Journal
AMERICAN JOURNAL OF OBSTETRICS AND GYNECOLOGY
Volume 211, Issue 6, Pages -Publisher
MOSBY-ELSEVIER
DOI: 10.1016/j.ajog.2014.06.037
Keywords
DNA methylation; gestational diabetes mellitus; leptin; maternal obesity; placenta
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Funding
- National Institutes of Health (NIH) (NIH-National Institute of Mental Health) [R01MH094609]
- National Institutes of Health (NIH) (NIH-National Institute of Environmental Health Sciences) [R01ES022223, P01 ES022832]
- National Institutes of Health (NIH) (US Environmental Protection Agency) [RD83544201]
- National Institutes of Health (NIH) (NIH-National Cancer Institute) [P30CA23108]
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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 (beta = 1.89, P = .04), as did those demonstrating prepregnancy obesity (beta = 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 (beta = 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.
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