‐ and folate pathway‐related genes changed in response to FA supplementation and that the changes were different in NW and obese women. Specific pathways influenced by folate status and exhibiting a differential response in obesity are being explored. Grant Funding Source : Funded in part by HATCH #GEO00706, #GEO00707 and the Obesity Initiative at the University of Georgia