The present study was conducted to test the hypothesis that low concentrations of coated ZnO, as a substitute for a high concentration of ZnO (2250 mg Zn/kg), could improve intestinal immunity function and regulate microbiota composition, thus alleviating the incidence of diarrhoea in weaned piglets. A total of eighty-four cross-bred piglets, weaned at an age of 28 (sem 1) d, were allocated randomly, on the basis of average initial body weight (7·72 (sem 0·65) kg), to seven treatment groups as follows: a 250 mg Zn (ZnO)/kg group (low Zn; LZ) and a 2250 mg Zn (ZnO)/kg group (high Zn; HZ) that were offered diets containing ZnO at 250 and 2250 mg Zn/kg, respectively; and five experimental groups in which coated ZnO was added at 250, 380, 570, 760 and 1140 mg Zn/kg basal diet, respectively. The trial lasted 2 weeks. The results indicated that, compared with LZ treatment, supplementation with coated ZnO at 380 or 570 mg Zn/kg reduced (P< 0·05) diarrhoea index, increased (P< 0·05) duodenal villus height and the ratio of villus height:crypt depth, up-regulated (P< 0·05) the gene expression of insulin-like growth factor 1, zonula occludens protein-1, occludin, IL-10 and transforming growth factor β1, and elevated (P< 0·05) secretory IgA concentration in the jejunal mucosa. Microbiota richness and the Shannon diversity index were also decreased (P< 0·05). Furthermore, piglets in the group fed coated ZnO at 380 or 570 mg Zn/kg did not differ from those in the HZ-fed group in relation to the aforementioned parameters. Collectively, a low concentration of coated ZnO (380 or 570 mg Zn/kg) can alleviate the incidence of diarrhoea by promoting intestinal development, protecting the intestinal mucosal barrier from damage, stimulating the mucosal immune system and regulating the microbiota composition.

Growth retardation reduces the incomes of livestock farming. However, effective nutritional interventions to promote compensatory growth and the mechanisms involving digestive tract microbiomes and transcripts have yet to be elucidated. In this study, Qinghai plateau yaks, which frequently suffer from growth retardation due to malnutrition, were used as an experimental model. Young growth-retarded yaks were pastured (GRP), fed basal ration (GRB), fed basal ration addition cysteamine hydrochloride (CSH; GRBC) or active dry yeast (ADY; GRBY). Another group of growth normal yak was pastured as a positive control (GNP). After 60-day nutritional interventions, the results showed that the average daily gain (ADG) of GRB was similar to the level of GNP, and the growth rates of GRBC and GRBY were significantly higher than the level of GNP (P < 0.05). Basal rations addition of CSH or ADY either improved the serum biochemical indexes, decreased serum LPS concentration, facilitated ruminal epithelium development and volatile fatty acids (VFA) fermentation of growth-retarded yaks. Comparative transcriptome in rumen epithelium between growth-retarded and normal yaks identified the differentially expressed genes mainly enriched in immune system, digestive system, extracellular matrix and cell adhesion pathways. CSH addition and ADY addition in basal rations upregulated ruminal VFA absorption (SLC26A3, PAT1, MCT1) and cell junction (CLDN1, CDH1, OCLN) gene expression, and downregulated complement system (C2, C7) gene expression in the growth-retarded yaks. 16S rDNA results showed that CSH addition and ADY addition in basal rations increased the rumen beneficial bacterial populations (Prevotella_1, Butyrivibrio_2, Fibrobacter) of growth-retarded yaks. The correlation analysis identified that ruminal VFAs and beneficial bacteria abundance were significantly positively correlated with cell junction and VFA absorption gene expressions and negatively correlated with complement system gene expressions on the ruminal epithelium. Therefore, CSH addition and ADY addition in basal rations promoted rumen health and body growth of growth-retarded yaks, of which basal ration addition of ADY had the optimal growth-promoting effects. These results suggested that improving nutrition and probiotics addition is a more effective method to improve growth retardation caused by gastrointestinal function deficiencies.

In the body of an animal, glutamine is a plentiful and very useful amino acid. Glutamine consumption in the body of animals in normal or disease conditions is the same or higher than the glucose. Many in vivo as well as in vitro experiments have been conducted to evaluate the importance of glutamine. Glutamine is a valuable nutrient for the proliferation of the lymphocytes. It also plays a crucial role in the production of cytokines, macrophages, phagocytic, and neutrophil to kill the bacteria. Most of the metabolic organs like the liver, gut, and skeletal muscles control the circulation and availability secretion of glutamine. In catabolic and hypercatabolic conditions, glutamine can turn out to be essential and plays a vital role in metabolism; however, availability may be compromised due to the impairment of homeostasis in the inter-tissue metabolism of amino acids. This is why the supplementation of glutamine is commonly used in clinical nutrition and is especially recommended to immune-suppressed persons. Despite this, in catabolic and hyper-catabolic conditions, it is challenging due to the amino acid concentration in plasma/bloodstream and glutamine should be provided via either the oral, enteral or parenteral route. However, the effect of glutamine as an immune-based supplement has been previously recognized as many research studies conducted in vivo and in-vitro evaluated the beneficial effects of glutamine. Hence, the present study delivers a combined review of glutamine metabolism in essential organs of the cell immune system. In this review, we have also reviewed the metabolism and action of glutamine and crucial problems due to glutamine supplementation in catabolic conditions.

Epizootic rabbit enteropathy (ERE) is reproduced successfully in the present study by feeding rabbits a low-fibre diet, and high-throughput sequencing and quantitative real-time PCR (qPCR) analysis were applied to examine the microbial variations in the stomach, small intestine and caecum. The evenness was disturbed and the richness was decreased in the ERE groups. When the rabbits were suffering from ERE, the abundance of the Firmicutes was decreased in three parts of the digestive tract, whereas the Proteobacteria was increased in the stomach and caecum, the Bacteroidetes and Verrucomicrobia were increased in the small intestine. Correlation analysis showed that the reduced concentrations of TVFA and butyrate in the caeca of the ERE group were attributed to the decreased abundances of genera such as Lactobacillus, Alistipes and other fibrolytic bacteria and butyrate- producing bacteria such as Eubacterium and Faecalibacterium. It is concluded that, in terms of microorganisms, the overgrowth of Bacteroides fragilis, Clostridium perfringen, Enterobacter sakazakii and Akkermansia muciniphila and inhibition of Bifidobacterium spp. and Butyrivibrio fibrisolvens in the stomach, small intestine and caecum resulted in a decrease in butyrate yield, leading to the incidence of ERE, and the probability of developing ERE could be manipulated by adjusting the dietary fibre level.