4.5 Article

Global Methylation in the Placenta and Umbilical Cord Blood From Pregnancies With Maternal Gestational Diabetes, Preeclampsia, and Obesity

Journal

REPRODUCTIVE SCIENCES
Volume 21, Issue 1, Pages 131-137

Publisher

SAGE PUBLICATIONS INC
DOI: 10.1177/1933719113492206

Keywords

global methylation; fetal programming; placenta; umbilical cord blood; gestational diabetes mellitus; preeclampsia; obesity; birth outcomes

Funding

  1. National Institutes of Health (NIH) from NIMH [K01 MH080062]
  2. NCRR [P20 RR018728]
  3. Queens College
  4. CUNY Research Enhancement Grant
  5. Venture Capital Research Funding Program of the Mount Sinai Children's Environmental Health Center
  6. NATIONAL CENTER FOR RESEARCH RESOURCES [P20RR018728] Funding Source: NIH RePORTER
  7. NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES [P30ES023515] Funding Source: NIH RePORTER
  8. NATIONAL INSTITUTE OF MENTAL HEALTH [K01MH080062] Funding Source: NIH RePORTER

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Emerging evidence indicates that maternal medical risk during pregnancy, such as gestational diabetes mellitus (GDM), preeclampsia, and obesity, predisposes the offspring to suboptimal development. However, the underlying biological/epigenetic mechanism in utero is still unknown. The current pilot study (N = 50) compared the levels of global methylation in the placenta and umbilical cord blood among women with and without each risk condition (GDM, preeclampsia, and obesity) and explored whether the levels of global methylation were associated with fetal/infant growth. Results show that global methylation levels in the placenta were lower in patients with gestational diabetes (P = .003) and preeclampsia (P = .05) but higher with obesity (P = .01). Suggestive negative associations were found between global methylation level in the placenta and infant body length and head circumference. While preliminary, it is possible that the placenta tissue, but not umbilical cord blood, may be epigenetically programmed by maternal GDM, preeclampsia, and obesity to carry out its own specific functions that influence fetal growth.

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