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Placenta DNA Methylation Adaptation to Maternal Glucose Tolerance in Pregnancy

View ORCID ProfileAndres Cardenas, Valerie Gagné-Ouellet, Catherine Allard, Diane Brisson, Patrice Perron, Luigi Bouchard, Marie-France Hivert
doi: https://doi.org/10.1101/224139
Andres Cardenas
1Division of Chronic Disease Research Across the Lifecourse, Department of Population Medicine, Harvard Medical School and Harvard Pilgrim Health Care Institute, Boston, MA, USA;
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  • ORCID record for Andres Cardenas
Valerie Gagné-Ouellet
2Centre de Recherche du Centre Hospitalier Universitaire de Sherbrooke, Sherbrooke, Quebec, Canada;
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Catherine Allard
2Centre de Recherche du Centre Hospitalier Universitaire de Sherbrooke, Sherbrooke, Quebec, Canada;
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Diane Brisson
3Lipidology Unit, Community Genomic Medicine Centre and ECOGENE-21, Department of Medicine, Université de Montréal, Saguenay, QC, Canada;
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Patrice Perron
2Centre de Recherche du Centre Hospitalier Universitaire de Sherbrooke, Sherbrooke, Quebec, Canada;
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Luigi Bouchard
2Centre de Recherche du Centre Hospitalier Universitaire de Sherbrooke, Sherbrooke, Quebec, Canada;
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Marie-France Hivert
1Division of Chronic Disease Research Across the Lifecourse, Department of Population Medicine, Harvard Medical School and Harvard Pilgrim Health Care Institute, Boston, MA, USA;
2Centre de Recherche du Centre Hospitalier Universitaire de Sherbrooke, Sherbrooke, Quebec, Canada;
4Diabetes Unit, Massachusetts General Hospital, Boston, MA, USA
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  • For correspondence: MHIVERT@PARTNERS.ORG
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ABSTRACT

Maternal hyperglycemia during pregnancy is associated with 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 levels post-load were 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). Methylation levels correlated with expression in placental tissue for all 4 CpG sites in PDE4B (rs: 0.26–0.35, P<0.01), LDLR (rs: 0.22, P=0.03) and at TNFRSF1B (rs: -0.25, P=0.01). Our study provides evidence that maternal glucose response during pregnancy is associated with DNA methylation of genes within the placenta that are partially under epigenetic control.

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  • Competing financial interest: The authors declare no competing financial interests.

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The copyright holder for this preprint is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under a CC-BY-NC-ND 4.0 International license.
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Posted November 22, 2017.
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Placenta DNA Methylation Adaptation to Maternal Glucose Tolerance in Pregnancy
Andres Cardenas, Valerie Gagné-Ouellet, Catherine Allard, Diane Brisson, Patrice Perron, Luigi Bouchard, Marie-France Hivert
bioRxiv 224139; doi: https://doi.org/10.1101/224139
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Placenta DNA Methylation Adaptation to Maternal Glucose Tolerance in Pregnancy
Andres Cardenas, Valerie Gagné-Ouellet, Catherine Allard, Diane Brisson, Patrice Perron, Luigi Bouchard, Marie-France Hivert
bioRxiv 224139; doi: https://doi.org/10.1101/224139

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