上海交通大学学报(医学版) ›› 2026, Vol. 46 ›› Issue (7): 990-996.doi: 10.3969/j.issn.1674-8115.2026.07.018

• 综述 • 上一篇    

绝经后卵泡刺激素水平升高对女性代谢影响的研究进展

林雪枫, 赖东梅()   

  1. 上海交通大学医学院附属国际和平妇幼保健院妇产科,上海市胚胎源性疾病重点实验室,上海 200030
  • 收稿日期:2025-10-27 接受日期:2025-12-18 出版日期:2026-07-08 发布日期:2026-07-08
  • 通讯作者: 赖东梅,主任医师,博士;电子信箱:laidongmei@hotmail.com
  • 基金资助:
    国家自然科学基金(82271664);上海市卫生健康委员会项目(202240345);上海市细胞治疗临床医学研究中心项目(23J41900100);上海交通大学医学院“双百人”项目(20191425)

Research progress in the impact of elevated follicle-stimulating hormone levels on metabolic changes in postmenopausal women

Lin Xuefeng, Lai Dongmei()   

  1. Shanghai Key Laboratory of Embryo Original Diseases; Department of Gynecology and Obstetrics, The International Peace Maternity and Child Health Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200030, China
  • Received:2025-10-27 Accepted:2025-12-18 Online:2026-07-08 Published:2026-07-08
  • Contact: Lai Dongmei, E-mail: laidongmei@hotmail.com.
  • Supported by:
    National Natural Science Foundation of China(82271664);Program of Shanghai Municipal Health Commission(202240345);Program of Shanghai Clinical Research Center for Cell Therapy(23J41900100);“Two-hundred Talents” Program of Shanghai Jiao Tong University of Medicine(20191425)

摘要:

下丘脑-垂体-卵巢轴(hypothalamic-pituitary-ovarian axis,HPO)是控制女性月经周期的核心内分泌系统。HPO各组分之间通过复杂的激素调节网络相互作用,共同调节女性生殖健康。其中,垂体分泌的卵泡刺激素(follicle-stimulating hormone,FSH)在卵泡发育及类固醇激素合成中发挥关键作用。而雌激素又通过负反馈调控下丘脑和垂体,从而维持HPO的动态平衡。随着女性进入绝经期,卵巢功能衰退导致雌激素水平显著下降,使得其负反馈作用减弱,FSH水平持续升高。众多研究表明,绝经后高FSH状态并不局限于生殖系统的改变,还可能通过卵泡刺激素受体(follicle-stimulating hormone receptor,FSHR)作用于脂肪组织、胰岛和骨组织等多个非生殖靶器官,参与能量代谢重塑和代谢稳态调节。研究显示,FSH水平升高与脂质代谢紊乱、脂肪组织炎症及心血管疾病风险密切相关。在糖代谢方面,FSH通过作用于胰岛β细胞上的FSHR,抑制葡萄糖刺激的胰岛素分泌(glucose-stimulated insulin secretion,GSIS),最终导致血糖稳态失调。在骨代谢中,FSH可直接增强破骨细胞活性,加速骨吸收,其作用在一定程度上独立于雌激素水平下降。该文就FSH水平升高对绝经后女性的脂质代谢、糖代谢及骨代谢影响的研究进展进行综述,并探讨其临床意义及面临的挑战。

关键词: 下丘脑-垂体-卵巢轴, 卵泡刺激素, 卵泡刺激素受体, 脂质代谢, 糖代谢, 骨代谢

Abstract:

The hypothalamic-pituitary-ovarian axis (HPO) is the core endocrine system regulating the female menstrual cycle. The components of the HPO operate within a complex hormonal regulatory network to maintain reproductive health. Follicle-stimulating hormone (FSH), secreted by the pituitary gland, is essential for follicular development and steroidogenesis, whereas estrogen provides negative feedback to the hypothalamus and pituitary to preserve the dynamic balance of the HPO. With the onset of menopause, ovarian failure leads to a marked decline in estrogen levels, weakening this feedback loop and resulting in sustained elevations of circulating FSH. Accumulating evidence indicates that high FSH levels in postmenopausal women have effects extending beyond the reproductive system, acting through the follicle-stimulating hormone receptor (FSHR) expressed in adipose tissue, pancreatic islets, and bone to participate in energy metabolic remodeling and the regulation of metabolic homeostasis. Current findings suggest that elevated FSH is associated with lipid metabolic disturbances, adipose tissue inflammation, and an increased risk of cardiovascular disease. In glucose metabolism, FSH acts through FSHR expressed on pancreatic β cells to inhibit glucose-stimulated insulin secretion (GSIS), ultimately leading to impaired glucose homeostasis. In bone metabolism, FSH directly enhances osteoclast activity and promotes bone resorption, with part of this effect being independent of estrogen deficiency. This review summarizes advances in understanding the roles of elevated FSH levels in lipid, glucose, and bone metabolism in postmenopausal women and highlights the potential clinical implications and remaining challenges in this field.

Key words: hypothalamic-pituitary-ovarian axis (HPO), follicle-stimulating hormone (FSH), follicle-stimulating hormone receptor (FSHR), lipid metabolism, glucose metabolism, bone metabolism

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