内分泌学
多囊卵巢
内科学
胰岛素抵抗
烟酰胺单核苷酸
蛋白激酶B
胰岛素
生物
医学
化学
细胞凋亡
NAD+激酶
酶
生物化学
烟酰胺腺嘌呤二核苷酸
作者
Qian Zhang,Jiaming Zhang,Haoxuan Xue,Xi Chen,Meixiang Li,Shenghua Chen,Zhiling Li,Leonardo A. Sechi,Qian Wang,Giampiero Capobianco,Xiaocan Lei
标识
DOI:10.1002/mnfr.202400340
摘要
Scope Polycystic ovary syndrome (PCOS) is a common endocrine disorder that can lead to insulin resistance (IR) and dysregulation of glucose metabolism, resulting in an imbalance in the endometrial environment, which is unfavorable for embryo implantation of PCOS. This study aims to investigate whether nicotinamide mononucleotide (NMN) improves the stability of the endometrium in a rat model of PCOS and identifies whether it is related to reduce IR and increase glycolysis levels and its potential signaling pathway. Methods and results Female Sprague‐Dawley (SD) rats are fed letrozole and a high‐fat diet (HFD) to form the PCOS model, then the model rats are treated with or without NMN. It randomly divided into control, PCOS, and PCOS‐NMN groups according to the feeding and treating method. Compared with the PCOS group, the regular estrous cycles are restored, the serum androgen ( p <0.01) and fasting insulin levels ( p <0.05) are reduced, and endometrial morphology ( p <0.05) is improved in NMN‐PCOS group. Furthermore, NMN inhibits endometrial cell apoptosis, improves endometrial decidualization transition, reduces IR, restores the expression of glycolysis rate‐limiting enzymes, and activates the PI3K/AKT pathway in the uterus. Conclusions These results suggest that NMN enhances endometrial tissue homeostasis by decreasing uterine IR and regulating the glycolysis through the PI3K/AKT pathway.
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