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Maternal obesity induces the meiotic defects and epigenetic alterations during fetal oocyte development [RNA-seq]

GSE263548 Mus musculus Expression profiling by high throughput sequencing 4 samples Submitted 2024/08/21 Platform GPL24247
Summary
It has been widely reported that obesity adversely impacts reproductive performance of females. However, the effects of maternal obesity on fetal germ cells remain poorly understood. In the present study, by employing a high-fat diet (HFD)-based mouse model, we found that maternal obesity disrupts the chromosomal synapsis and homologous recombination during fetal oogenesis. Moreover, transcriptomic profiling revealed the potential molecular network controlling this process. Of note, the global hypermethylation of genomic DNA in fetal oocytes from obese mouse was detected. Importantly, time-restricted feeding (TRF) of obese mice not only ameliorated the meiotic defects, but also partly restored the epigenetic remodeling in fetal oocytes. In sum, we provide the evidence showing the deficit fetal oogenesis in obese mother, implicating a mechanism underlying the intergenerational effects of environmental insults. TRF may represent a potentially effective approach for mitigating fertility issues in obese patients.
Published in
Maternal Obesity Induces the Meiotic Defects and Epigenetic Alterations During Fetal Oocyte Development
Tang S, Wu H, Chen Q et al. · Advanced science (Weinheim, Baden-Wurttemberg, Germany) 2024 · PMID 38868907 · doi:10.1002/advs.202309184
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Also filed as BioProject PRJNA1098030 and SRA study SRP500535. Searching any of these in the dataset finder brings you back here.

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