RESEARCH Chenodeoxycholic acid fortified diet drives ovarian steroidogenesis to improve embryo implantation through enhancing uterine receptivity via progesterone receptor signaling pathway in rats

文献类型： 外文期刊

第一作者： Chen, Meixia

作者： Chen, Meixia;Zhao, Xiaoyi;Liu, Hui;Zhu, Longlong;Wang, Sixin;Zhang, Dongyang;Wang, Jing;Zhao, Xiaoyi;Chang, Zhuo;Zhu, Longlong

作者机构：

关键词： Chenodeoxycholic acid; Embryo implantation; Metabolome; Ovarian steroid hormone; Progesterone receptor

期刊名称：JOURNAL OF NUTRITIONAL BIOCHEMISTRY （ 影响因子：4.9； 五年影响因子：5.5 ）

ISSN： 0955-2863

年卷期： 2024 年 134 卷

页码：

收录情况： SCI

摘要： Infertility is a worldwide reproductive health problem influenced by the embryo implantation efficiency. We previously revealed that dietary chenodeoxycholic acid (CDCA) positively influence the early embryo implantation. But how CDCA regulate embryo implantation is largely unexplored. Herein, we investigated the mechanism behind CDCA's regulation on embryo implantation in rats. Results showed that CDCA promoted uterine receptivity, leading to increased number of implantation sites. Mechanistically, CDCA reshaped maternal amino acid metabolism and enhanced serum progesterone levels. CDCA enhanced ovarian progesterone synthesis by improving steroidogenesis-related protein (StAR and CYP11A1) expression via Takeda G-protein-coupled receptor 5. Elevated progesterone exaggerated uterine progesterone but weakened the estradiol signaling in the CDCA group, contributing to better uterine receptive for embryo implantation. Additionally, elevated transcription repressor Stat5b induced the down-regulation of progesterone-metabolizing enzyme 20-hydroxysteroid dehydrogenase 20 alpha-HSD, complementally explained uterine progesterone signaling enhancement. Overall, our data revealed that CDCA drove ovarian steroidogenesis to improve embryo implantation through enhancing uterine receptivity via progesterone receptor pathway in rats. Therefore, CDCA diet may be a potential favorable nutritional strategy for infertility and pregnancy management. (c) 2024 Elsevier Inc. All rights are reserved, including those for text and data mining, AI training, and similar technologies.

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