Central injection of epidermal growth factor (EGF) induces hypophagia via D₁ dopaminergic and β₂ adrenergic receptors in broiler chickens

TL;DR

Injecting EGF into the brain of baby chickens reduces their food intake, and this effect is linked to specific brain receptors.

Contribution

This study is the first to show that EGF suppresses appetite in chickens via D₁ dopaminergic and β₂ adrenergic receptors.

Findings

EGF at 100 and 200 ng significantly reduced food consumption in broiler chickens.

The appetite-suppressing effect of EGF was enhanced by l-DOPA and blocked by SCH23390 and ICI 118,551.

Antagonists for other receptors had no effect on EGF-induced anorexia.

Abstract

In avian species, the central nervous system orchestrates feeding behavior through intricate interplay among diverse neurotransmitter pathways. Epidermal Growth Factor (EGF), a key peptide in cell growth and repair, has been implicated in appetite control in mammals, but its role in avian species remains unexplored. The present study was conducted to investigate the effect of central infusion of EGF on food consumption in neonatal broilers and to determine the possible involvement of dopaminergic and adrenergic systems. In a series of experiments, 5-day-old male broilers were subjected to intracerebroventricular (ICV) injections following a 3-hour fasting period. In experiment 1, chicks received an ICV injection of either the control solution or EGF at doses of 50, 100, or 200 ng. Experiments 2-10 evaluated the effects of co-injection of EGF (200 ng) with various pharmacological agents and receptor antagonists: SCH23390 (D₁-dopaminergic), AMI-193 (D₂-dopaminergic), l-DOPA (dopamine precursor), 6-OHDA (dopaminergic neurotoxin), prazosin (α₁-adrenergic), yohimbine (α₂-adrenergic), metoprolol (β₁-adrenergic), ICI 118,551 (β₂-adrenergic), and SR 59230R (β₃-adrenergic). At 30, 60, and 120 minutes after the infusion, cumulative food consumption was recorded. The results showed that EGF (100 and 200 ng) significantly and dose-dependently reduced cumulative feed consumption compared to the control group (P < 0.05). The anorexigenic effect of EGF (200 ng) was potentiated by co-injection with l-DOPA (P < 0.05). Conversely, the anorexigenic effect of EGF was attenuated by co-infusion of SCH23390, 6-OHDA, and ICI 118,551 with EGF (P < 0.05). Antagonists for α₁, α₂, β₁, and β₃ adrenergic receptors, as well as D₂ dopaminergic receptors, had no significant effect on EGF-induced anorexia (P ≥ 0.05). These findings demonstrate, for the first time, that central EGF acts as an appetite-suppressing peptide in broilers, and its effect is specifically mediated through interactions with D₁ dopaminergic and β₂ adrenergic receptor systems.

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