ArticleClinical epigenetics2023
Impact of intrauterine exposure to maternal diabetes on preterm birth: fetal DNA methylation alteration is an important mediator.
Article in Clinical epigenetics, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 8 citations in OpenAlex.
- Intrauterine exposure to maternal diabetes and the risk of developing epilepsy in children: a national cohort study of 2.3 million children.BMC medicine · 2026Article
- Identifying epigenetic and microbial biomarkers for preterm birth using DNA methylation and gut microbiome data.Frontiers in cellular and infection microbiology · 2026Article
- In-utero exposure to maternal diabetes and DNA methylation alterations in the Next Generation birth cohort.Clinical epigenetics · 2025Article
- Extracellular Vesicles Alter Trophoblast Function in Pregnancies Complicated by COVID-19.Journal of extracellular vesicles · 2025Article
- The Hidden Impact of Gestational Diabetes: Unveiling Offspring Complications and Long-Term Effects.Life (Basel, Switzerland) · 2025Review
- Early life epigenetics and childhood outcomes: a scoping review.Pediatric research · 2025Article
- Genomics and multiomics in the age of precision medicine.Pediatric research · 2025Review
- Gestational diabetes complicated with preterm birth: a retrospective cohort study.BMC pregnancy and childbirth · 2024Article
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Authors and funding
8 authors at 5 institutions in 1 country.
Funding
Abstract
backgroundIn utero exposure to diabetes has been shown to contribute to preterm birth, though the underlying biological mechanisms are yet to be fully elucidated. Fetal epigenetic variations established in utero may be a possible pathway. This study aimed to investigate whether in utero exposure to diabetes was associated with a change in newborn DNA methylation, and whether the identified CpG sites mediate the association between diabetes and preterm birth in a racially diverse birth cohort population.
methodsThis study included 954 mother-newborn pairs. Methylation levels in the cord blood were determined using the Illumina Infinium MethylationEPIC BeadChip 850 K array platform. In utero exposure to diabetes was defined by the presence of maternal pregestational or gestational diabetes. Preterm birth was defined as gestational age at birth less than 37 weeks. Linear regression analysis was employed to identify differentially methylated CpG sites. Differentially methylated regions were identified using the DMRcate Package.
results126 (13%) newborns were born to mothers with diabetes in pregnancy and 173 (18%) newborns were born preterm, while 41 newborns were born both preterm and to mothers with diabetes in pregnancy. Genomic-wide CpG analysis found that eighteen CpG sites in cord blood were differentially methylated by maternal diabetes status at an FDR threshold of 5%. These significant CpG sites were mapped to 12 known genes, one of which was annotated to gene Major Histocompatibility Complex, Class II, DM Beta (HLA-DMB). Consistently, one of the two identified significant methylated regions overlapped with HLA-DMB. The identified differentially methylated CpG sites mediated the association between diabetes in pregnancy and preterm birth by 61%.
conclusionsIn this US birth cohort, we found that maternal diabetes was associated with altered fetal DNA methylation patterns, which substantially explained the link between diabetes and preterm birth.
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