The objectives of this review are to investigate the quantitative, compositional, and structural differences of β-glucans and the functional effects of β-glucans on the intestinal health and growth of nursery pigs. Banning antibiotic feed supplementation increased the research demand for antibiotic alternatives to maintain the intestinal health and growth of nursery pigs. It has been proposed that β-glucans improve the growth efficiency of nursery pigs through positive impacts on their intestinal health. However, based on their structure and source, their impacts can be extensively different. β-glucans are non-starch polysaccharides found in the cell walls of yeast (Saccharomyces cerevisiae), bacteria, fungi (Basidiomycota), and cereal grains (mainly barley and oats). The total β-glucan content from cereal grains is much greater than that of microbial β-glucans. Cereal β-glucans may interfere with the positive effects of microbial β-glucans on the intestinal health of nursery pigs. Due to their structural differences, cereal β-glucans also cause digesta viscosity, decreasing feed digestion, and decreasing nutrient absorption in the GIT of nursery pigs. Specifically, cereal β-glucans are based on linear glucose molecules linked by β-(1,3)- and β-(1,4)-glycosidic bonds with relatively high water-soluble properties, whereas microbial β-glucans are largely linked with β-(1,3)- and β-(1,6)-glycosidic bonds possessing insoluble properties. From the meta-analysis, the weight gain and feed intake of nursery pigs increased by 7.6% and 5.3%, respectively, through the use of yeast β-glucans (from Saccharomyces cerevisiae), and increased by 11.6% and 6.9%, respectively, through the use of bacterial β-glucans (from Agrobacterium sp.), whereas the use of cereal β-glucans did not show consistent responses. The optimal use of yeast β-glucans (Saccharomyces cerevisiae) was 50 mg/kg in nursery pig diets based on a meta-analysis. Collectively, use of microbial β-glucans can improve the intestinal health of nursery pigs, enhancing immune conditions, whereas the benefits of cereal β-glucans on intestinal health were not consistent.

The objective of this review is to investigate the impacts of aflatoxins, particularly aflatoxin B1 (AFB₁), on intestinal microbiota, intestinal health, and growth performance in monogastric animals, primarily chickens and pigs, as well as dietary interventions to mitigate these effects. Aflatoxin B1 contamination in feeds disrupts intestinal microbiota, induces immune responses and oxidative damage, increases antioxidant activity, and impairs jejunal cell viability, barrier function, and morphology in the small intestine. These changes compromise nutrient digestion and reduce growth performance in animals. The negative impact of AFB₁ on the % change in average daily gain (ΔADG) of chickens and pigs was estimated based on meta-analysis: ΔADG (%)_chicken = −0.13 × AFB₁ intake per body weight (ng/g·d) and ΔADG (%)_pig = −0.74 × AFB₁ intake per body weight (µg/kg·d), indicating that increasing AFB₁ contamination linearly reduces the growth of animals. To mitigate the harmful impacts of AFB₁, various dietary strategies have been effective. Mycotoxin-detoxifying agents include mycotoxin-adsorbing agents, such as clay and yeast cell wall compounds, binding to AFB₁ and mycotoxin-biotransforming agents, such as specific strains of Bacillus subtilis and mycotoxin-degrading enzyme, degrading AFB₁ into non-toxic metabolites such as aflatoxin D1. Multiple mycotoxin-detoxifying agents are often combined and used together to improve the intestinal health and growth of chickens and pigs fed AFB₁-contaminated feeds. In summary, AFB₁ negatively impacts intestinal microbiota, induces immune responses and oxidative stress, disrupts intestinal morphology, and impairs nutrient digestion in the small intestine, leading to reduced growth performance. Supplementing multi-component mycotoxin-detoxifying agents in feeds could effectively adsorb and degrade AFB₁ co-contaminated with other mycotoxins prior to its absorption in the small intestine, preventing its negative impacts on the intestinal health and growth performance of chickens and pigs.

The objectives of this review are to investigate how benzoic acid can mitigate the negative effects of weaning stress, improve the intestinal microbiota, intestinal health, and growth of nursery pigs, determine the optimal dose level of benzoic acid for the growth rate in nursery pigs, and compare the efficacy of benzoic acid and other acids in pig feeds. After weaning, pigs are exposed to less lactose and solid feed with high acid-binding capacity at infrequent intervals, causing an increase in digesta pH, reducing protein digestion, and increasing ammonia-producing bacteria in the stomach. Benzoic acid supplementation has improved the intestinal health and growth of nursery pigs through its antimicrobial properties and pH reduction in the digesta. The positive modulation of luminal microbiota in the small intestine of pigs by benzoic acid improves intestinal morphology and enhances nutrient utilization, especially nitrogen, of nursery pigs. Benzoic acid supplementation of up to 1% in feeds also increases hippuric acid contents in the urine of nursery pigs, decreasing urinary pH, which is related to ammonia emission and barn conditions in intensive pig production. Supported by the beneficial impacts of benzoic acid, the growth performance of nursery pigs was also improved. However, excessive benzoic acid (over 2.5% up to 5%) in feeds reduces the growth performance of nursery pigs. Thus, this review conducted a meta-analysis of the results from 16 papers to determine the optimal dose level of benzoic acid for body weight gain of nursery pigs, which was found to be 0.60%. The efficacy of benzoic acid was similar to that of other organic acids, including citric acid, fumaric acid, formic acid, and formate salts. Collectively, benzoic acid supplementation can positively modulate the luminal and mucosal microbiota in the small intestine, increase nutrient utilization and intestinal health, decrease urinary pH, and improve the growth performance of nursery pigs.

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 [(e^lnRR − 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.