The gut-brain axis in avian appetite regulation: Integrating peripheral signals with central neurocircuitry.

The precise regulation of energy homeostasis is essential for sustainable poultry production. Dysregulation of the avian gut-brain axis (GBA) contributes to metabolic disorders such as ascites and sudden death syndrome, impaired feed efficiency, and welfare problems in high-yield broilers. The avian GBA is a specialized bidirectional network that integrates hormonal, neural, and microbial signals to match feeding behavior with acute nutrient availability and long-term metabolic demands. Unique avian traits include a simplified gustatory system, lack of a functional T1R2 sweet receptor, a divergent leptin system, and distinct microbiota composition; these traits necessitate a species-specific framework for appetite control. This narrative review synthesizes current knowledge on how peripheral signals from the gastrointestinal tract, pancreas, liver, adipose tissue, and microbiota are encoded and conveyed to central command centers to regulate feed intake in poultry. We first outline nutrient sensing and gut-derived hormones with complex or divergent actions in birds (ghrelin, peptide YY, somatostatin), then summarize canonical satiety peptides (cholecystokinin, proglucagon-derived peptides, amylin, bombesin-like peptides, and neuromedin U) and long-term metabolic cues (leptin, insulin, insulin-like growth factors, liver-expressed antimicrobial peptide-2). At the central level, we describe how arcuate neuropeptide Y/agouti-related peptide (NPY/AgRP) and pro-opiomelanocortin/cocaine- and amphetamine-regulated transcript (POMC/CART) neurons, downstream hypothalamic nuclei, and brainstem relays integrate these inputs into a dynamic balance between opposing orexigenic and anorexigenic neurochemical effector pathways. Finally, we link these mechanistic insights to potential practical strategies for improving feed conversion, reducing metabolic disease, and enhancing resilience to environmental stressors. These strategies include dietary and microbiota-targeted interventions, receptor-level modulation, and the use of divergent genetic lines.