Insulin Resistance as a Determinant of Menstrual Irregularities in Women of Reproductive Age With and Without Polycystic Ovary Syndrome
Metabolic Determinants of Menstrual Dysfunction
DOI:
https://doi.org/10.69750/dmls.02.012.0180Keywords:
Insulin resistance, menstrual irregularities, polycystic ovary syndrome, reproductive age, HOMA-IRAbstract
Background: The menstrual abnormalities are often reproductive disorders among women of reproductive age and are more often linked to underlying endocrine and metabolic disorders. Polycystic ovary syndrome (PCOS) is well known to result in insulin resistance; its role in causing menstrual irregularities independently of PCOS in non-PCOS women is a poorly researched area.
Objective: To evaluate insulin resistance as a factor leading to menstrual irregularities in women of reproductive age, and to provide a comparative analysis between women with and without polycystic ovary syndrome.
Methods: This is a comparative cross-sectional study carried out between December 2024 and July 2025. One hundred and ten females with 18-40 years with menstrual abnormalities were recruited and split into the PCOS (n= 55) and non-PCOS (n= 55) groups. After an overnight fast, the levels of fasting plasma glucose and fasting serum insulin were measured, and insulin resistance was evaluated using the Homeostatic Model Assessment of Insulin Resistance (HOMA-IR). Menstrual patterns and anthropometric parameters were measured, and statistical analysis was done to establish correlations of insulin resistance and menstrual irregularities.
Results: PCOS women showed drastically higher fasting insulin concentrations and HOMA-IR rates than non-PCOS women. However, the insulin resistance was also observed in a significant number of non-PCOS women. An increment in the HOMA-IR values of both groups had an important relationship with the severity of menstrual irregularities. The multivariational outcome was an insulin resistance, which is an independent predictor of menstrual irregularities adjusted by age and body mass index.
Conclusion: Insulin resistance is a significant factor in the occurrence of menstrual abnormalities in reproductively-aged women, irrespective of PCOS presence. Regular metabolic screening can help in the diagnosis and specific treatment of menstrual dysfunction.
Downloads
References
Pirotta S, Joham A, Grieger JA, et al. Obesity and the risk of infertility, gestational diabetes, and type 2 diabetes in polycystic ovary syndrome. Semin Reprod Med. 2020;38(6):342-51. doi:10.1055/s-0041-1726866
Hoeger KM, Dokras A, Piltonen T. Update on PCOS: consequences, challenges, and guiding treatment. J Clin Endocrinol Metab. 2021;106(3):e1071-83. doi:10.1210/clinem/dgaa839
Rahmatnezhad L, Moghaddam-Banaem L, Behroozi-Lak T, et al. Association of insulin resistance with polycystic ovary syndrome phenotypes and patients’ characteristics. Reprod Biol Endocrinol. 2023;21(1):113. doi:10.1186/s12958-023-01160-z
Zhao H, Zhang J, Cheng X, et al. Insulin resistance in polycystic ovary syndrome across various tissues: pathogenesis, evaluation, and treatment. J Ovarian Res. 2023;16(1):9. doi:10.1186/s13048-022-01091-0
Genazzani A. Inositols: reflections on how to choose the appropriate one for PCOS. Gynecol Endocrinol. 2020;36(12):1045-6. doi:10.1080/09513590.2020.1846697
Lawrence MC. Understanding insulin and its receptor from their three-dimensional structures. Mol Metab. 2021;52:101255. doi:10.1016/j.molmet.2021.101255
James DE, Stöckli J, Birnbaum MJ. The aetiology and molecular landscape of insulin resistance. Nat Rev Mol Cell Biol. 2021;22(11):751-71. doi:10.1038/s41580-021-00390-6
Xu J, Dun J, Yang J, et al. Letrozole rat model mimics human polycystic ovarian syndrome and changes in insulin signaling pathways. Med Sci Monit. 2020;26:e923073. doi:10.12659/MSM.923073
Zeng X, Xie YJ, Liu YT, et al. Polycystic ovarian syndrome: correlation between hyperandrogenism, insulin resistance and obesity. Clin Chim Acta. 2020;502:214-21. doi:10.1016/j.cca.2019.11.003
Tian Y, Li J, Su S, et al. PCOS-GWAS susceptibility variants and their association with insulin resistance. Front Endocrinol (Lausanne). 2020;11:274. doi:10.3389/fendo.2020.00274
Li M, Chi X, Wang Y, et al. Trends in insulin resistance: insights into mechanisms and therapeutic strategies. Signal Transduct Target Ther. 2022;7(1):216. doi:10.1038/s41392-022-01073-0
Herman R, Sikonja J, Jensterle M, et al. Insulin metabolism in polycystic ovary syndrome: secretion, signaling, and clearance. Int J Mol Sci. 2023;24(4):3140. doi:10.3390/ijms24043140
Hernández-Jiménez JL, Barrera D, Espinoza-Simón E, et al. Polycystic ovarian syndrome: feedback effects of hyperandrogenism and insulin resistance. Gynecol Endocrinol. 2022;38(1):2-9. doi:10.1080/09513590.2021.2003326
Zhu Q, Yao Y, Xu L, et al. Elevated SAA1 promotes insulin resistance in ovarian granulosa cells in PCOS. Reprod Biol Endocrinol. 2022;20(1):4. doi:10.1186/s12958-021-00873-3
Tan M, Cheng Y, Zhong X, et al. LNK promotes granulosa cell apoptosis in PCOS via AKT-FOXO3 signaling. Aging (Albany NY). 2021;13(3):4617-33. doi:10.18632/aging.202421
Yang X, Wang K, Lang J, et al. miR-133a-3p promotes ovarian insulin resistance in obese PCOS patients. BMC Womens Health. 2022;22(1):412. doi:10.1186/s12905-022-01994-6
Jiang NX, Zhao WJ, Shen HR, et al. Hyperinsulinemia impairs decidualization via AKT-NR4A1 signaling in PCOS-related infertility. J Ovarian Res. 2024;17(1):31. doi:10.1186/s13048-023-01334-8
Wang K, Li Y, Chen Y. Androgen excess: a hallmark of polycystic ovary syndrome. Front Endocrinol (Lausanne). 2023;14:1273542. doi:10.3389/fendo.2023.1273542
Dietz de Loos ALP, Jiskoot G, Timman R, et al. Improvements in PCOS phenotype severity during lifestyle intervention. Reprod Biomed Online. 2021;43(2):298-309. doi:10.1016/j.rbmo.2021.05.008
Lei R, Chen S, Li W. Advances in the correlation between insulin resistance and infertility. Front Endocrinol (Lausanne). 2024;15:1288326. doi:10.3389/fendo.2024.1288326
Downloads
PlumX Metrics
Published
Issue
Section
License
© The Author(s) 2025. Open Access This article is licensed under a Creative Commons Attribution 4.0 International License , which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third-party material in this article are included in the article’s Creative Commons license unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you must obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/ . The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/ ) applies to the data made available in this article, unless otherwise stated in a credit line to the data.
How to Cite
