Human genetic studies have associated Neuronatin gene variants with anorexia nervosa (AN) and obesity. Studies on the expression of the Neuronatin gene product, a proteolipid, are lacking. We investigated the relationship between circulating Neuronatin, body mass index (BMI), body composition (BC), physical activity (PA), and psychometric outcomes in patients with AN, normal weight, and obesity. Plasma Neuronatin was measured by ELISA in (1) 79 subjects of five BMI categories (AN/BMI < 17.5 kg/m2; normal weight/BMI 18.5–25 kg/m2; obesity/BMI 30–40 kg/m2; obesity/BMI 40–50 kg/m2; obesity/BMI > 50 kg/m2) with assessment of BC (bioimpedance analysis; BIA); (2) 49 women with AN (BMI 14.5 ± 1.8 kg/m2) with measurements of BC (BIA) and PA (accelerometry); (3) 79 women with obesity (BMI 48.8 ± 7.8 kg/m2) with measurements of anxiety (GAD-7), stress (PSQ-20), depression (PHQ-9) and eating behavior (EDI-2). Overall, a positive correlation was found between Neuronatin and BMI (p = 0.006) as well as total fat mass (FM; p = 0.036). In AN, Neuronatin did not correlate with BMI, FM, or PA (p > 0.05); no correlations were found between Neuronatin and psychometric outcomes in obesity (p > 0.05). The findings suggest an FM-dependent peripheral Neuronatin expression. The decreased Neuronatin expression in AN provides evidence that Neuronatin is implicated in the pathogenesis of eating disorders.
