Placenta DNA Methylation Adaptation to Maternal Glucose Tolerance in Pregnancy

Andres Cardenas, Valerie Gagné-Ouellet, Catherine Allard, Diane Brisson, Patrice Perron, Luigi Bouchard and Marie-France Hivert

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Received: 10th November 17

Maternal hyperglycemia during pregnancy is associated with excess fetal growth and adverse perinatal and developmental outcomes. Placental epigenetic maladaptation may underlie these associations. We performed an epigenome-wide association study of term placentas and prenatal maternal glucose response 2-hour post oral glucose challenge at 24-30 weeks of gestation among 448 mother-infant pairs. Maternal glucose post-load was strongly associated with lower DNA methylation of 4 CpGs (FDR q<0.05) within the Phosphodiesterase 4B gene (PDE4B). Additionally, three other CpGs were differentially methylated relative to maternal glucose response within the TNFRSF1B; LDLR; and BLM genes (FDR q<0.05). DNA methylation correlated with expression of these genes in placental tissue for CpG sites in PDE4B (rs: 0.26-0.35, P<0.01), LDLR (rs: 0.22, P=0.03) and TNFRSF1B (rs: -0.25, P=0.01). Our study provides evidence that maternal glucose response during pregnancy is associated with placental DNA methylation of genes whose expression levels are partially under epigenetic control.

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This is an abstract of a preprint hosted on an independent third party site. It has not been peer reviewed but is currently under consideration at Nature Communications.

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