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Abstract
Castration is widely used in poultry and livestock to enhance fat metabolism and improve the flavor, tenderness and juiciness of meat. However, the genetic regulatory mechanism underlying castration consequences have not been clarified. To investigate the key metabolites affecting the quality of capons and the key regulatory mechanisms, Qingyuan partridge roosters were subjected to castration. Metabolic profiling was used to detect differential metabolites in the breast muscle of both capon and control groups. Additionally, an integrative analysis of transcriptomics and proteomics was conducted to explore the genetic regulation mechanisms influencing meat quality. The results indicated that the muscle fiber density and shear force of capons was lower than that of normal chickens, and the fat percentage of capon group (CAM) was higher than control group (COM). The expression of the metabolite inostine-5’-monophosphate (IMP) was lower in capons, and lipid metabolites (PC (10:0/10:0), PC (6:0/13:1), LPC 22:6, LPC 18:2, LPE 18:1, LPE 20:4) were higher in capons. Metabolic pathways were found to be a common signaling pathway in all omics. Glutamate-ammonia ligase (GLUL),acetyl-CoA carboxylase beta (ACACB),1-acylglycerol-3-phosphate O-acyltransferase 2 (AGPAT2),4-hydroxy-2-oxoglutarate aldolase 1 (HOGA1) and glutathione S-transferase alpha 2 (GSTA2) regulate the expression of citric acid, arachidonic acid, palmitic acid, isocitric acid, and betaine. These findings highlight the key mechanisms contributing to the meat quality differences between capons and normal chickens.
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