Insulin Resistance Exacerbates Hyperandrogenism and Hormonal Imbalance in Polycystic Ovary Syndrome: A Case-Control Study
DOI:
https://doi.org/10.46649/t5vrd366Keywords:
Polycystic Ovary Syndrome, Insulin Resistance, Luteinizing Hormone (LH), Follicle Stimulating Hormone (FSH), Testosterone, HyperandrogenismAbstract
Background: Polycystic ovary syndrome (PCOS) is a prevalent endocrine disorder that is characterized by hyperandrogenism, ovarian dysfunction, and metabolic disturbances. Insulin resistance (IR), present in 50–70% of PCOS cases, exacerbates hormonal imbalances by stimulating ovarian androgen synthesis and suppressing sex hormone-binding globulin (SHBG). Objective: This study aimed to evaluate the role of insulin resistance in driving hyperandrogenism and hormonal dysregulation in PCOS patients compared with healthy controls. Methods: This case-control study included 60 women diagnosed with PCOS (Rotterdam criteria) and 30 age-matched healthy controls. Participants were recruited from a fertility center, excluding smokers, those with chronic conditions, and those taking medications affecting the outcomes. Fasting blood samples collected on menstrual cycle day 2 were analyzed for glucose, insulin, LH, FSH, and testosterone. Insulin resistance was assessed via HOMA-IR. Results: PCOS patients exhibited significantly higher BMI (p = 0.004), hirsutism (86.7% vs. 0%, p < 0.001), and menstrual irregularities (80% vs. 6.7%, p < 0.001) than controls. Metabolic parameters, including fasting glucose (104.32 ± 15.23 vs. 86.47 ± 7.08 mg/dL), insulin (14.91 ± 3.01 vs. 8.22 ± 2.47 µU/mL), and HOMA-IR (3.77 ± 1.01 vs. 1.74 ± 0.52), were elevated in PCOS (p < 0.001). Hormonal profiles showed increased LH (10.12 ± 1.84 vs. 4.21 ± 1.4 IU/mL), FSH (6.13 ± 1.48 vs. 4.23 ± 1.2 IU/mL), and testosterone (2.11 ± 0.86 vs. 0.73 ± 0.48 ng/mL) in PCOS (p < 0.001). Conclusion: Insulin resistance is a central driver of hyperandrogenism and hormonal dysregulation in PCOS, perpetuating metabolic and reproductive dysfunctions.
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