Unraveling the Therapeutic Role of Myoinositol in Polycystic Ovary Syndrome
Polycystic ovary syndrome (PCOS) is a multifaceted endocrine disorder affecting a significant number of women of reproductive age. It is characterized by irregular menstrual cycles, hyperandrogenism, and polycystic ovaries, contributing to infertility and metabolic disturbances. Inositol, particularly myo-inositol (MI), has emerged as a promising therapeutic approach for managing PCOS symptoms. Myo-inositol is an essential component of cell membranes and a precursor to several important signaling pathways. Recent studies have highlighted its beneficial effects on insulin sensitivity, ovarian function, and hormonal regulation in women with PCOS. This review states the potential mechanisms through which myo-inositol modulates insulin resistance, a key metabolic feature of PCOS, and its impact on ovarian function, including its role in improving oocyte quality and promoting regular menstrual cycles. Furthermore, the combination of myo-inositol with D-chiro-inositol (DCI) has been studied for its synergistic effects in managing PCOS symptoms. By evaluating the current literature, this review provides insights into the clinical efficacy of myo-inositol as a safe and effective adjunct in the management of PCOS, with particular emphasis on its role in restoring metabolic balance and improving reproductive outcomes. The review also discusses the challenges and areas for future research to further elucidate the optimal dosing, treatment regimens, and long-term outcomes of myo-inositol therapy for PCOS.
Authors
- Malak Shariff
- Kelly J. Rohan (ORCID: https://orcid.org/0000-0002-8935-8409)
- Valanka Melicia Fernandes
- Mamta Saraf
- Zoya Sadaf
- D R Bhalavikashini
- Sai Krishna Mohana Kondra
- Samuel Bilgates Brettlee
Publication Details
- Journal
- International journal of research and scientific innovation
- Published
- 2025-01-01
- DOI
- https://doi.org/10.51244/ijrsi.2025.12040112
- Primary Topic
- Ovarian function and disorders
- Type
- article
- Field-Weighted Citation Impact
- 0.00