Background <p>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.</p> Methods <p>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&#xa0;µg). In experiment 2, birds received ICV injection of saline, B5063 (NPY₁ receptor antagonist, 1.25&#xa0;µg), adropin (2&#xa0;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 (NPY₂ receptor antagonist, 1.25&#xa0;µg), SML0891 (NPY₅ receptor antagonist, 1.25&#xa0;µg), SHU9119 (MC3/MC4 receptor antagonist, 0.5 nmol) and MCL0020 (MC4 receptor antagonist, 0.5 nmol). At 30, 60, and 120&#xa0;min subsequent to ICV injection, cumulative food intake was evaluated.</p> Results <p>Adropin produced a significant reduction in food intake in a dose-responsive manner compared with control animals (<i>p</i> &lt; 0.05). Co-injection of B5063 alongside adropin intensified the hypophagic response elicited by adropin (<i>p</i> &lt; 0.05). Furthermore, the anorexigenic response triggered by adropin was negated when SHU9119 and MCL0020 were given alongside it (<i>p</i> &lt; 0.05). Adropin-mediated suppression of feeding was unaffected by the administration of SF22 and SML0891 (<i>p</i> &gt; 0.05).</p> Conclusion <p>These findings suggest that the NPY₁, MC3, and MC4 receptors contribute to the hypophagic response triggered by adropin.</p>