Newborns of obese parents have altered DNA methylation patterns at imprinted genes
Genomic Imprinting
Differentially methylated regions
MEG3
Methylated DNA immunoprecipitation
DOI:
10.1038/ijo.2013.193
Publication Date:
2013-10-25T07:34:42Z
AUTHORS (11)
ABSTRACT
Several epidemiologic studies have demonstrated associations between periconceptional environmental exposures and health status of the offspring in later life. Although these environmentally related effects been attributed to epigenetic changes, such as DNA methylation shifts at imprinted genes, little is known about potential maternal paternal preconceptional overnutrition or obesity.We examined parental obesity relation profiles multiple human genes important normal growth development, as: maternally expressed gene 3 (MEG3), mesoderm-specific transcript (MEST), paternally (PEG3), pleiomorphic adenoma gene-like 1 (PLAGL1), epsilon sarcoglycan 10 (SGCE/PEG10) neuronatin (NNAT).We measured percentages differentially methylated regions (DMRs) by bisulfite pyrosequencing extracted from umbilical cord blood leukocytes 92 newborns. Preconceptional obesity, defined BMI ⩾30 kg m(-2), was ascertained through standardized questionnaires.After adjusting for confounders cluster effects, significantly associated with lower levels MEST (β=-2.57; s.e.=0.95; P=0.008), PEG3 (β=-1.71; s.e.=0.61; P=0.005) NNAT (β=-3.59; s.e.=1.76; P=0.04) DMRs. Changes detected other loci were follows: β-coefficient +2.58 (s.e.=1.00; P=0.01) PLAGL1 DMR -3.42 (s.e.=1.69; MEG3 DMR.We found altered outcomes imprint regulatory children born obese parents, compared non-obese parents. In spite small sample size, our data suggest a influence life-style on (re)programming marks during gametogenesis early development. More specifically, significant independent association offspring's suggests susceptibility developing sperm insults. The acquired instability may be carried onto next generation increase risk chronic diseases adulthood.
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