This study was to determine the effects of dietary emodin (ED) on the intestinal mucosal barrier, nuclear factor kappa-B (NF-κB) pathways, and gut microbial flora in lipopolysaccharide (LPS)-induced piglets. Twenty-four weaned piglets were chosen and 4 treatments were created by randomly distributing piglets into CON, ED, LPS, and ED_LPS groups. Experiments were done in a 2 × 2 factorial arrangement and maintained for 21d. Dietary treatment (a basal diet or 300mg/kg ED) and immunological challenge (LPS or sterile saline) were 2 major factors. Intraperitoneal injections of LPS or sterilized saline were given to piglets on d 21. Six hours after the LPS challenge, all piglets were euthanized for sample collection and analysis. The results showed that piglets of the ED_LPS group had higher (P < 0.05) villus height to crypt depth ratio (VCR), and lower (P < 0.05) plasma D-lactate and diamine oxidase (DAO) than the LPS group. Furthermore, ED inhibited (P < 0.05) the decrease of glutathione peroxidase (GSH-Px) and catalase (CAT) activities and increase of malonaldehyde level (P < 0.05) in jejunal mucosa induced by LPS. The mRNA levels of pro-inflammatory cytokine genes (IL-6, IL-1β, and TNF-α) were significantly reduced (P < 0.05), and the mRNA levels of antioxidant enzyme genes (GPX-1, SOD2 and CAT), as well as protein and mRNA levels of tight junction proteins (occludin, claudin-1, and ZO-1), were also significantly increased (P < 0.05) by ED addition in LPS-induced piglets. Meanwhile, ED supplementation significantly decreased the LPS-induced protein levels of cyclooxygenase-2 and phosphorylation levels of NF-κB p65 and IκBα in jejunal mucosa. Emodin had a significant effect on the composition of gut microbial flora at various taxonomic positions as indicated by 16S RNA sequencing. The acetic acid, isobutyric acid, valeric acid, and isovaleric acid concentrations in the cecum were also increased by ED addition in pigs (P < 0.05). Furthermore, the correlation analysis revealed that some intestinal microbiota had a potential relationship with jejunal VCR, plasma D-lactate and DAO, jejunal mucosa GSH-Px and CAT activity, and cecal short-chain fatty acid concentration. These data suggest that ED is effective in alleviating LPS-induced intestinal mucosal barrier injury by modulating gut microbiota in piglets.

Intensive production can cause immunological stress in commercial broilers. Chlorogenic acid (CGA) regulates the intestinal microbiota, barrier function, and immune function in chickens. As complex interrelations regulate the dynamic interplay between gut microbiota, the host, and diverse health outcomes, the aim of this study was to elucidate the immunoregulatory mechanisms of CGA using multi-omics approaches. A total of 240 one-day-old male broilers were assigned to a 2 × 2 factorial design with 2 CGA levels (0 or 500 mg/kg) either with or without dexamethasone (DEX) injection for a 21-day experimental period. Therefore, there were 4 dietary treatments: control, DEX, CGA, and DEX + CGA, with 6 replicates per treatment. CGA supplementation improved (P< 0.05) growth performance, jejunal morphology, jejunal barrier function, and immune function in DEX-treated broilers. Moreover, in DEX + CGA-treated broilers, the increase in gut microbiome diversity (P< 0.05) was consistent with a change in taxonomic composition, especially in the Clostridiales vadin BB60_group. Additionally, the levels of short-chain fatty acids increased remarkably (P< 0.01) after CGA supplementation. This was consistent with the Kyoto Encyclopedia of Genes and Genomes analysis results that the "pyruvate fermentation to butanoate" pathway was more enriched (P< 0.01) in the DEX + CGA group than in the DEX group. Proteomics revealed that CGA treatment increased the expression of several health-promoting proteins, thymosin beta (TMSB4X) and legumain (LGMN), which were verified by multiple reaction monitoring. Metabolomics revealed that CGA treatment increased the expression of health-promoting metabolites (2,4-dihydroxy benzoic acid and homogentisic acid). Proteomic and metabolic analyses showed that CGA treatment regulated the peroxisome proliferator-activated receptor (PPAR) and mitogen-activated protein kinase (MAPK) pathways. Western blotting results support these findings. Pearson’s correlation analyses showed correlations (P< 0.01) between altered immune function, jejunal barrier function, different microbiota, proteins, and metabolites parameters. Overall, our data indicate that CGA treatment increased growth performance and improved the immunological functions of DEX-treated broilers by regulating gut microbiota and the PPAR and MAPK pathways. The results offer novel insights into a CGA-mediated improvement in immune function and intestinal health.

