Doha Mohamad Khalifeh, Gabriella Gulyás, Renáta Knop, Gebrehaweria K Reda, Gergő Kalló, Csaba Szabó, Éva Csösz, Levente Czeglédi
Feed intake determines nutrient utilization and production efficiency in poultry, yet hepatic mechanisms underlying responses to acute nutritional challenges remain insufficiently characterized. This study aimed to identify the liver proteins and pathways associated with feed intake regulation in Japanese quails (Coturnix japonica) subjected to different nutritional challenges. Eighteen 12-wk-old male quails (245.20 g ± 0.213) were housed individually and allocated to ad libitum control, 24 h feed-deprived, or 24 h low metabolizable energy groups (n = 6/group). The basal diet contained 18% crude protein and 12.13 MJ/kg energy, whereas the low-energy diet had 6.30 MJ/kg and 11.60% crude protein. Liver proteins were extracted, identified, quantified, combined with STRING-based functional analysis. In total, 856 proteins were identified, of which 563 met the filtering criteria. Compared with the control, the low-energy diet induced 85 differentially abundant proteins (DAPs) through increasing oxidative phosphorylation, fatty acid β-oxidation, mitochondrial substrate supply, and RNA-binding/translation, with decreased ER-Golgi trafficking, intracellular transport, and glycolysis-associated proteins. Feed deprivation yielded 81 DAPs by emphasizing mitochondrial respiratory chain assembly and oxidative phosphorylation, lipid oxidation, and detoxification, while suppressing ribosomal biogenesis, protein turnover, and fed-state metabolic processing. Direct comparison had 76 DAPs and revealed that low energy maintains active cytoplasmic translation/ribosome biogenesis and xenobiotic metabolism, while feed deprivation enriches carboxylic acid metabolism and mitochondrial protection against oxidative stress. Quail liver demonstrated distinct proteomic responses to energy reduction compared with complete feed withdrawal. Notably, oxidative phosphorylation and lipid utilization emerged as central adaptive mechanisms and potential biomarker pathways in response to nutritional stress.