Recent years have witnessed growing interest in the role of peptides in animal nutrition. Chemical, enzymatic, or microbial hydrolysis of proteins in animal by-products or plant-source feedstuffs before feeding is an attractive means of generating high-quality small or large peptides that have both nutritional and physiological or regulatory functions in livestock, poultry and fish. These peptides may also be formed from ingested proteins in the gastrointestinal tract, but the types of resultant peptides can vary greatly with the physiological conditions of the animals and the composition of the diets. In the small intestine, large peptides are hydrolyzed to small peptides, which are absorbed into enterocytes faster than free amino acids (AAs) to provide a more balanced pattern of AAs in the blood circulation. Some peptides of plant or animal sources also have antimicrobial, antioxidant, antihypertensive, and immunomodulatory activities. Those peptides which confer biological functions beyond their nutritional value are called bioactive peptides. They are usually 2–20 AA residues in length but may consist of >20 AA residues. Inclusion of some (e.g. 2–8%) animal-protein hydrolysates (e.g., porcine intestine, porcine mucosa, salmon viscera, or poultry tissue hydrolysates) or soybean protein hydrolysates in practical corn- and soybean meal-based diets can ensure desirable rates of growth performance and feed efficiency in weanling pigs, young calves, post-hatching poultry, and fish. Thus, protein hydrolysates hold promise in optimizing the nutrition of domestic and companion animals, as well as their health (particularly gut health) and well-being.

This article summarizes current experimental knowledge on the efficacy, possible mechanisms and feasibility in the application of phytogenic products as feed additives for food-producing animals. Phytogenic compounds comprise a wide range of plant-derived natural bioactive compounds and essential oils are a major group. Numerous studies have demonstrated that phytogenic compounds have a variety of functions, including antimicrobial/antiviral, antioxidative and anti-inflammation effects and improvement in the palatability of feed and gut development/health. However, the mechanisms underlying their functions are still largely unclear. In the past, there has been a lack of consistency in the results from both laboratory and field studies, largely due to the varied composition of products, dosages, purities and growing conditions of animals used. The minimal inhibitory concentration (MIC) of phytogenic compounds required for controlling enteric pathogens may not guarantee the best feed intake, balanced immunity of animals and cost-effectiveness in animal production. The lipophilic nature of photogenic compounds also presents a challenge in effective delivery to the animal gut and this can partially be resolved by microencapsulation and combination with other compounds (synergistic effect). Interestingly, the effects of photogenic compounds on anti-inflammation, gut chemosensing and possible disruption of bacterial quorum sensing could explain a certain number of studies with different animal species for the better production performance of animals that have received phytogenic feed additives. It is obvious that phytogenic compounds have good potential as an alternative to antibiotics in feed for food animal production and the combination of different phytogenic compounds appears to be an approach to improve the efficacy and safety of phytogenic compounds in the application. It is our expectation that the recent development of high-throughput and “omics” technologies can significantly advance the studies on the mechanisms underlying phytogenic compounds’ functions and, therefore, guide the effective use of the compounds.

Significance: Hydroxyproline is a structurally and physiologically important imino acid in animals. It is provided from diets and endogenous synthesis, and its conversion into glycine enhances the production of glutathione, DNA, heme, and protein. Furthermore, oxidation of hydroxyproline by hydroxyproline oxidase (OH-POX) plays an important role in cell antioxidative reactions, survival, and homeostasis. Understanding the mechanisms whereby hydroxyproline participates in metabolism and cell signaling can improve the nutrition and health of animals and humans. Recent Advances: Hydroxyproline is highly abundant in milk and is utilized for renal synthesis of glycine to support neonatal growth, development, and survival. The oxidation of hydroxyproline by mitochondrial OH-POX generates reactive oxygen species (ROS). Enhanced ROS production contributes to the regulation of oxidative defense, apoptosis, angiogenesis, tumorigenesis, hypoxic responses, and cell survival in animals. Critical Issues: Although dietary hydroxyproline enters the portal circulation, its utilization by the portal-drained viscera is unknown. Pathways for hydroxyproline metabolism and their regulation at the molecular, cellular, and whole-body levels remain to be defined. Furthermore, the mechanisms responsible for hydroxyproline-derived ROS and related metabolites to induce cell survival or apoptosis are unknown. Future Directions: Interorgan metabolism of hydroxyproline (including synthesis, catabolism, and flux) in animals must be quantified using isotope technologies. Efforts should also be directed toward studying dietary, hormonal, and epigenetic regulation of OH-POX expression at transcriptional and translational levels. Another emerging research need is to understand the roles of cellular redox and signaling networks involving both ROS and Δ ¹ -pyrroline-3-hydroxy-5-carboxylate in nutrition, health, and disease.

