A bird's-eye overview of molecular mechanisms regulating feed intake in chickens-with mammalian comparisons

Abstract

In recent decades, a lot of research has been conducted to explore poultry feeding behavior. However, up to now, the processes behind poultry feeding behavior remain poorly understood. The review generalizes modern expertise about the hormonal regulation of feeding behavior in chickens, focusing on signaling pathways mediated by insulin, leptin, and ghrelin and regulatory pathways with a cross-reference to mammals. This overview also summarizes state-of-the-art research devoted to hypothalamic neuropeptides that control feed intake and are prime candidates for predictors of feeding efficiency. Comparative analysis of the signaling pathways that mediate the feed intake regulation allowed us to conclude that there are major differences in the processes by which hormones influence specific neuropeptides and their contrasting roles in feed intake control between two vertebrate clades.

Keywords: Chicken; Feed intake; Hormone; Hypothalamus; Neuropeptide; Signaling pathway.

Fig. 1

AMPK/mTOR signaling pathway involved in regulation of feed intake in chickens (created with BioRender.com). AMP = adenosine monophosphate; ATP = adenosine triphosphate; LKB1 = liver kinase B1; AMPK = adenosine-monophosphate activated protein kinase; TSC1/TSC2 = tuberous sclerosis complex 1/2; Rheb = Ras homologue enriched in brain; mTOR = mammalian target of rapamycin; Raptor = regulatory-associated protein of mTOR; 4E-BP 1= 4E-binding protein 1; S6K = S6 kinase; Akt = protein kinase B; mTORC1 = mTOR complex 1; mTORC2 = mTOR complex 2; Rag = recombination-activating gene protein.

Fig. 2

Overview of leptin and insulin signaling pathways in the hypothalamus of chickens regulating neuropeptide genes (created with BioRender.com). The mechanism of insulin action in chickens may differ from what is known in mammals. FOXO1 signaling is significantly different between broilers and laying hens. In broilers, there is a slight phosphorylation of FOXO1 and no significant change in the expression of the anorexigenic neuropeptide POMC. While the opposite pattern is shown for laying hens, which is similar to the characteristic of mammals. Note: Pattern of a chicken indicates differences in signaling pathway compared to mammals. IR = insulin receptor; IRS-1 = insulin receptor substrate-1; JAK2 = Janus tyrosine kinase 2; PI3K = phosphoinositide 3-kinase; PIP2 = phosphatidylinositol 4,5-bisphosphate; PIP3 = phosphatidylinositol (3,4,5)-triphosphate; PDK-1 = phosphoinositide-dependent protein kinase-1; Akt = protein kinase B; mTORC1 = mammalian target of rapamycin complex 1; mTORC2 = target of rapamycin complex 2; S6K = S6 kinase; FOXO1 = forkhead box protein O1; STAT3 = signal transducer and transcription 3; POMC = proopiomelanocortin; SOCS3 = suppressor of cytokine signaling 3; NPY = neuropeptide Y.

Fig. 3

Detailed leptin signaling pathway in the hypothalamus of chickens (adapted from “Cytokine Signaling through the JAK-STAT Pathway”, by BioRender.com (2023). Retrieved from https://app.biorender.com/biorender-templates). The mechanism of leptin action in chickens may differ from what is known in mammals. In SOCS3-mediated inhibition of leptin signaling, chicken SOCS3 probably does not interact with p-Tyr986 in the intracellular domain of chicken LEPR, but directly binds to JAK2. In contrast to mammals, leptin is more likely to affect feeding behavior of chickens through the expression of the orexigenic neuropeptide NPY (but not AgRP), without affecting the expression of anorexigenic POMC. Note: The pattern of a chicken indicates differences in signaling pathway compared to mammals. LEPR = leptin receptor; JAK2 = Janus tyrosine kinase 2; STAT3 = signal transducer and transcription 3; SOCS3 = suppressor of cytokine signaling 3; NPY = neuropeptide Y.