Telomere Dysfunction in Oocytes and Embryos From Obese Mice.
Juan Ge1, Congyang Li1, Hongzheng Sun1
1State Key Laboratory of Reproductive Medicine, Suzhou Municipal Hospital, Nanjing Medical University, Nanjing, China.
Frontiers in Cell and Developmental Biology
|February 8, 2021
Summary
Maternal obesity causes telomere shortening in eggs and embryos, impacting fertility. This study reveals telomere dysfunction as a key pathway linking obesity to impaired reproductive outcomes.
Area of Science:
- Reproductive biology
- Molecular genetics
- Cellular aging
Background:
- Maternal obesity is linked to reduced oocyte and embryo quality.
- The underlying molecular mechanisms require further investigation.
Purpose of the Study:
- To investigate the impact of maternal obesity on telomere status in oocytes and early embryos.
- To explore telomere dysfunction as a potential molecular pathway in obesity-related reproductive impairment.
Main Methods:
- Utilized a high-fat diet (HFD) mouse model to induce maternal obesity.
- Assessed telomere length, telomerase reverse transcriptase expression, telomerase activity, and telomere dysfunction-induced foci (TIFs).
- Analyzed aneuploidy frequency and blastocyst apoptosis rates.
Main Results:
- Obese mice exhibited significant telomere shortening in oocytes and embryos.
- Reduced telomerase reverse transcriptase expression and telomerase activity were observed.
- Increased TIFs indicated telomere dysfunction in oocytes and embryos from HFD mice.
- HFD oocytes and embryos showed higher aneuploidy rates and increased blastocyst apoptosis.
Conclusions:
- Maternal obesity leads to telomere dysfunction in oocytes and embryos.
- Telomere dysfunction is a likely molecular mechanism contributing to impaired oocyte quality and embryo development in obese mothers.
- Findings highlight the importance of addressing maternal metabolic health for reproductive success.
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