Serum BDNF as an integrative neuro-immunometabolic marker in adolescent polycystic ovary syndrome: divergent dietary and inflammatory associations across weight phenotypes
Abstract
Background Polycystic ovary syndrome (PCOS) in adolescence is characterized by hormonal imbalance, low-grade inflammation, oxidative stress, and metabolic dysfunction. Brain-derived neurotrophic factor (BDNF) regulates energy homeostasis and neuroimmune signaling and may act as a neuroimmunometabolic integrator in PCOS. Methods Forty adolescent females with PCOS (26 normal weight and 14 with overweight and obesity) were evaluated. Serum BDNF, omega-3 fatty acids (EPA, DHA), uric acid, metabolic and hormonal indices, and total antioxidant capacity (T-AOC) were measured. Dietary intake and physical activity were assessed using validated tools. Results Serum BDNF concentrations did not differ between BMI phenotypes. After FDR correction, significant dietary associations were observed only in normal-weight participants, including energy, protein, fat, and unsaturated fatty acids. No dietary associations remained significant in patients with overweight and obesity. Across both phenotypes, BDNF was positively associated with IL-1β, MDA, T-AOC, EPA, and uric acid. IL-6, TNF- α , and DHA remained significant only in normal-weight participants. No associations were found with CRP, lipid profile, sex hormones, or glucose–insulin parameters. Conclusion Circulating BDNF was associated with dietary, inflammatory, and oxidative parameters, with limited evidence for endocrine associations. These findings suggest that BDNF may reflect an integrated neuroimmunometabolic profile in adolescent PCOS and should be considered exploratory, requiring confirmation in longitudinal studies.
Fields of Study & Subjects
Ovarian function and disorders
Nerve injury and regeneration
Hypothalamic control of reproductive hormones
Publication details
- Journal / source
- Frontiers in Nutrition
- Publisher
- Frontiers Media SA
- Volume
- 13
- Pages
- 1830074–1830074
- Publication date
- 21 May 2026
- Language
- EN