Immunosaccharides such as β-glucans and fructooligosaccharide (FOS) strengthen the host’s immune responses. This study examined the influences of three levels of the β-1, 3 glucan-FOS combination on Red tilapia performance. Four diets were prepared: T0 as a control, while T0.5, T1, and T1.5 indicate the addition of β-1, 3 glucan-FOS mixture at 0.5%, 1%, and 1.5%, respectively. Then, 240 red Tilapia (Oreochromis niloticus x O. mossambicus) (weight 6.1 ± 0.07gm) were allocated into four groups, and every group was fed tested diets for 56 days. After the feeding trial, growth parameters, erythrogram profile, liver and kidney function testes, glucose, histopathological analysis, and gene expressions for antioxidants, catalase (CAT) and glutathione peroxidase (GPX) besides growth hormone (GH) and insulin-like growth factor 1 IGF1-related markers were assessed. Red tilapia fed T0.5, T1, and T1.5 exhibited consistent growth, survival rate, and homeostasis compared with the control group. Different supplement concentrations displayed varying levels of responses. The hepatorenal biomarkers (alanine transaminase (ALT = SGPT) and aspartate transaminase (AST = SGOT), alkaline phosphatase (ALP = ALK), urea, and creatinine) and glucose showed a significant reduction in the supplemented groups compared with the control, especially in the T1 and T1.5 groups. The intestinal morphometric study revealed that fish group fed on T1 represented the best result, whereas group T1.5, followed by group T0.5, was moderately treated, compared to the control. The real-time quantitative reverse transcription PCR (qRT-PCR) analysis displayed up-regulated expression of antioxidant and growth-correlated genes in the T1.5 groups. After 56 days, the β-1,3 glucan-FOS fed groups also exhibited an increase in survival rates compared to the control when challenged with a pathogenic Vibrio alginolyticus. Current findings suggest that inclusion of β-1,3 glucan-FOS in diets could enhance red tilapia biochemical parameters, growth, and protection against pathogenic V. alginolyticus infection.
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