The quality of pork determines consumers' purchase intention, which directly affects the economic value of pork. Minimizing the proportion of inferior pork and producing high quality pork are the ultimate goals of the pig industry. Muscle energy metabolism, serving as a regulative hub in organism energy expenditure and storage as a fat deposit, is compatible with myofiber type composition, affecting meat color, intramuscular fat content, tenderness, pH values and drip loss. Increasing data illustrate that dietary nutrients and bioactive ingredients affect muscle energy metabolism, white adipose browning and fat distribution, and myofiber type composition in humans, and rodents. Recently, some studies have shown that modulating muscle energy metabolism and lipid accumulation through nutritional approaches could effectively improve meat quality. This article reviews the progress and development in this field, and specifically discusses the impacts of dietary supply of amino acids, lipids, and gut microbiota as well as maternal nutrition on skeletal muscle energy metabolism, lipid accumulation and meat quality of pigs, so as to provide comprehensive overview with respect to effective avenues for improving meat quality.

This study investigated the effects of using soy protein concentrate (SPC) to replace animal protein supplements on mucosa-associated microbiota, intestinal health, and growth performance of nursery pigs. Fifty-six newly weaned pigs (BW = 6.4 ± 0.6 kg) were allotted to 5 treatments in a randomized complete block design. Pigs were fed for 35 d in 3 phases (P; 1, 2, 3) for 10, 12, 13 d, respectively. Dietary treatments were: (1) basal diet with fish meal (P1: 4%, P2: 2%, and P3: 1%), poultry meal (P1: 10%, P2: 8%, and P3: 4%), and blood plasma (P1: 4%, P2: 2%, and P3: 1%), where SPC replacing none (NC); (2) basal diet with SPC replacing fish meal (RFM); (3) basal diet with SPC replacing poultry meal (RPM); (4) basal diet with SPC replacing blood plasma (RBP); and (5) basal diet with SPC replacing all animal protein supplements (PC). Growth performance was recorded for each phase. Pigs were euthanized on d 35 to collect jejunal mucosa and tissue to evaluate intestinal health and microbiota, and ileal digesta to measure apparent ileal digestibility (AID) of nutrients. Data were analyzed using the MIXED procedure of SAS. Overall, RFM, RPM, and RBP did not affect growth performance, whereas PC decreased (P < 0.05) ADG and ADFI. The RPM increased (P < 0.05) Prevotella stercorea and decreased (P < 0.05) Helicobacter rappini. The PC decreased (P < 0.05) H. rappini, whilst increasing (P < 0.05) Prevotella copri, Propionibacterium acnes, and Pelomonas aquatica. The RFM tended to increase (P = 0.096) immunoglobulin A in the jejunum. The PC tended to decrease (P = 0.078) jejunal crypt cell proliferation. There were no differences in the villus height, AID of nutrients, intestinal inflammation, and intestinal oxidative stress among treatments. In conclusion, SPC can replace fish meal, poultry meal, or blood plasma individually without affecting growth performance and intestinal health, and AID of nutrients of nursery pigs. Particularly SPC replacing poultry meal benefitted intestinal health by reducing H. rappini and increasing P. stercorea. However, SPC replacing all three animal protein supplements reduced growth of nursery pigs mainly by reducing feed intake.

