From Gut to Ovary: The Expanding Role of GLP-1 Analogues in PCOS and Fertility in Women
Background: Polycystic ovary syndrome (PCOS) is a common endocrine disorder marked by hyperandrogenism, ovulatory dysfunction, and insulin resistance. Conventional treatments often fail to address the underlying metabolic disturbances contributing to infertility. Aim: To critically evaluate the role of GLP-1 receptor agonists in managing metabolic and reproductive dysfunctions in women with PCOS. Methods: A narrative review was conducted using structured searches in PubMed, Scopus, Web of Science, and ResearchGate, covering publications from 2002 to 2025. Eligible studies included original articles, randomized trials, reviews, and meta-analyses on GLP-1 receptor agonists in the context of PCOS. Results: GLP-1 receptor agonists, particularly liraglutide and semaglutide, have demonstrated efficacy in reducing insulin resistance, lowering serum androgens, and restoring ovulation. Clinical data show improved menstrual regularity and increased pregnancy rates in both natural and assisted reproduction contexts. Safety remains favorable, with gastrointestinal side effects being most common and typically transient. Conclusions: GLP-1 receptor agonists represent a promising therapeutic option in PCOS, offering dual metabolic and reproductive benefits. Further randomized studies are needed to define their role in fertility treatment protocols and ensure reproductive safety.
Authors
- Agnieszka Marianowska
- Maciej Karasiński (ORCID: https://orcid.org/0009-0001-3961-0717)
- Katarzyna Krzyżanowska
- Wiktoria Dzierzgowska
- Aleksandra Maria Śledziewska (ORCID: https://orcid.org/0009-0006-3782-9201)
- Julia Delfina Latocha (ORCID: https://orcid.org/0009-0009-8438-864X)
- Szymon Antoni Kaźmierczak (ORCID: https://orcid.org/0009-0004-3678-5126)
Publication Details
- Journal
- Archiv Euromedica
- Published
- 2025-08-29
- DOI
- https://doi.org/10.35630/2025/15/4.017
- Primary Topic
- Ovarian function and disorders
- Type
- article
- Field-Weighted Citation Impact
- 0.00