Adipokine Dysregulation in Obese and Non-Obese Polycystic Ovary Syndrome (PCOS) Patients: Association With Visceral Adiposity Index and Metabolic Risk.

Background Polycystic ovary syndrome (PCOS) is a multifactorial endocrine disorder characterized by metabolic and reproductive abnormalities. Obesity exacerbates PCOS-associated insulin resistance, inflammation, and hormonal imbalances, potentially influencing adipokine secretion. This study evaluated variations in adipokines between obese and non-obese PCOS patients and their association with the Visceral Adiposity Index (VAI), metabolic parameters, and disease severity. Methods A cross-sectional study was conducted at a tertiary care center in North India on 90 women diagnosed with PCOS using the Rotterdam 2003 criteria. Participants were categorized into obese (n=45) and non-obese (n=45) groups based on body mass index (BMI). Clinical, biochemical, and inflammatory markers were assessed, including leptin, adiponectin, resistin, tumor necrosis factor alpha (TNF-α), and interleukin-6 (IL-6). Metabolic parameters such as fasting glucose, insulin, homeostatic model assessment for insulin resistance (HOMA-IR), and lipid profile were evaluated. Pearson correlation and receiver operating characteristic (ROC) analyses were used to assess associations and diagnostic accuracy. Results Obese PCOS patients had significantly higher leptin (24.5 ± 6.2 vs. 14.2 ± 5.8 ng/mL, p<0.001) and lower adiponectin (5.2 ± 1.4 vs. 7.8 ± 1.9 µg/mL, p=0.002) than non-obese counterparts. Resistin, TNF-α, and IL-6 were also elevated in the obese group (p<0.05). Obesity was associated with increased fasting glucose (mean difference = 5.6 mg/dL, 95% CI: 0.2-11.0, p=0.043), insulin (mean difference = 4.1 µIU/mL, 95% CI: 2.1-6.1, p<0.001), HOMA-IR (mean difference = 1.2, 95% CI: 0.7-1.7, p<0.001), triglycerides (mean difference = 24.3 mg/dL, 95% CI: 3.1-45.5, p=0.025), and lower high-density lipoprotein cholesterol (HDL-C) (mean difference = -6.2 mg/dL, 95% CI: -11.4 to -1.0, p=0.018). Leptin correlated positively with BMI (r=0.742, p<0.001) and VAI (r=0.763, p<0.001), while adiponectin showed a negative correlation (r=-0.515, p=0.010). ROC analysis indicated that leptin had the highest diagnostic accuracy for predicting obesity in PCOS (area under the curve [AUC] =0.85, 95% CI: 0.79-0.91, p<0.001). Conclusion Obesity in PCOS is associated with significant alterations in adipokine profiles, metabolic dysfunction, and elevated inflammatory markers. Leptin demonstrated the strongest association with obesity and metabolic disturbances, supporting its potential as a biomarker for identifying metabolic risk in PCOS. Targeted interventions addressing adipokine imbalances may help mitigate metabolic complications in obese PCOS patients.