Statistical tables are an essential component of scientific papers and reports in biomedical and agricultural sciences. Measurements in these tables are summarized as mean ± SEM for each treatment group. Results from pairwise-comparison tests are often included using letter displays, in which treatment means that are not significantly different, are followed by a common letter. However, the traditional manual processes for computation and presentation of statistically significant outcomes in MS Word tables using a letter-based algorithm are tedious and prone to errors. Using the R package ‘Shiny’, we present a web-based program freely available online, at https://houssein-assaad.shinyapps.io/TwoWayANOVA/ . No download is required. The program is capable of rapidly generating publication-ready tables containing two-way analysis of variance (ANOVA) results. Additionally, the software can perform multiple comparisons of means using the Duncan, Student-Newman-Keuls, Tukey Kramer, Westfall, and Fisher’s least significant difference (LSD) tests. If the LSD test is selected, multiple methods (e.g., Bonferroni and Holm) are available for adjusting p-values. Significance statements resulting from all pairwise comparisons are included in the table using the popular letter display algorithm. With the application of our software, the procedures of ANOVA can be completed within seconds using a web-browser, preferably Mozilla Firefox or Google Chrome, and a few mouse clicks. To our awareness, none of the currently available commercial (e.g., Stata, SPSS and SAS) or open-source software (e.g., R and Python) can perform such a rapid task without advanced knowledge of the corresponding programming language. The new and user-friendly program described in this paper should help scientists perform statistical analysis and rapidly generate publication-ready MS-Word tables for two-way ANOVA. Our software is expected to facilitate research in agriculture, biomedicine, and other fields of life sciences.

The intestinal epithelium (IE) forms an indispensible barrier and interface between the intestinal interstitium and the luminal environment. The IE regulates water, ion and nutrient transport while providing a barrier against toxins, pathogens (bacteria, fungi and virus) and antigens. The apical intercellular tight junctions (TJ) are responsible for the paracellular barrier function and regulate trans-epithelial flux of ions and solutes between adjacent cells. Increased intestinal permeability caused by defects in the IE TJ barrier is considered an important pathogenic factor for the development of intestinal inflammation, diarrhea and malnutrition in humans and animals. In fact, defects in the IE TJ barrier allow increased antigenic penetration, resulting in an amplified inflammatory response in inflammatory bowel disease (IBD), necrotizing enterocolitis and ischemia-reperfusion injury. Conversely, the beneficial enhancement of the intestinal TJ barrier has been shown to resolve intestinal inflammation and apoptosis in both animal models of IBD and human IBD. Autophagy (self-eating mechanism) is an intracellular lysosome-dependent degradation and recycling pathway essential for cell survival and homeostasis. Dysregulated autophagy has been shown to be directly associated with many pathological processes, including IBD. Importantly, the crosstalk between IE TJ and autophagy has been revealed recently. We showed that autophagy enhanced IE TJ barrier function by increasing transepithelial resistance and reducing the paracellular permeability of small solutes and ions, which is, in part, by targeting claudin-2, a cation-selective, pore-forming, transmembrane TJ protein, for lysosome (autophagy)-mediated degradation. Interestingly, previous studies have shown that the inflamed intestinal mucosa in patients with active IBD has increased claudin-2 expression. In addition, inflammatory cytokines (for example, tumor necrosis factor-α, interleukin-6, interleukin-13, and interleukin-17) whose levels are increased in IBD patients cause an increase in claudin-2 expression and a claudin-2-dependent increase in TJ permeability. Thus, the role of claudin-2 in intestinal pathological processes has been attributed, in part, to the increase of intestinal TJ permeability. Claudin-2 represents a new therapeutic target in treating IBD, diarrhea and malnutrition in animals and humans.

Tributyrin (TBU) is a good dietary source of butyrate and has beneficial effects on the maintenance of normal intestinal morphology. The present study tested the hypothesis that dietary TBU supplementation could alleviate intestinal injury in the acetic acid (ACA)-induced porcine model of colitis. A total of eighteen piglets (25 d old) were randomly allocated to one of three treatment groups (control, ACA and TBU). The control and ACA groups were fed a basal diet and the TBU group was fed the basal diet supplemented with 0·1 % TBU. On day 15 of the trial, under anaesthesia, a soft catheter was inserted into the rectum of piglets (20–25 cm from the anus), followed by administration of either saline (control group) or ACA (10 ml of 10 % ACA solution for ACA and TBU groups). On day 22 of the trial, after venous blood samples were collected, piglets were killed to obtain mid-ileum and mid-colon mucosae. Compared with the control group, the ACA group exhibited an increase (P< 0·05) in lymphocyte counts, creatinine, PGE₂, and malondialdehyde concentrations and diamine oxidase and inducible NO synthase activities in the plasma and lymphocyte density in the colon and a decrease in insulin concentrations and glutathione peroxidase activity, ileal villus height:crypt depth ratios and goblet cell numbers in the colon. These adverse effects of ACA were attenuated by TBU supplementation. Moreover, TBU prevented the ACA-induced increase in caspase-3 levels while enhancing claudin-1 protein and epidermal growth factor receptor (EGFR) mRNA expression in the colonic mucosa. Collectively, these results indicate that dietary supplementation with 0·1 % TBU alleviates ACA-induced intestinal injury possibly by inhibiting apoptosis, promoting tight-junction formation and activating EGFR signalling.