Affiliation:
1. State Key Laboratory of Reproductive Medicine and Offspring Health Changzhou Maternity and Child Health Care Hospital Changzhou Medical Center Nanjing Medical University Nanjing 211166 China
2. Department of Nutrition and Food Hygiene School of Public Health Nanjing Medical University Nanjing 211166 China
3. Suzhou Municipal Hospital Nanjing Medical University Nanjing 211166 China
Abstract
AbstractIt 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, it is discovered that maternal obesity disrupts the chromosomal synapsis and homologous recombination during fetal oogenesis. Moreover, transcriptomic profiling reveales the potential molecular network controlling this process. Of note, the global hypermethylation of genomic DNA in fetal oocytes from obese mouse is detected. Importantly, time‐restricted feeding (TRF) of obese mice not only ameliorate the meiotic defects, but also partly restore the epigenetic remodeling in fetal oocytes. In sum, the evidence are provided 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.
Funder
National Key Research and Development Program of China
National Natural Science Foundation of China
Natural Science Foundation of Jiangsu Province