DNA methylation profiles in diabetic embryos

2025 · doi:10.1101/2025.10.17.683187
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This study examined whether maternal diabetes alters global DNA methylation patterns in mouse embryos and whether such epigenetic changes affect neural tube closure–related genes. Using nondiabetic and diabetic embryo groups, the authors found no significant difference in the overall distribution of DNA methylation levels, but observed lower methylation at differentially methylated CpGs near transcription start sites, gene bodies, and transcription end sites in diabetic embryos, with increased methylation in CpG islands. Maternal diabetes also caused differential methylation of CpGs in promoter and gene body regions of genes including Sphk1, Twist1, and Shroom3, and altered expression of three genes. The paper relates DNA methylation to neural tube defect mechanisms induced by maternal diabetes but does not explicitly discuss endometriosis or adenomyosis; it was included in the corpus via a keyword match in the upstream search index.

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Abstract

Maternal diabetes leads to neural tube defects (NTDs) in offspring. DNA methylation could be associated with NTDs induced by maternal diabetes. This study investigated whether maternal diabetes disturbs global DNA methylation of the embryos and possible influence on neural tube closure related genes. Our study showed that there was no significant difference in the overall distribution of DNA methylation levels between nondiabetic and diabetic embryos. The methylation levels of differentially methylated CpGs (dmCpGs) around transcription start sites, gene body and transcription end sites were higher in nondiabetic embryos than that in diabetic embryos. However, there was an increased methylation level of dmCpGs in CpG islands in diabetic embryos compared to that of nondiabetic embryos. Meanwhile, maternal diabetes significantly resulted in differential methylation of CpGs in promoter and gene bodies region of genes such as Sphingosine kinase-1 (Sphk1), twist basic helix-loop-helix transcription factor 1 (Twist1) and shroom family member 3 (Shroom3) and gene expression levels of three genes were altered by maternal diabetes. This study demonstrates that changes of DNA methylation in diabetic embryos led to aberrant expression of genes that may be involved in the pathophysiology of NTDs induced by maternal diabetes.
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Abstract Maternal diabetes leads to neural tube defects (NTDs) in offspring. DNA methylation could be associated with NTDs induced by maternal diabetes. This study investigated whether maternal diabetes disturbs global DNA methylation of the embryos and possible influence on neural tube closure related genes. Our study showed that there was no significant difference in the overall distribution of DNA methylation levels between nondiabetic and diabetic embryos. The methylation levels of differentially methylated CpGs (dmCpGs) around transcription start sites, gene body and transcription end sites were higher in nondiabetic embryos than that in diabetic embryos. However, there was an increased methylation level of dmCpGs in CpG islands in diabetic embryos compared to that of nondiabetic embryos. Meanwhile, maternal diabetes significantly resulted in differential methylation of CpGs in promoter and gene bodies region of genes such as Sphingosine kinase-1 (Sphk1), twist basic helix-loop-helix transcription factor 1 (Twist1) and shroom family member 3 (Shroom3) and gene expression levels of three genes were altered by maternal diabetes. This study demonstrates that changes of DNA methylation in diabetic embryos led to aberrant expression of genes that may be involved in the pathophysiology of NTDs induced by maternal diabetes. Competing Interest Statement The authors have declared no competing interest.

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