In-utero exposure to maternal diabetes and DNA methylation alterations in the Next Generation birth cohort
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View abstract on PubMed
Summary
This summary is machine-generated.Maternal diabetes during pregnancy alters offspring DNA methylation (DNAm). The timing of exposure, whether pregestational type 2 diabetes (T2D) or gestational diabetes mellitus (GDM), results in distinct DNAm patterns, potentially influencing T2D risk in youth.
Area Of Science
- Epigenetics
- Developmental Biology
- Endocrinology
Background
- Rising incidence of youth-onset type 2 diabetes (T2D).
- In-utero exposure to maternal diabetes is a risk factor for offspring T2D.
- Higher risk associated with pregestational T2D compared to gestational diabetes mellitus (GDM).
Purpose Of The Study
- Investigate epigenome-wide DNA methylation (DNAm) alterations.
- Determine if timing of prenatal diabetes exposure differentially alters DNAm.
- Hypothesize differential risk is reflected in DNAm changes due to timing of exposure.
Main Methods
- Epigenome-wide analysis of cord blood DNAm.
- Study included newborns exposed to pregestational T2D (n=99), GDM (n=70), and controls (n=41).
- Statistical models adjusted for covariates including sex, maternal age, BMI, and cell type proportions.
Main Results
- Identified differentially methylated sites and regions associated with GDM and T2D exposure.
- Found common and distinct DNAm patterns between GDM and T2D exposures.
- Identified specific CpG sites in PTPRN2 associated with T2D risk and previously linked to youth T2D.
Conclusions
- In-utero maternal diabetes exposure is linked to offspring DNAm alterations.
- Timing of maternal diabetes exposure (GDM vs. T2D) yields distinct DNAm signatures.
- Identified potential early-life biomarkers for exposure and T2D risk in offspring.
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