State Key Laboratory of Reproductive Medicine, Nanjing Medical University, Nanjing 211166, China.
Key Laboratory of Human Functional Genomics of Jiangsu Province, Department of Biochemistry and Molecular Biology, Nanjing Medical University, Nanjing 211166, China.
Int J Mol Sci. 2022 Apr 27;23(9):4797. doi: 10.3390/ijms23094797.
Obesity induced by a high-fat diet (HFD) leads to the excessive consumption of primordial follicles (PFs) in the ovaries. There is systemic chronic inflammation under HFD conditions, but no previous studies have explored whether there is a certain causal relationship between HFD-induced chronic inflammation and the overactivation of PFs. Here, we showed that HFD causes disorders of intestinal microflora in mice, with five Gram-negative bacteria showing the most profound increase at the genus level compared to the normal diet (ND) groups and contributes to the production of endotoxin. Endotoxin promotes M1 macrophage infiltration in the ovaries, where they exhibit proinflammatory actions by secreting cytokines IL-6, IL-8, and TNFα. These cytokines then boost the activation of PFs by activating Signal Transducer and Activator of Transcription 3 (STAT3) signaling in follicles. Interestingly, transplantation of the HFD intestinal microflora to the ND mice partly replicates ovarian macrophage infiltration, proinflammation, and the overactivation of PFs. Conversely, transplanting the ND fecal microbiota to the HFD mice can alleviate ovarian inflammation and rescue the excessive consumption of PFs. Our findings uncover a novel and critical function of gut microbes in the process of PF overactivation under HFD conditions, and may provide a new theoretical basis for the microbial treatment of patients with premature ovarian insufficiency caused by HFD.
高脂肪饮食(HFD)引起的肥胖会导致卵巢中原始卵泡(PFs)的过度消耗。在 HFD 条件下存在全身性慢性炎症,但以前的研究尚未探讨 HFD 诱导的慢性炎症与 PFs 的过度激活之间是否存在某种因果关系。在这里,我们表明 HFD 会导致小鼠肠道微生物群紊乱,与正常饮食(ND)组相比,五种革兰氏阴性菌在属水平上的增加最为明显,并导致内毒素的产生。内毒素促进卵巢中 M1 巨噬细胞浸润,它们通过分泌细胞因子 IL-6、IL-8 和 TNFα 发挥促炎作用。这些细胞因子通过激活卵泡中的信号转导和转录激活因子 3(STAT3)信号通路,从而促进 PFs 的激活。有趣的是,将 HFD 肠道微生物群移植到 ND 小鼠中部分复制了卵巢巨噬细胞浸润、促炎和 PFs 的过度激活。相反,将 ND 粪便微生物群移植到 HFD 小鼠中可以减轻卵巢炎症并挽救 PFs 的过度消耗。我们的发现揭示了肠道微生物在 HFD 条件下 PF 过度激活过程中的新的关键功能,并为使用微生物治疗由 HFD 引起的卵巢早衰患者提供了新的理论依据。