Abstract:
Background: Oxytocin (OT), a hypothalamic neuropeptide, is increasingly recognized for its role in energy balance, appetite regulation, and metabolic homeostasis. While leptin has been extensively studied as a driver of obesity-related inflammation and hepatic steatosis, the role of oxytocin in human metabolic dysfunction and disordered eating behaviors remains underexplored. In Uzbekistan, where obesity prevalence is rising due to rapid lifestyle transitions, there is an urgent need to identify novel biomarkers for early risk stratification and targeted interventions.
Objective: This study aimed to investigate the associations of plasma oxytocin and leptin levels with obesity-related metabolic markers, liver dysfunction (ALT, AST, hepatic steatosis index), and disordered eating behaviors.
Methods: A cross-sectional analysis was conducted in 100 adults (mean age 38.5 ± 12.1 years; mean BMI 35.2 ± 8.1 kg/m²), 70% of whom were female. Participants underwent anthropometric and biochemical assessment, including plasma oxytocin, leptin, HOMA-IR, TG, WHR, ALT, AST, and liver fat indices. Eating behavior was evaluated using EDE-Q subscales (e.g., emotional eating, binge frequency). Pearson correlations, multivariate linear regressions, and cluster analyses were used to explore associations, controlling for age, sex, and BMI.
Results: Lower oxytocin levels were significantly associated with higher BMI (r = -0.32, p = 0.002), greater insulin resistance (HOMA-IR: r = -0.41, p < 0.001), increased ALT (r = -0.36, p < 0.001), and more frequent binge eating episodes (r = -0.28, p = 0.01). Leptin showed strong positive correlations with ALT (r = 0.52, p < 0.001) and HOMA-IR (r = 0.55, p < 0.001). In adjusted regression models, oxytocin remained an independent negative predictor of both insulin resistance (β = -0.041, p = 0.001) and elevated liver enzymes (β = -0.027, p = 0.02), while leptin positively predicted ALT levels (β = 0.003, p = 0.01). A high-risk subgroup characterized by “low oxytocin–high leptin” profiles exhibited significantly worse metabolic and behavioral outcomes.
Conclusions: Oxytocin appears to exert a protective influence against metabolic dysfunction, liver injury, and disordered eating in individuals with obesity, potentially counterbalancing leptin’s adverse effects. These findings support further investigation into oxytocin as a therapeutic target in obesity-related conditions, including NAFLD and eating disorders, particularly in resource-limited settings such as Uzbekistan.
