Maternal obesity and gestational diabetes are associated with placental leptin DNA methylation

Objective In this study, we aimed to investigate relationships between maternal prepregnancy obesity and gestational diabetes mellitus and placental leptin DNA methylation. Study Design This study comprises data on 535 mother-infant dyads enrolled in the Rhode Island Child Health Study, a prospectiv...

Full description

Saved in:
Bibliographic Details
Published in:American journal of obstetrics and gynecology 2014-12, Vol.211 (6), p.654.e1-654.e9
Main Authors: Lesseur, Corina, MD, PhD, Armstrong, David A., MS, Paquette, Alison G., BS, Li, Zhigang, PhD, Padbury, James F., MD, Marsit, Carmen J., PhD
Format: Article
Language:English
Subjects:
Adult
Body Mass Index
Cohort Studies
Diabetes, Gestational - genetics
DNA methylation
DNA Methylation - genetics
Female
gestational diabetes mellitus
Humans
Infant, Newborn
leptin
Leptin - genetics
Linear Models
Logistic Models
Male
maternal obesity
Multivariate Analysis
Obesity - genetics
Obstetrics and Gynecology
placenta
Placenta - metabolism
Pregnancy
Pregnancy Complications - genetics
Promoter Regions, Genetic - genetics
Prospective Studies
Young Adult
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Objective In this study, we aimed to investigate relationships between maternal prepregnancy obesity and gestational diabetes mellitus and placental leptin DNA methylation. Study Design This study comprises data on 535 mother-infant dyads enrolled in the Rhode Island Child Health Study, a prospective cohort study of healthy term pregnancies. Prepregnancy body mass index was calculated from self-reported anthropometric measures and gestational diabetes mellitus diagnoses gathered from inpatient medical records. DNA methylation of the leptin promoter region was assessed in placental tissue collected at birth using quantitative bisulfite pyrosequencing. Results In a multivariable regression analysis adjusted for confounders, infants exposed to gestational diabetes mellitus had higher placental leptin methylation (β = 1.89, P  = .04), as did those demonstrating prepregnancy obesity (β = 1.17, P  = .06). Using a structural equations model, we observed that gestational diabetes mellitus is a mediator of the effects of prepregnancy obesity on placental leptin DNA methylation (β = 0.81, 95% confidence interval, 0.27–2.71). Conclusion Our results suggest that the maternal metabolic status before and during pregnancy can alter placental DNA methylation profile at birth and potentially contribute to metabolic programming of obesity and related conditions.
ISSN:0002-9378
1097-6868
DOI:10.1016/j.ajog.2014.06.037