Investigating the role of melanocortinergic, glutamatergic and neuropeptide Y systems on hypophagia caused by gastric inhibitory polypeptide (GIP) in broilers

TL;DR

This study explores how GIP affects appetite in broilers and finds that its effects are mediated by melanocortin and NMDA receptors.

Contribution

The study identifies the involvement of melanocortin and NMDA receptor systems in GIP-induced hypophagia in broilers.

Findings

GIP at 6 and 12 nmol significantly reduced food intake in broilers.

The anorexigenic effect of GIP was blocked by MC3/MC4 and NMDA receptor antagonists.

NPY Y1, Y2, and Y5 receptors were not involved in GIP's effects.

Abstract

Appetite control and the metabolic rate of energy expenditure are under the influence of a broad suite of biochemical messengers, which include peptide-based signals, hormonal agents, and neurotransmitters. This research sought to examine the correlation between melanocortinergic, glutamatergic, and neuropeptide Y (NPY) systems with gastric inhibitory polypeptide (GIP) in the modulation of appetite and consummatory behavior. In experiment 1, broilers were injected with GIP at various doses (3, 6 and 12 nmol) in addition to saline. The experimental design for the second trial involved four distinct ICV treatment groups: a saline control, SHU9119 (a MC3/4 melanocortin receptor antagonist, 0.5 nmol), GIP (12 nmol), and a co-infusion of SHU9119 and GIP. Experiments 3 through 11 followed a protocol analogous to that of experiment 2. The sole modification was the substitution of SHU9119 with specific receptor antagonists, administered via intracerebroventricular (ICV) injection. These antagonists targeted the following receptors and their respective doses: MC4 (HS024, 0.5 nmol), NMDA (MK-801, 15 nmol), AMPA (CNQX, 390 nmol), mGluR1 (AIDA, 2 nmol), mGluR2 (LY341495, 150 nmol), mGluR3 (UBP1112, 2 nmol), NPY1 (BMS193885, 1.25 µg), NPY2 (CYM9484, 1.25 µg), and NPY5 (L-152804, 1.25 µg). Cumulative feed intake was subsequently measured at 30, 60, and 120-minute post-infusion intervals. Based on the results, GIP at doses of 6 and 12 nmol induced a significant reduction in food consumption relative to the control group (P < 0.05). This anorexigenic effect of GIP was significantly attenuated by the co-infusion of either the MC3/MC4 receptor antagonist SHU9119 (P < 0.05) or the NMDA receptor antagonist MK-801 (P < 0.05). The collected data imply that signaling cascades dependent on NMDA and melanocortin (MC3/MC4) receptors potentially mediate the anorectic effect of GIP in neonatal broilers, a process which appears independent of NPY Y1, Y2, and Y5 receptor involvement.

Image, graphical abstract

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