Impact of Dietary β-Mannans on the Intestinal-Nutritional Interface and Growth Performance of Chickens and Pigs: Challenges and Strategies via Exogenous β-Mannanase Based on Meta-Analysis

The objectives of this review were to elucidate the physiological challenges induced by dietary β-mannans and to review the underlying modes of action of exogenous β-mannanase on the intestinal microbiota, intestinal health, nutrient utilization, and growth performance of chickens and pigs. The highly branched structure of β-mannans, particularly those with a high proportion of soluble β-mannans, can increase digesta viscosity and negatively modulate intestinal health by increasing the abundance of opportunistic pathogenic microbiota and reducing the abundance of bacteria associated with favorable metabolic outputs, such as short-chain fatty acids, in the small intestine. Furthermore, intact β-mannans are recognized by the intestinal immune system due to structural similarity to pathogen-associated molecular patterns in the small intestine, triggering unnecessary inflammatory responses. These combined factors damage intestinal structure and tight junction proteins and reduce nutrient utilization and growth performance in monogastric animals. Dietary β-mannanase supplementation can mitigate these challenges by breaking down the β-mannan structure. This enzymatic action reduces digesta viscosity and increases prebiotic manno-oligosaccharides in the small intestine, which positively modulates the diversity and abundance of intestinal microbiota, reduces immune responses, enhances intestinal barrier function and structure, and increases nutrient utilization. These gastrointestinal improvements enhance growth performance. Meta-analysis using a log response ratio scale (lnRR) showed that as dietary β-mannans increased, the mitigating effects of β-mannanase on intestinal health and growth performance of chickens became pronounced. When back-transformed to the percentage scale [(elnRR − 1) × 100], β-mannanase supplementation was estimated to reduce digesta viscosity in the small intestine by an average of 44.3% (slope on the log-scale = −0.584; 95% confidence interval: −65.0 to −11.3%; p < 0.05) and to increase average daily gain by an average of 5.23% (slope on the log-scale = 0.051; 95% confidence interval: 2.33 to 8.22%; p < 0.01) when dietary β-mannan content is 1% (DM basis). Further research, however, is warranted to refine model-derived estimates by considering variations in enzyme efficacy, non-standardized enzyme activity units, variable doses across studies, and the absence of a formal risk-of-bias assessment. In particular, the number of studies conducted in pigs was insufficient to allow meta-analysis, highlighting the need for further research to clarify β-mannanase efficacy across different dietary β-mannans. In conclusion, dietary β-mannanase serves as a valuable strategy that positively influences the intestinal microbiota, intestinal health, and nutrient utilization, thereby enhancing the growth performance of animals fed high β-mannan diets through the degradation of β-mannans.