Diana L Juvinao-Quintero1, Andres Cardenas2, Patrice Perron3,4, Luigi Bouchard3,5,6, Sharon M Lutz1,7, Marie-France Hivert1,4,8. 1. Division of Chronic Disease Research Across the Life Course, Department of Population Medicine, Harvard Pilgrim Health Care Institute, Harvard Medical School, Boston, MA 02215, USA. 2. Division of Environmental Health Sciences, School of Public Health & Center for Computational Biology, University of California, Berkeley, CA 94720-7360, USA. 3. Centre de Recherche du Centre Hospitalier Universitaire de Sherbrooke, Sherbrooke, QC, J1H 5N4, Canada. 4. Department of Medicine, Université de Sherbrooke, Sherbrooke, QC, J1H 5N4, Canada. 5. Department of Medical Biology, Centre Intégré Universitaire en Santé et Services Sociaux Saguenay-Lac-Saint-Jean, Hôpital Universitaire de Chicoutimi, Saguenay, QC, G7H 5H6, Canada. 6. Department of Biochemistry & Functional Genomics, Université de Sherbrooke, Sherbrooke, QC, J1K 2R1, Canada. 7. Department of Biostatistics, Harvard TH Chan School of Public Health, Boston, MA 02215, USA. 8. Diabetes Unit, Massachusetts General Hospital, Boston, MA 02114, USA.
Abstract
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.
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.
Entities:
Keywords:
DNA methylation; cord blood; insulinemia; maternal glycemia; oral glucose tolerance test; pregnancy; principal component analysis
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