Effect of residual feed intake phenotype–nutritional treatment interaction on the growth performance, plasma metabolic variables and somatotropic axis gene expression of growing ewes

Abstract

This study aimed to evaluate the effect of residual feed intake (RFI) phenotype and nutritional treatment interaction on the growth performance, plasma variables and gene expression levels within the somatotropic axis. Growing ewes [n = 52, initial bodyweight (BW) = 17.5 ± 0.5 kg, 2 months of age] were offered ad libitum access to diets for 63 days and ranked based on RFI phenotype. Thirty ewes with the highest and lowest RFI values were selected and randomly assigned to three nutritional treatments based on dry matter intake (DMI), which are ad libitum (AL), low restriction (LR) and high restriction (HR) groups, respectively. Each nutritional treatment group included ewes with high (n = 5) and low RFI (n = 5) values. During nutritional treatment (from Day 64 to Day 138), plasma samples were obtained to measure metabolite and hormone concentrations. Tissues of the hypothalamus, pituitary, liver, and Longissimus dorsi muscle (LM) were harvested at the end of the experiment (Day 138) to measure the gene expression level within the somatotropic axis. Muscle growth hormone receptor mRNA abundance of low RFI ewes tended to be greater (P = 0.09) under AL feeding, but this difference was abolished by underfeeding (P > 0.10). Low RFI ewes under HR treatment showed slightly greater growth performance, which was accompanied with lower pituitary somatostain receptor 2 mRNA abundance (P < 0.05), plasma non-esterified fatty acid concentration (P < 0.05), and greater concentration of triglyceride (P < 0.05), compared with ewes classified as high RFI group. Our results suggested that ewes categorised as low RFI showed higher resistance to the condition of high feed restriction, which might be attributed to less intensity of fat mobilisation under negative energy balance. The mechanism underlying resistance to such feed restriction was presumably through action of somatostain receptor 2 and was potentially mediated by inhibitory effects of somatostatin on growth hormone release but not basal growth hormone secretion.