Open AccessAssociations between an integrated component of maternal glycemic regulation in pregnancy and cord blood DNA methylation
Author(s) -
Diana L. Juvinao-Quintero,
Andrés Cárdenas,
Patrice Perron,
Luigi Bouchard,
Sharon M. Lutz,
MarieFrance Hivert
Publication year - 2021
Publication title -
epigenomics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.265
H-Index - 60
eISSN - 1750-1911
pISSN - 1750-192X
DOI - 10.2217/epi-2021-0220
Subject(s) - dnam , dna methylation , txnip , pregnancy , cord blood , biology , epigenetics , gestational diabetes , placenta , endocrinology , medicine , glycemic , insulin , fetus , gestation , immunology , genetics , gene expression , gene , oxidative stress , thioredoxin
Background: Previous studies suggest that fetal programming to hyperglycemia in pregnancy is due to modulation of DNA methylation (DNAm), but they have been limited in their maternal glycemic characterization. Methods: In the Gen3G study, we used a principal component analysis to integrate multiple glucose and insulin values measured during the second trimester oral glucose tolerance test. We investigated associations between principal components and cord blood DNAm levels in an epigenome-wide analysis among 430 mother-child pairs. Results: The first principal component was robustly associated with lower DNAm at cg26974062 ( TXNIP ; p = 9.9 × 10 -9 ) in cord blood. TXNIP is a well-known DNAm marker for type 2 diabetes in adults. Conclusion: We hypothesize that abnormal glucose metabolism in pregnancy may program dysregulation of TXNIP across the life course.