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Panoramic Elucidation of the Molecular Mechanisms Underpinning the Epigenetic Impact of Gestational Diabetes Mellitus on Offspring

ABSTRACT: Background: Gestational diabetes mellitus (GDM), a common pregnancy complication with profound effects on maternal and offspring health, involves epigenetic modifications, particularly DNA methylation, but the molecular mechanisms elevating metabolic disease risk in offspring remain elusive. Methods: Integrating public data with whole-genome methylation data from umbilical cord blood of GDM fetuses as the validation cohort, this study characterizes GDM-associated epigenetic features and develops a predictive model validated across external datasets to assess potential long-term health risks in offspring. Results:We identified consistent patterns of differential methylation in the offspring of GDM, with key DMPs associated with glucose homeostasis and insulin sensitivity genes. Pathway analysis revealed enrichment in insulin signaling, AMPK activation, and adipocytokine signaling pathways. Our predictive model demonstrated robust performance across different sample sizes (AUC=0.89 in public data, AUC=0.82 in validation cohort). CpG sites associated with PPARG and INS genes showed persistent predictive significance across datasets. Conclusions:This study provides a comprehensive characterization of the epigenetic landscape in the offspring of GDM, revealing consistent methylation patterns and pathway enrichments across diverse datasets. The developed predictive model holds potential for assessing health risks of GDM in offspring, advancing understanding of GDM pathophysiology and offering epigenetic biomarkers for future diagnostic, therapeutic, and preventive strategies.

ORGANISM(S): Homo sapiens

PROVIDER: GSE284448 | GEO | 2025/05/07

REPOSITORIES: GEO

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Project description:Chronic injury in kidney transplants remains a major cause of graft loss. The aim of this study was to identify a predictive gene set capable of classifying renal grafts at risk for progressive injury due to fibrosis.The Genomics of Chronic Allograft Rejection (GoCAR) study is a prospective, multicenter study. Biopsies obtained prospectively 3 months after transplantation from renal allograft recipients (n=159) with stable renal function were analyzed for gene expression by microarray. Genes were sought which correlated with subsequent 12-month Chronic Allograft Damage Index (CADI) but neither CADI in the 3 month biopsy nor other histological or clinical parameters. We identified a set of 13 genes that was independently predictive for the development of fi brosis at 1 year (ie, CADI-12 >=2). The gene set had high predictive capacity (area under the curve [AUC] 0·967), which was superior to that of baseline clinical variables (AUC 0·706) and clinical and pathological variables (AUC 0·806). Furthermore routine pathological variables were unable to identify which histologically normal allografts would progress to fi brosis (AUC 0·754), whereas the predictive gene set accurately discriminated between transplants at high and low risk of progression (AUC 0·916). The 13 genes also accurately predicted early allograft loss (AUC 0·842 at 2 years and 0·844 at 3 years). We validated the predictive value of this gene set in an independent cohort from the GoCAR study (n=45, AUC 0·866) and two independent, publically available expression datasets (n=282, AUC 0·831 and n=24, AUC 0·972). Biopsies obtained prospectively 3 months after transplantation from renal allograft recipients (n=159) with stable renal function were analyzed for gene expression by Affymetrix exon arrays. Genes that were specifically correlated with 12-month Chronic Allograft Damage Index (CADI) but neither CADI in the 3 month biopsy nor other histological or clinical parameters were identified by correlation analysis. The minimal geneset was further identified to predict the progressors/non progressors and validated by qPCR in an independent cohort and two public datasets. This dataset is part of the TransQST collection.

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Panoramic Elucidation of the Molecular Mechanisms Underpinning the Epigenetic Impact of Gestational Diabetes Mellitus on Offspring

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