Modulation of feeding behavior by central adropin injection in neonatal broiler chicks: evidence for NPY and melanocortin signaling pathways involvement

Adropin, a peptide hormone encoded by the Energy Homeostasis Associated (Enho) gene, is involved in regulating food intake, energy homeostasis, and diverse metabolic functions; it is predominantly produced in the liver and brain and exerts its effects on both central and peripheral tissues. This study aimed to evaluate the impact of intracerebroventricular (ICV) adropin administration on food intake and its interactions with NPY and melanocortin systems. This research encompassed 6 experiments organized into 4 distinct groups. In experiment 1, chickens received ICV injections of saline or adropin (0.5, 1, and 2 µg). In experiment 2, birds received ICV injection of saline, B5063 (NPY 1 receptor antagonist, 1.25 µg), adropin (2 µg) and co-injection of the B5063 + adropin. Experiments 3 to 6 mirrored the methodology of experiment 2, with the sole modifications being the substitution of B5063 with SF22 (NPY 2 receptor antagonist, 1.25 µg), SML0891 (NPY 5 receptor antagonist, 1.25 µg), SHU9119 (MC3/MC4 receptor antagonist, 0.5 nmol) and MCL0020 (MC4 receptor antagonist, 0.5 nmol). At 30, 60, and 120 min subsequent to ICV injection, cumulative food intake was evaluated. Adropin produced a significant reduction in food intake in a dose-responsive manner compared with control animals ( p < 0.05). Co-injection of B5063 alongside adropin intensified the hypophagic response elicited by adropin ( p < 0.05). Furthermore, the anorexigenic response triggered by adropin was negated when SHU9119 and MCL0020 were given alongside it ( p < 0.05). Adropin-mediated suppression of feeding was unaffected by the administration of SF22 and SML0891 ( p > 0.05). These findings suggest that the NPY 1 , MC3, and MC4 receptors contribute to the hypophagic response triggered by adropin.