Location: Arkansas Children's Nutrition CenterTitle: Maternal adiposity in the absence of excessive gestational weight gain is associated with distinct changes in DNA methylation patterns in umbilical cords of infants) Author
Submitted to: Federation of American Societies for Experimental Biology Conference
Publication Type: Abstract only
Publication Acceptance Date: 2/19/2014
Publication Date: 4/15/2014
Citation: Thakali, K., Saben, J., Faske, J.B., Lindsey, F., Gomez-Acevedo, H., Badger, T.M., Andres, A., Shankar, K. 2014. Maternal adiposity in the absence of excessive gestational weight gain is associated with distinct changes in DNA methylation patterns in umbilical cords of infants [abstract]. The FASEB Journal. 28(1 Supplement):271.1. Interpretive Summary:
Technical Abstract: Maternal obesity has been hypothesized to lead to developmental programming of excessive weight and adiposity in offspring. In addition, excessive gestational weight gain (GWG) is also a demonstrated determinant of later-life adiposity. We examined genome-wide DNA methylation (Infinium® HumanMethylation450K BeadChip) in umbilical cords (UC) from lean (Ln, BMI<25) and overweight/obese women (OB, BMI=25) who gained weight within Institute of Medicine guidelines to specifically identify the epigenetic influence of maternal obesity. Offspring birth weight and infant adiposity at 2 wk did not differ between groups. Multivariable linear regression analysis of CpG methylation against maternal fat mass at 12 wk while controlling for maternal age, mode of delivery, infant birth-weight and sex identified 1,269 CpG sites whose methylation status was associated with maternal adiposity (p<0.05). Of these, 54% sites were located in 5'-UTR and proximal promoter (-1500 bp) regions. Gene ontology analysis identified processes related to fat cell differentiation to be hypomethylated and processes related to RNA stability to be hypermethylated in OB compared to Ln UCs. Our data suggest that maternal adiposity in the absence of excessive GWG is associated with epigenetic modifications of fetal tissue that may contribute to the development of obesity in offspring.