The objective of this study was to investigate the effects of dietary crude protein (CP) concentrations, grain types and arginine:lysine ratios on performance parameters of broiler chickens. The 2 × 2 × 2 factorial array of dietary treatments harnessed two CP concentrations (210 and 170 g/kg), two feed grains (wheat and sorghum), and two arginine:lysine ratios (104 and 110). Each dietary treatment was offered to 7 replicates of 14 birds per floor pen, a total of 784 off-sex male, Ross 308 broilers, from 14 to 35 d post-hatch. The dietary CP reduction compromised weight gain by 10.0% (2078 versus 2310 g/bird) as a main effect and FCR by 7.51% (1.474 versus 1.371), subject to an interaction. In a three-way interaction (P= 0.008), expanded arginine:lysine ratios improved FCR by 2.30% in 170 g/kg CP, sorghum-based diets but compromised FCR by 2.12% in corresponding wheat-based diets. Sorghum was the more suitable feed grain in reduced-CP diets as sorghum generated significant advantages in weight gain of 7.59% (2154 versus 2002 g/kg) and FCR of 6.94% (1.421 versus 1.527) in birds offered 170 g/kg CP diets. Both dietary CP and feed grain generated significant and divergent impacts in apparent ileal digestibility coefficients for the majority of 16 assessed amino acids. Dietary CP reductions increased non-bound amino acid inclusions (NBAA) in wheat-based diets (48.96 versus 9.80 g/kg) to a greater extent than sorghum-based diets (35.3 versus 9.50 g/kg) and increasing dietary NBAA inclusions were linearly associated with compromised weight gain (r＝-0.834; P < 0.001) and FCR (r = 0.862; P < 0.001). Increasing ratios of free arginine to lysine plasma concentrations were linearly (r＝-0.466; P = 0.004) related to improvements in FCR. The implications of the observed outcomes are discussed and possible explanations are advanced.

The objective of this study was to reveal the effect of rumen degradable starch (RDS) on bile acid metabolism and liver transcription in dairy goats using metabolomics and transcriptomics. Eighteen Guanzhong dairy goats of a similar weight and production level (body weight = 45.8 ± 1.54kg, milk yield = 1.75 ± 0.08kg, and second parity) were randomly assigned to 3 treatment groups where they were fed a low RDS (LRDS, RDS = 20.52% DM) diet, medium RDS (MRDS, RDS = 22.15% DM) diet, or high RDS (HRDS, RDS = 24.88% DM) diet, respectively. The goats were fed with the experimental diets for 5 weeks. On the last day of the experiment, all goats were anesthetized, and peripheral blood and liver tissue samples were collected. The peripheral blood samples were used in metabolomic analysis and white blood cell (WBC) count, whereas the liver tissue samples were used in transcriptomic analysis. Based on the metabolomics results, the relative abundances of primary bile acids in the peripheral blood were significantly reduced in the group that was fed the HRDS diet (P < 0.05). The WBC count was significantly increased in the HRDS group compared with that in the LRDS and MRDS groups (P < 0.01), indicating that there was inflammation in the HRDS group. Transcriptomic analysis showed that 4 genes related to bile acid secretion (genes: MDR1, RXRα, AE2, SULT2A1) were significantly downregulated in the HRDS group. In addition, genes related to the immune response were upregulated in the HRDS group, suggesting the HRDS diet induced a hepatic inflammatory response mediated by lipopolysaccharides (LPS) (gene: LBP), activated the Toll-like receptor 4 binding (genes: S100A8, S100A9) and the NF-kappa B signaling pathway (genes: LOC106503980, LOC108638497, CD40, LOC102180880, LOC102170970, LOC102175177, LBP, LOC102168903, LOC102185461, LY96 and CXCL8), triggered inflammation and complement responses (genes: C1QB, C1QC, and CFD). The HRDS diet induced a hepatic inflammatory response may be mediated by activating the Toll-like receptor 4 binding and NF-kappa B signaling pathway after free LPS entered the liver. The changes of bile acids profile in blood and the downregulation of 4 key genes (MDR1, RXRα, AE2, SULT2A1) involved in bile secretion in liver are probably related to liver inflammation.

