ArticleMolecular endocrinology (Baltimore, Md.)2009
Maternal diabetes causes mitochondrial dysfunction and meiotic defects in murine oocytes.
Article in Molecular endocrinology (Baltimore, Md.), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 99 papers.
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Who cites it
99 citing papers in PubMed, 245 citations in OpenAlex.
- Associations between free fatty acids, cumulus oocyte complex morphology and ovarian function during in vitro fertilization.Fertility and sterility · 2011Trial
- Heterogeneity in secondary follicle development buffers the lifespan of activated oocytes to optimize female fertility in mice.Nature aging · 2026Article
- Inositol and Berberine Synergistically Reprogram Endocrine and Ovarian Metabolism in Polycystic Ovary Syndrome.Cell proliferation · 2026Article
- Moderate NEFA reprogram early follicular development and oocyte competence: evidence for a targetable redox mechanism.Frontiers in nutrition · 2026Article
- The role of metabolic reprogramming in oocyte development: research progress and prospects.Frontiers in reproductive health · 2026Review
- PINK1 functions in mitophagy and mitochondrial homeostasis during mice oocyte maturation.Cell & bioscience · 2025Article
- The potential protective effects of curcumin on the diabetic ovary: Experimental and molecular approaches.Histology and histopathology · 2025Review
- Nicotinamide riboside supplementation protects against maternal diabetes-associated decline in oocyte quality.Reproduction (Cambridge, England) · 2025Article
- The Importance of Mitochondrial Processes in the Maturation and Acquisition of Competences of Oocytes and Embryo Culture.International journal of molecular sciences · 2025Review
- Investigating developmental characteristics of biopsied blastocysts stratified by mitochondrial copy numbers using time-lapse monitoring.Reproductive biology and endocrinology : RB&E · 2024Article
- Embryos from Prepubertal Hyperglycemic Female Mice Respond Differentially to Oxygen Tension In Vitro.Cells · 2024Article
- Article
- Risks of using mitoquinone during in vitro maturation and its potential protective effects against lipotoxicity-induced oocyte mitochondrial stress.Journal of assisted reproduction and genetics · 2024Article
- Article
- Association of Mitochondrial Variants with the Joint Occurrence of Polycystic Ovary Syndrome and Hashimoto's Thyroiditis.Antioxidants (Basel, Switzerland) · 2023Article
- Human follicular fluid elicits select dose- and age-dependent effects on mouse oocytes and cumulus-oocyte complexes in a heterologous in vitro maturation assay.Molecular human reproduction · 2023Article
- Review
- Polycystic Ovary Syndrome and Oxidative Stress-From Bench to Bedside.International journal of molecular sciences · 2023Review
- Effects of adverse fertility-related factors on mitochondrial DNA in the oocyte: a comprehensive review.Reproductive biology and endocrinology : RB&E · 2023Review
- Coenzyme Q10 Stimulate Reproductive Vatality.Drug design, development and therapy · 2023Review
39 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
The adverse effects of maternal diabetes on embryo development and pregnancy outcomes have recently been shown to occur as early as the one-cell zygote stage. The hypothesis of this study was that maternally inherited mitochondria in oocytes from diabetic mice are abnormal and thus responsible in part for this latency of developmental compromise. In ovulated oocytes from diabetic mice, transmission electron microscopy revealed an alteration in mitochondrial ultrastructure, and the quantitative analysis of mitochondrial DNA copy number demonstrated an increase. The levels of ATP and tricarboxylic acid cycle metabolites in diabetic oocytes were markedly reduced compared with controls, suggesting a mitochondrial metabolic dysfunction. Abnormal distribution of mitochondria within maturing oocytes also was seen in diabetic mice. Furthermore, oocytes from diabetic mice displayed a higher frequency of spindle defects and chromosome misalignment in meiosis, resulting in increased aneuploidy rates in ovulated oocytes. Collectively, our results suggest that maternal diabetes results in oocyte defects that are transmitted to the fetus by two routes: first, meiotic spindle and chromatin defects result in nondisjunction leading to embryonic aneuploidy; second, structural and functional abnormalities of oocyte mitochondria, through maternal transmission, provide the embryo with a dysfunctional complement of mitochondria that may be propagated during embryogenesis.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.