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<p>C-type natriuretic peptide (CNP), belonging to the natriuretic peptide group, has recently emerged as a potential modulator of feeding behavior in mammalian species. This study aimed to examine the impact of central infusion of CNP-22 on feeding behavior in neonatal broilers and to elucidate its interaction with the dopaminergic, malanocortinergic, and neuropeptide Y (NPY) systems. Across ten separate experiments, broilers were systematically allocated into four different treatment groups for each experiment. In the initial experiment, neonatal chickens (Ross-308) received ICV injections of saline or CNP-22 at escalating doses (0.75, 1.5, and 3 nmol). Subsequent experiments assessed the interplay between CNP-22 (3 nmol); L-DOPA, a precursor of dopamine; 6-hydroxydopamine (6-OHDA), a neurotoxin targeting dopaminergic neurons; SCH23390, an antagonist of D1 dopamine receptors; AMI-193, an antagonist of D2 dopamine receptors; SHU9119, an antagonist of melanocortin 3 and 4 receptors; HS 024, a selective melanocortin 4 receptor antagonist; BMS193885, an antagonist of the neuropeptide Y1 receptor; CYM9484, an antagonist of the neuropeptide Y2 receptor; and L-152,804, which functions as an antagonist at neuropeptide Y5 receptors. Treatments included individual injections and simultaneous co-administrations of CNP-22 with these pharmacological agents. Feed consumption was measured for 120&#xa0;min post-infusion. When CNP-22 was administered at concentrations of 1.5 and 3 nmol, a progressive decline in meal consumption was observed, correlating with increasing dosage (<i>P</i> &lt; 0.05). Co-infusion of BMS193885 + CNP-22 enhanced the anorexigenic effect induced by CNP-22 (<i>P</i> &lt; 0.05). However, simultaneous infusion of 6-OHDA, SCH23390, and SHU9119 with CNP-22 markedly decreased CNP-22-induced anorexia (<i>P</i> &lt; 0.05). The data indicate that CNP-22 administration suppresses feeding behavior in young broiler chickens, a process potentially mediated via the D1, MC3/MC4, and NPY1 receptors pathways.</p> Graphical abstract <p></p>

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Central administration of C-type natriuretic peptide (CNP) modulates food consumption in broilers: involvement of dopaminergic, melanocortinergic, and neuropeptide Y receptors

  • 期刊论文

  • 发表日期：

    2025年11月3日

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  • Ghazaleh Alidadiani,
  • Morteza Zendehdel,
  • Kimia Mahdavi

摘要

C-type natriuretic peptide (CNP), belonging to the natriuretic peptide group, has recently emerged as a potential modulator of feeding behavior in mammalian species. This study aimed to examine the impact of central infusion of CNP-22 on feeding behavior in neonatal broilers and to elucidate its interaction with the dopaminergic, malanocortinergic, and neuropeptide Y (NPY) systems. Across ten separate experiments, broilers were systematically allocated into four different treatment groups for each experiment. In the initial experiment, neonatal chickens (Ross-308) received ICV injections of saline or CNP-22 at escalating doses (0.75, 1.5, and 3 nmol). Subsequent experiments assessed the interplay between CNP-22 (3 nmol); L-DOPA, a precursor of dopamine; 6-hydroxydopamine (6-OHDA), a neurotoxin targeting dopaminergic neurons; SCH23390, an antagonist of D1 dopamine receptors; AMI-193, an antagonist of D2 dopamine receptors; SHU9119, an antagonist of melanocortin 3 and 4 receptors; HS 024, a selective melanocortin 4 receptor antagonist; BMS193885, an antagonist of the neuropeptide Y1 receptor; CYM9484, an antagonist of the neuropeptide Y2 receptor; and L-152,804, which functions as an antagonist at neuropeptide Y5 receptors. Treatments included individual injections and simultaneous co-administrations of CNP-22 with these pharmacological agents. Feed consumption was measured for 120 min post-infusion. When CNP-22 was administered at concentrations of 1.5 and 3 nmol, a progressive decline in meal consumption was observed, correlating with increasing dosage (P < 0.05). Co-infusion of BMS193885 + CNP-22 enhanced the anorexigenic effect induced by CNP-22 (P < 0.05). However, simultaneous infusion of 6-OHDA, SCH23390, and SHU9119 with CNP-22 markedly decreased CNP-22-induced anorexia (P < 0.05). The data indicate that CNP-22 administration suppresses feeding behavior in young broiler chickens, a process potentially mediated via the D1, MC3/MC4, and NPY1 receptors pathways.

Graphical abstract