ArticleNature communications2025
Gestational diabetes mellitus causes genome hyper-methylation of oocyte via increased EZH2.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Article
- Integrated metabolomic and proteomic analyses reveal global reprogramming of oocyte metabolism following AFB1 exposure.Cell communication and signaling : CCS · 2026Article
- Obesity-Associated Gestational Diabetes Promotes Cellular Heterogeneity and Dysfunction in Neonatal Offspring-Islets.Nutrients · 2026Article
- Epigenetic editing of marine medaka (Zoological research · 2026Article
- How Early-Life Programming During Embryogenesis Imprints Cellular Memory.International journal of molecular sciences · 2025Review
- Intrauterine hyperglycemia impairs mouse primordial germ cell development and fertility by sex-specific epigenetic reprogramming interference.Cell discovery · 2025Article
- Review
- Modes of action of traditional Chinese medicine for diabetic infertility: from molecular pathways to clinical evidence.American journal of clinical and experimental immunology · 2025Review
- Liquid-liquid phase separation in gastric cancer: identifying novel biomarkers and therapeutic targets through gene signature analysis.Frontiers in immunology · 2025Article
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Authors and funding
18 authors.
Funding
Abstract
Gestational diabetes mellitus (GDM), a common pregnancy disease, has long-term negative effects on offspring health. Epigenetic changes may have important contributions to that, but the underlying mechanisms are not well understood. Here, we report the influence of GDM on DNA methylation of offspring (GDF1) oocytes and the possible mechanisms. Our results show that GDM induces genomic hyper-methylation of offspring oocytes, and at least a part of the altered methylation is inherited by F2 oocytes, which may be a reason for the inheritance of metabolic disorders. We further find that GDM exposure increases the expression of Ezh2 in oocytes. Ezh2 regulates DNA methylation via DNMT1, and Ezh2 knockdown reduces the genomic methylation level of GDF1 oocytes. These results suggest that GDM may induce oocyte genomic hyper-methylation of offspring via enhancing the Ezh2 expression recruiting more DNMT1 into nucleus.
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