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The mammalian target of rapamycin (mTOR) signaling pathway functions as a key regulator, coordinating diverse cellular responses to environmental cues, and is essential for regulating metabolic homeostasis and reproductive processes.Previous studies have shown that gut dysbiosis-induced inflammation negatively affects male reproductive fertility in mice.However, research on its impact on female fertility and oocyte quality remains limited.Accordingly, the present study investigated the role of mTOR signaling in reproductive dysfunction induced by gut dysbiosis in female mice.To induce dysbiosis, 10-11-week-old female mice received antibiotic treatment for 4 weeks.Following treatment, serum, organs, and tissues were collected to assess the role of mTOR.Serum levels of glucose, cholesterol, ammonia, and sex hormones were measured, and RT-PCR was performed to analyze the levels of mTOR-related genes in the ovary and uterus.Our findings revealed a significant reduction in serum glucose levels, indicating that the intestinal microbiome regulates glucose homeostasis.Additionally, cholesterol levels were significantly higher in dysbiosis-induced mice (WD) than in the control mice (W/O).Furthermore, significantly lower levels of follicle-stimulating hormone and luteinizing hormone were observed in the WD group than in the control group.The relative gene expression levels of Mtor, Rictor, p53, PI3K, Akt1, p70s6k, and Rheb were significantly upregulated, whereas Raptor was suppressed in the ovaries and uterus of WD mice.In conclusion, antibiotic-induced gut dysbiosis appears to be associated with female reproductive dysfunction and changes in mTOR pathway, which is consistent with previous studies on reproductive disorders associated with gut dysbiosis.
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Gamage et al. (2026) studied this question.
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