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In utero exposure to dietary lipotropes affects DNA methylation and gene expression in mammary glands of offspring (1033.9)
Author(s) -
Cho Kwang Bog,
Mabasa Lawrence,
Cho Kyongshin,
Crane Courtney,
Choi WooSik,
Park Chung
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.1033.9
Subject(s) - dna methylation , offspring , methylation , biology , dnmt1 , lactation , weaning , epigenetics , endocrinology , medicine , methyltransferase , gene expression , mammary gland , andrology , gene , pregnancy , genetics , cancer , breast cancer
Lipotropes are methyl group‐containing essential nutrients (i.e., methionine, choline, folic acid, and vitamin B12) that play key roles in one‐carbon metabolism. One‐carbon metabolism provides methyl groups for biological methylation pathways, including DNA methylation which controls the expression of genes. The objective of the study was to determine the extent to which maternal dietary lipotropes affect DNA methylation and the expression of genes in mammary glands of the offspring. Pregnant rats were fed either the control or lipotropes supplemented diet until parturition, at which point, rats were fed the control diet until weaning. At weaning, randomly selected female offspring from each group were kept on the control diet until they were bred for collection of the mammary tissues. Tissues were analyzed for global DNA methylation and gene expression. Maternal dietary lipotropes significantly increased DNA methylation in mammary tissues of the offspring [P=0.04]. Transcription of DNA methyltransferase 1 (Dnmt1) [P=0.01] and beta‐casein (Csn2) [P=0.01] genes was increased by maternal methyl diet. While, Dnmt1 is responsible for establishing and regulating methylation patterns, Csn2 is a marker for mammary cell differentiation. Thus, data may be informative to studies aimed at improving mammary development and lactation potential. Grant Funding Source : NIH‐National Cancer Institute