The Renin-Angiotensin System and Metabolic Dysfunction in PCOS: Associations Between Angiotensin Peptides, HOMA-IR, and BMI
DOI:
https://doi.org/10.24237/04.02.784Keywords:
Polycystic Ovary Syndrome, Renin Angiotensin System, Metabolic dysfunction, BMI, IRAbstract
Polycystic Ovary Syndrome (PCOS) is a multifactorial disorder that affects both the metabolic and endocrine systems, characterized by chronic anovulation, hyperandrogenism, and insulin resistance. It is strongly associated with obesity, diabetes, and metabolic disturbances, with evidence suggesting that androgens may directly stimulate the renin–angiotensin system (RAS). This case–control study aimed to investigate the correlation of angiotensin peptides, HOMA-IR, and BMI in women with PCOS. A total of 90 reproductive-age women were enrolled, including 45 newly diagnosed PCOS patients (according to Rotterdam criteria) and 45 age-matched healthy controls. The levels of renin, angiotensin II, angiotensin 1–7, fasting insulin, and BMI were measured, and statistical analyses were performed using SPSS. Group comparisons were performed using the Mann–Whitney U test and independent samples t-test, whereas one-way ANOVA was applied to evaluate variations across BMI categories within the PCOS cohort. Correlations were evaluated using Spearman’s and Pearson’s methods, with statistical significance set at p < 0.05. Compared with controls, PCOS patients showed no significant differences in renin (p = 0.254) and angiotensin II (p = 0.114) levels, whereas HOMA-IR, angiotensin 1–7, and BMI were significantly elevated (all p < 0.01). Correlation analysis within the PCOS group revealed a negative relationship between renin and HOMA-IR (p = 0.045, r = –0.3). These findings highlight RAS alterations in PCOS, particularly reduced angiotensin 1–7 levels, which may indicate impaired protective RAS activity and its association with insulin resistance. Furthermore, elevated angiotensin II levels in women over 25 years suggest potential age-related RAS dysregulation, reinforcing the role of RAS imbalance in PCOS pathophysiology.
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