ArticleDiabetic medicine : a journal of the British Diabetic Association2022
Gestational diabetes mellitus, epigenetic age and offspring metabolism.
Article in Diabetic medicine : a journal of the British Diabetic Association, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 14 citations in OpenAlex.
- Association of prenatal glycemic marker cumulative exposure with placental DNA methylation change.The Journal of clinical endocrinology and metabolism · 2026Article
- Placental epigenetic age and adolescent blood pressure: the Extremely Low Gestational Age Newborn cohort.Pediatric research · 2025Article
- Gestational diabetes mellitus causes genome hyper-methylation of oocyte via increased EZH2.Nature communications · 2025Article
- Severe drought exposure in utero associates to children's epigenetic age acceleration in a global climate change hot spot.Nature communications · 2024Article
- Epigenetic age acceleration is associated with speed of pubertal growth but not age of pubertal onset.Scientific reports · 2024Article
- Predictive value of ultrasonic artificial intelligence in placental characteristics of early pregnancy for gestational diabetes mellitus.Frontiers in endocrinology · 2024Article
- Maternal Hyperglycemia in Pregnancy and Offspring Internalizing and Externalizing Behaviors.Maternal and child health journal · 2023Article
- Epigenetic Age Acceleration in Mothers and Offspring 4-10 Years after a Pregnancy Complicated by Gestational Diabetes and Obesity.Metabolites · 2022Article
- Gestational diabetes mellitus, epigenetic age and offspring metabolism.Diabetic medicine : a journal of the British Diabetic Association · 2022Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
aimsNo reports examine the relationship between in-utero exposure to gestational diabetes mellitus (GDM), offspring epigenetic age acceleration (EAA), and offspring insulin sensitivity.
methodsUsing data from a cohort study, we examined associations between GDM in-utero exposure and offspring EAA at approximately 10 years of age, using separate regression models adjusting for offspring chronological age and sex. We also examined associations between EAA with updated homeostasis model assessment of insulin sensitivity and secretion (HOMA2-S and HOMA2-β) measured at approximately 10 and 16 years of age, using mixed linear regression models accounting for repeated measures after adjustment for offspring chronological age and sex.
resultsCompared to unexposed offspring (n = 91), offspring exposed to GDM (n = 88) had greater EAA or older extrinsic age compared to chronological age (β-coefficient 2.00, 95% confidence interval [0.71, 3.28], p = 0.0025), but not greater intrinsic EAA (β-coefficient -0.07, 95% CI [-0.71, 0.57], p = 0.93). Extrinsic EAA was associated with lower insulin sensitivity (β-coefficient -0.018, 95% CI [-0.035, -0.002], p = 0.03) and greater insulin secretion (β-coefficient 0.018, 95% CI [0.006, 0.03], p = 0.003), and these associations persisted after further adjustment for measures of maternal and child adiposity. No associations were observed between intrinsic EAA and insulin sensitivity and secretion, before or after adjustment for measures of maternal and child adiposity.
conclusionsIn this study, children exposed to GDM experience greater extrinsic EAA, which is associated with lower insulin sensitivity and greater insulin secretion. Further studies are needed to determine the directionality of these associations.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.