Neurotrophin and Adipokine Signatures Associated with Visceral Adiposity–Driven Cardiometabolic and Endocrine Risk in Polycystic Ovary Syndrome

Polycystic ovary syndrome (PCOS) is a heterogeneous endocrine–metabolic disorder as-sociated with insulin resistance (IR), visceral adiposity, and increased cardiometabolic risk. The visceral adiposity index (VAI) is a validated surrogate marker of adipose tissue dysfunction, but its relationship with circulating neurotrophins and adipokine balance in PCOS remains incompletely understood. In this study, 100 women with PCOS were strati-fied into lower- (n = 50) and higher-risk (n = 50) groups according to VAI. Anthropometric measures, fasting glucose and insulin concentrations, lipid profile, and serum levels of brain-derived neurotrophic factor (BDNF), nerve growth factor-β (NGFβ), leptin, adi-ponectin, and resistin were assessed. HOMA-IR, adipokine ratios and atherogenic indices were calculated. Multivariate regression revealed that BDNF was independently associ-ated with VAI and non-HDL-cholesterol, whereas NGFβ was independently associated with HDL-cholesterol and estradiol, indicating neurotrophin associations with metabolic and endocrine parameters independent of general adiposity. Correlation heatmap and network analyses demonstrated interconnected clusters linking visceral adiposity, IR, dyslipidemia, adipokine imbalance, and neurotrophins, with the leptin/adiponectin ratio emerging as a central integrative marker. These findings indicate that VAI-defined car-diometabolic risk in PCOS is accompanied by distinct and opposing neurotrophin–adipokine signatures, highlighting neurotrophin–adipokine networks underlying visceral adiposity-driven cardiometabolic and endocrine risk.