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13 results on '"Yuan, Suzhen"'

8. Analysis of Ovarian Injury Associated With COVID-19 Disease in Reproductive-Aged Women in Wuhan, China: An Observational Study

Author

Ding, Ting, primary, Wang, Tian, additional, Zhang, Jinjin, additional, Cui, Pengfei, additional, Chen, Zhe, additional, Zhou, Su, additional, Yuan, Suzhen, additional, Ma, Wenqing, additional, Zhang, Minli, additional, Rong, Yueguang, additional, Chang, Jiang, additional, Miao, Xiaoping, additional, Ma, Xiangyi, additional, and Wang, Shixuan, additional

Published
2021
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13. High-fat diet-induced L-saccharopine accumulation inhibits estradiol synthesis and damages oocyte quality by disturbing mitochondrial homeostasis.

Author

Wen J, Feng Y, Xue L, Yuan S, Chen Q, Luo A, Wang S, and Zhang J

Subjects
Animals, Female, Mice, Fecal Microbiota Transplantation, Infertility, Female microbiology, Infertility, Female metabolism, Infertility, Female etiology, Ovary metabolism, Ovary microbiology, Diet, High-Fat adverse effects, Estradiol metabolism, Estradiol biosynthesis, Oocytes metabolism, Oocytes drug effects, Gastrointestinal Microbiome drug effects, Mitochondria metabolism, Mitochondria drug effects, Dysbiosis microbiology, Homeostasis, Mice, Inbred C57BL
Abstract

High-fat diet (HFD) has been linked to female infertility. However, the specific age at which HFD impacts ovarian function and the underlying mechanisms remain poorly understood. Here, we administered a HFD to female mice at various developmental stages: pre-puberty (4 weeks old), post-puberty (6 weeks old), young adult (9 weeks old), and middle age (32 weeks old). Our observations indicated that ovarian function was most significantly compromised when HFD was initiated at post-puberty. Consequently, post-puberty mice were chosen for further investigation. Through transplantation of fecal bacteria from the HFD mice to the mice on a normal diet, we confirmed that gut microbiota dysbiosis contributed to HFD-induced deteriorated fertility and disrupted estradiol synthesis. Utilizing untargeted and targeted metabolomics analyses, we identified L-saccharopine as a key metabolite, which was enriched in the feces, serum, and ovaries of HFD and HFD-FMT mice. Subsequent in vitro and in vivo experiments demonstrated that L-saccharopine disrupted mitochondrial homeostasis by impeding AMPKα/MFF-mediated mitochondrial fission. This disruption ultimately hindered estradiol synthesis and compromised oocyte quality. AICAR, an activator of AMPKα, ameliorated L-saccharopine induced mitochondrial damage in granulosa cells and oocytes, thereby enhancing E2 synthesis and improving oocyte quality. Collectively, our findings indicate that the accumulation of L-saccharopine may play a pivotal role in mediating HFD-induced ovarian dysfunction. This highlights the potential therapeutic benefits of targeting the gut microbiota-metabolite-ovary axis to address HFD-induced ovarian dysfunction.

Published
2024
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