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. 2014 Dec;211(6):654.e1-9.
doi: 10.1016/j.ajog.2014.06.037. Epub 2014 Jun 19.

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

Affiliations

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

Corina Lesseur et al. Am J Obstet Gynecol. 2014 Dec.

Abstract

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.

Keywords: DNA methylation; gestational diabetes mellitus; leptin; maternal obesity; placenta.

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Conflict of interest statement

The authors have no conflicts of interest to declare.

Figures

Figure 1
Figure 1
Structural equation model relating maternal prepregnancy obesity to placental LEP DNA methylation through gestational diabetes in RICHS participants (n=473). Model is adjusted for variables in the figure, birth weight group and maternal age (continuous). Odds ratios (OR) are provided from logistic regression when the outcome (in this case gestational diabetes) was dichotomous, and the betas provided individual paths are standardized partial regression coefficients that can be interpreted similar to betas for linear regression.

References

    1. Simmons D. Diabetes and obesity in pregnancy. Best Practice & Research Clinical Obstetrics & Gynaecology. 2011;25:25–36. - PubMed
    1. Gluckman PD, Hanson MA, Pinal C. The developmental origins of adult disease. Maternal & child nutrition. 2005;1:130–141. - PMC - PubMed
    1. Zambrano E, Nathanielsz PW. Mechanisms by which maternal obesity programs offspring for obesity: evidence from animal studies. Nutrition reviews. 2013;71:S42–S54. - PubMed
    1. Waterland RA, Michels KB. Epigenetic epidemiology of the developmental origins hypothesis. Annu Rev Nutr. 2007;27:363–388. - PubMed
    1. Jaenisch R, Bird A. Epigenetic regulation of gene expression: how the genome integrates intrinsic and environmental signals. Nature genetics. 2003;33:245–254. - PubMed

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