ArticleEpigenetics2015
Mendelian randomization supports causality between maternal hyperglycemia and epigenetic regulation of leptin gene in newborns.
Article in Epigenetics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers, 5 of them syntheses that pooled it.
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The trial behind it
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Who cites it
68 citing papers in PubMed, 5 syntheses or guidelines pooled it, 137 citations in OpenAlex.
- Epigenetic Mechanisms in Childhood Obesity.Annals of the New York Academy of Sciences · 2025Pooled it
- Methodological approaches, challenges, and opportunities in the application of Mendelian randomisation to lifecourse epidemiology: A systematic literature review.European journal of epidemiology · 2024Pooled it
- Prenatal medication exposure and epigenetic outcomes: a systematic literature review and recommendations for prenatal pharmacoepigenetic studies.Epigenetics · 2022Pooled it
- Mendelian randomisation approaches to the study of prenatal exposures: A systematic review.Paediatric and perinatal epidemiology · 2021Pooled it
- Mendelian Randomization and the Environmental Epigenetics of Health: a Systematic Review.Current environmental health reports · 2019Pooled it
- Trial
- Interactions between nutrition and the epigenome: how can it be harnessed for public health?Future science OA · 2026Article
- Epigenetics and childhood obesity: DNA methylation coordinates environment and gene regulation.Endocrine reviews · 2026Review
- Maternal obesity and the metabolic syndrome in reproductive health: assessing incretin-based interventions.Reviews in endocrine & metabolic disorders · 2026Review
- Epigenetic regulation in a high-sugar environment (Review).International journal of molecular medicine · 2026Review
- Clinical characteristics of pediatric attention deficit hyperactivity disorder patients born with low birth weight, small for gestational age, or preterm.Fukushima journal of medical science · 2026Article
- Epigenetic legacy of early-life undernutrition: methodological lessons from Dutch and Chinese famine studies.Frontiers in genetics · 2026Review
- Gestational Glucose Intolerance and Risk of Obesity in Childhood and Adolescence.The Journal of clinical endocrinology and metabolism · 2025Article
- Effects of perinatal variables on echocardiographic assessments of left ventricular dimensions in infants born large for gestational age: a prospective cohort analysis.Italian journal of pediatrics · 2025Article
- Exercise therapy for gestational diabetes mellitus: from basic to clinical.Frontiers in medicine · 2025Review
- Association of DNA Methylation with Infant Birth Weight in Women with Gestational Diabetes.Metabolites · 2024Review
- Cord blood DNA methylation of immune and lipid metabolism genes is associated with maternal triglycerides and child adiposity.Obesity (Silver Spring, Md.) · 2024Article
- Associations between nutrients in one-carbon metabolism and fetal DNA methylation in pregnancies with or without gestational diabetes mellitus.Clinical epigenetics · 2023Article
- Social Determinants of Health and Cerebral Small Vessel Disease: Is Epigenetics a Key Mediator?Journal of the American Heart Association · 2023Review
- Maternal glycemia in pregnancy is longitudinally associated with blood DNAm variation at the FSD1L gene from birth to 5 years of age.Clinical epigenetics · 2023Article
8 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 3 countries.
Funding
Abstract
Leptin is an adipokine that acts in the central nervous system and regulates energy balance. Animal models and human observational studies have suggested that leptin surge in the perinatal period has a critical role in programming long-term risk of obesity. In utero exposure to maternal hyperglycemia has been associated with increased risk of obesity later in life. Epigenetic mechanisms are suspected to be involved in fetal programming of long term metabolic diseases. We investigated whether DNA methylation levels near LEP locus mediate the relation between maternal glycemia and neonatal leptin levels using the 2-step epigenetic Mendelian randomization approach. We used data and samples from up to 485 mother-child dyads from Gen3G, a large prospective population-based cohort. First, we built a genetic risk score to capture maternal glycemia based on 10 known glycemic genetic variants (GRS10) and showed it was an adequate instrumental variable (β = 0.046 mmol/L of maternal fasting glucose per additional risk allele; SE = 0.007; P = 7.8 × 10(-11); N = 467). A higher GRS10 was associated with lower methylation levels at cg12083122 located near LEP (β = -0.072 unit per additional risk allele; SE = 0.04; P = 0.05; N = 166). Direction and effect size of association between the instrumental variable GRS10 and methylation at cg12083122 were consistent with the negative association we observed using measured maternal glycemia. Lower DNA methylation levels at cg12083122 were associated with higher cord blood leptin levels (β = -0.17 log of cord blood leptin per unit; SE = 0.07; P = 0.01; N = 170). Our study supports that maternal glycemia is part of causal pathways influencing offspring leptin epigenetic regulation.
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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.