Central β₂-adrenergic receptors mediate insulin-induced anorexia in broiler chickens

Insulin acts as a central anorexigenic signal in vertebrates, but its precise neuropharmacological mechanisms in avian species remain largely unelucidated. This study sought to delineate the involvement of specific central adrenergic receptor subtypes in the mechanism through which insulin suppresses feed intake in broiler chickens. To achieve this objective, six experiments were conducted using 264 neonatal broiler chicks receiving intracerebroventricular injections. The experimental design consisted of: 1) establishing a dose-response relationship for insulin (2.5, 5, and 10 ng), followed by 2) investigating potential interactions between insulin (10 ng) and selective adrenergic receptor antagonists including prazosin (α₁, 10 nmol), yohimbine (α₂, 13 nmol), metoprolol (β₁, 24 nmol), ICI 118,551 (β₂, 5 nmol), and SR59230R (β₃, 20 nmol). Total feed intake was assessed at three specific time points: 30, 60, and 120 min after the infusion of the treatment. Exogenous insulin administration elicited a robust, dose-responsive inhibition of feeding behavior in the subjects (P < 0.05). Co-infusion with the β2-adrenergic receptor antagonist ICI 118,551 markedly attenuated insulin's hypophagic effects (P < 0.05), whereas the administration of antagonists for alternative adrenergic receptor subtypes did not result in a statistically significant modulation of insulin's action (P ≥ 0.05). This investigation provides evidence supporting a central role for β₂-adrenergic receptors in the mediation of insulin's appetite-suppressing actions in broiler chickens. The results contribute to understanding of the neurochemical substrates governing avian feeding behavior and indicate potential targets for further investigation into metabolic regulation.