The rapid accumulation of organic acids, particularly lactate, has been suggested as the main cause of ruminal acidosis (RA) for ruminants fed high-concentrate diets. Previous research has shown that a gradual shift from low-to high-concentrate diets within 4 to 5 weeks effectively reduces the risk for RA. However, the mechanisms remain unknown. In this study, 20 goats were randomly allocated into four groups (n = 5) and fed with a diet containing a weekly increasing concentrate portion of 20%, 40%, 60%, and 80% over 28d. At d 7, 14, 21, and 28, one group (named C20, C40, C60, and C80 according to the last concentrate level that they received) was killed and the ruminal microbiome was collected. Ruminal acidosis was not detected in any of the goats during the experiment. Nonetheless, ruminal pH dropped sharply from 6.2 to 5.7 (P < 0.05) when dietary concentrate increased from 40% to 60%. A combined metagenome and metatranscriptome sequencing approach identified that this was linked to a sharp decrease in the abundance and expression of genes encoding nicotinamide adenine dinucleotide (NAD)-dependent lactate dehydrogenase (nLDH), catalyzing the enzymatic conversion of pyruvate to lactate (P < 0.01), whereas the expression of two genes encoding NAD-independent lactate dehydrogenase (iLDH), catalyzing lactate oxidation to pyruvate, showed no significant concomitant change. Abundance and expression alterations for nLDH- and iLDH-encoding genes were attributable to bacteria from Clostridiales and Bacteroidales, respectively. By analyzing the gene profiles of 9 metagenome bins (MAG) with nLDH-encoding genes and 5 MAG with iLDH-encoding genes, we identified primary and secondary active transporters as being the major types of sugar transporter for lactate-producing bacteria (LPB) and lactate-utilizing bacteria (LUB), respectively. Furthermore, more adenosine triphosphate was required for the phosphorylation of sugars to initiate their catabolic pathways in LPB compared to LUB. Thus, the low dependence of sugar transport systems and catabolic pathways on primary energy sources supports the acid tolerance of LUB from Bacteroidales. It favors ruminal lactate utilization during the adaptation of goats to a high-concentrate diet. This finding has valuable implications for the development of measures to prevent RA.

Endogenous protein leaving the ileum largely consists of accrued mucins from the upper gastrointestinal tract (GIT) that had resisted digestion. The amounts released rely on their mucosal generation during enteral feeding which vary with age as well as diet. These digestion resistant proteins of endogenous origin continue to be unavailable in the large intestine, whereas those of dietary origin provide amino acids that largely support the existing microbial population while denying limited amounts for absorption. Other mucins pre-exist within the large intestine as two layers at the lumen surface. A loose layer harboring a diverse microbial population is superimposed on the unstirred water layer (USWL) which simultaneously acts as an obstacle to microbes at the loose layer while performing as a molecular sieve for nutrients. The USWL is formed through interplay between enterocyte and goblet cells; however, the basis for presence of the loose layer is elusive. Large intestinal fermentation predominates within the colon of swine, whereas fowl employ their ceca. Motility within the colon of swine segregates fine materials into haustrae out-pocketings that parallel their placement within the ceca of fowl. Viscous mucins from small intestinal endogenous losses may envelop microbes within the large intestinal lumen to present successive adherents on the USWL that assemble its loose layer. The loose layer continually functions as a microbial reservoir in support of lumen fermentation. Microbial catabolism of mucin within the loose layer is known to be slow, but its proximity to the enterocyte is of advantage to enterocyte absorption with by-product amino acids fostering the USWL.

The emergence of safe and functional eggs for consumer acceptance has gained focus. The production of carotenoid-enriched eggs has received attention due to its multifunctional biological properties. Nutritional modification of laying hens' diet can be a strategy to produce such eggs. This review presents the chemistry of carotenoids in nature and eggs, the accumulation process of carotenoids into eggs, and the functions of carotenoids in eggs. Our findings showed that carotenoids can be deposited into the egg and contribute to improving its nutritive value. The biosynthesis, chemical structure, and metabolism pathways of carotenoids lead to the deposition of carotenoids into eggs in their original or metabolized forms. Also, some factors modulate the efficiency of carotenoids in fowls before accumulation into eggs. Carotenoid-enriched eggs may be promising, ensuring the availability of highly nutritive eggs. However, further studies are still needed to comprehend the full metabolism process and the extensive functions of carotenoids in eggs.