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
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.
Read in full at bioRxiv.
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 It has not been peer reviewed but is currently under consideration at Nature Communications.