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

TL;DR

This study explores how neurotrophins and adipokines relate to visceral fat and metabolic risks in women with PCOS.

Contribution

The study identifies distinct neurotrophin–adipokine signatures linked to visceral adiposity in PCOS.

Findings

BDNF is independently associated with VAI and non-HDL cholesterol.

NGFβ is independently linked to HDL cholesterol and estradiol.

The leptin/adiponectin ratio is a central marker in the neurotrophin–adipokine network.

Abstract

Polycystic ovary syndrome (PCOS) is a heterogeneous endocrine–metabolic disorder associated 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 stratified 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, adiponectin, and resistin were assessed. HOMA-IR, adipokine ratios and atherogenic indices were calculated. Multivariate regression showed that BDNF was independently associated with VAI and non-HDL cholesterol, whereas NGFβ was independently linked to HDL cholesterol and estradiol, highlighting neurotrophin relationships with metabolic and endocrine parameters beyond 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 suggest that within a PCOS population, VAI-defined cardiometabolic risk is associated with distinct neurotrophin–adipokine signatures, highlighting neurotrophin–adipokine networks underlying visceral adiposity-driven cardiometabolic and endocrine risk.

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