ArticleMolecular medicine reports2017
Maternal diabetes impairs the initiation of meiosis in murine female germ cells.
Article in Molecular medicine reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Intrauterine hyperglycemia impairs mouse primordial germ cell development and fertility by sex-specific epigenetic reprogramming interference.Cell discovery · 2025Article
- A visualized and quercetin-optimized three-dimensional culture model of mouse ovaries derived from fetal gonads.Acta biochimica et biophysica Sinica · 2025Article
- Long-term outcomes and potential mechanisms of offspring exposed to intrauterine hyperglycemia.Frontiers in nutrition · 2023Review
- Article
- Looking at the Future Through the Mother's Womb: Gestational Diabetes and Offspring Fertility.Endocrinology · 2021Review
- Maternal aerobic running during mid or late gestation improves the quality of oogenesis and folliculogenesis in the ovary of neonatal rats: An experimental study.International journal of reproductive biomedicine · 2021Article
- Pregnancy environment, and not preconception, leads to fetal growth restriction and congenital abnormalities associated with diabetes.Scientific reports · 2020Article
- Factors influencing establishment of the ovarian reserve and their effects on fertility.Animal reproductionArticle
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11 authors.
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Abstract
Gestational diabetes mellitus (GDM) is characterized by an initial diagnosis of glucose intolerance during pregnancy. There is increasing evidence supporting the association between GDM and the inhibited development of several organs in offspring. In the present study, a murine GDM model was established in mice by intraperitoneal injection of streptozotocin to evaluate the effect of maternal diabetes on the initiation of meiosis in female germ cells of offspring. The effect of GDM on the initiation of meiosis in the offspring was evaluated by reverse transcription-quantitative polymerase chain reaction, flow cytometry and hematoxylin and eosin staining. The results showed that, compared with the control group, fetal ovary growth was inhibited, the expression levels of meiosis‑specific genes, stimulated by retinoic acid gene 8, synaptonemal complex protein, and DNA meiotic recombinase were inhibited, and the number of primordial/primary follicles was reduced in the GDM group. These may have been induced by an increase of apoptosis and inhibition of growth, as the mRNA levels of p21, a vital G1 cell cycle inhibitor, and apoptotic genes were upregulated, whereas the expression levels of genes important in folliculogenesis were decreased in the GDM group. In conclusion, the data obtained in the present study suggested that maternal diabetes may impair the initiation of meiosis and ovarian growth via growth inhibition, cell cycle arrest and the induction of apoptosis.
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