Evidence map›Paper›PMID 41507059›Full record

ArticleThe Journal of clinical endocrinology and metabolism2026

Association of prenatal glycemic marker cumulative exposure with placental DNA methylation change.

Tesfa D Habtewold, Richard J Biedrzycki, Prabhavi Wijesiriwardhana, Nigus G Asefa, Fasil Tekola-Ayele

Abstract read
In one paragraph

Article in The Journal of clinical endocrinology and metabolism, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

2 citing papers in PubMed.

  1. Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors.

Tesfa D HabtewoldEpidemiology Branch, Division of Population Health Research, Division of Intramural Research, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD 20892, USA.ORCID 0000-0003-4476-518X
Richard J BiedrzyckiGlotech, Inc., Contractor for Division of Population Health Research, Division of Intramural Research, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD 20892, USA.
Prabhavi WijesiriwardhanaEpidemiology Branch, Division of Population Health Research, Division of Intramural Research, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD 20892, USA.
Nigus G AsefaLaboratory of Epidemiology and Population Sciences, National Institute on Aging, National Institutes of Health, Baltimore, MD 21224, USA.
Fasil Tekola-AyeleEpidemiology Branch, Division of Population Health Research, Division of Intramural Research, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD 20892, USA.ORCID 0000-0003-4194-9370

Funding

Eunice Kennedy Shriver National Institute of Child Health and Human DevelopmentNIDDK NIH HHSNIH HHS HHSN27500006NIH HHS HHSN27500008NIH HHS HHSN275200800002INIH HHS HHSN275200800003ICNIH HHS HHSN275200800012CNIH HHS HHSN275200800013CNIH HHS HHSN275200800014CNIH HHS HHSN275200800028CNIH HHS HHSN275201000009CNIMHD NIH HHS
6 · The paper itself

Abstract

backgroundMaternal glycemic dysregulation during pregnancy increases risk of pregnancy complications and long-term offspring health outcomes, potentially through DNA methylation alterations.

objectivesTo investigate the association between maternal glycemic marker concentration during pregnancy and placental DNA methylation, and to examine whether the methylation changes correlate with neonatal anthropometry.

methodsCumulative glycemic exposure was estimated using area under the curve for glucose (AUCgluc), insulin (AUCinsl), and glycated hemoglobin (AUCHbA1c), measured at 8-13, 16-22, 24-29, and 34-37 gestational weeks. Placental DNA methylation was measured using an Illumina array and tested for associations with AUCgluc, AUCHbA1c, and AUCinsl for all women and stratified by fetal sex. Correlations of the differentially methylated sites with neonatal anthropometry and placenta weight were also tested.

resultsFour sex-specific methylation associations were identified at FDR-adjusted P < .05. In women with male offspring, higher AUCgluc was associated with decreased methylation at cg23951198 (CBLN3 and KHNYN) and increased methylation at cg15608939 (NTN1), and higher AUCinsl was associated with decreased methylation at cg26529437 (ITGB8). In women with female offspring, higher AUCHbA1c associated with decreased methylation at cg05471842 (AMICA1). Higher methylation at the AUCgluc-associated cg15608939 in males and lower methylation at the AUCHbA1c-associated cg05471842 in females were correlated with increased birth weight, and lower methylation at the AUCgluc-associated cg23951198 in males was correlated with increased placental weight. Genes mapped to top CpGs were enriched for metabolic, immune, and inflammatory pathways and are linked to cardiometabolic diseases and traits.

conclusionIncreased glycemic marker exposure was associated with placental DNA methylation near genes enriched for inflammatory and cardiometabolic pathways. Placenta-mediated epigenetic mechanisms may link maternal glycemic dysregulation and offspring disease risk.

Indexed as

Blood GlucoseDiabetes, GestationalDNA MethylationPlacentaPrenatal Exposure Delayed EffectsAdultBiomarkersBirth WeightDevelopmental Origins of Health and DiseaseEpigenesis, GeneticFemaleGlycated HemoglobinHumansInfant, NewbornInsulinMaleBiomarkersBlood GlucoseGlycated HemoglobinInsulinblood glucose area under the curveglycemic markersmaternal hyperglycemiaplacental DNA methylationspregnancysex-specific

Identifiers

PMID41507059
PMCPMC13183445

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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.