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Porcine epidemic diarrhea virus (PEDV) has become a challenging problem in pig industry worldwide, causing significant profit losses. Lactobacillus rhamnosus GG (LGG) has been regarded as a safe probiotic strain and has been shown to exert protective effects on the intestinal dysfunction caused by PEDV. This study evaluated the effect of LGG on the gut health of lactating piglets challenged with PEDV. Fifteen piglets at 7 days of age were equally assigned into 3 groups (5 piglets per group): 1) control group (basal diet); 2) PEDV group: (basal diet + PEDV challenged); 3) LGG + PEDV group (basal diet + 3×10 9 CFU/pig/day LGG + PEDV). The trial lasted 11 days including 3 days of adaptation. The treatment with LGG was from D4 to D10. PEDV challenge was carried out on D8. PEDV infection disrupted the cell structure, undermined the integrity of the intestinal tract, and induced oxidative stress, and intestinal damage of piglets. Supplementation of LGG improved intestinal morphology, enhanced intestinal antioxidant capacity, and alleviated jejunal mucosal inflammation and lipid metabolism disorders in PEDV-infected piglets, which may be regulated by LGG by altering the expression of TNF signaling pathway, PPAR signaling pathway, and fat digestion and absorption pathway., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2024 Xu, Zhang, Wu, Zhang, Li, Li, Yu, Zhang, Zhao, Wang, Hou and Wu.)

Glycerol-lactate esters are energy supplements for exercise, but effects of trilactic glyceride (TLG) on intestinal function and hepatic metabolism are unknown. We found that dietary supplementation with 0.5% TLG to weanling piglets decreased plasma concentrations of low-density lipoprotein and gamma-glutamyl transferase but increased those of D-xylose and high-density lipoprotein. TLG supplementation enhanced mRNA levels for fatty acid synthase (FASN) and SLC27A2 in white adipose tissue; insulin receptor in duodenum; aquaporin-8 in ileum, jejunum and colon; aquaporin-10 in duodenum and ileum; nuclear factor like-2 in jejunum and colon; glutathione S -transferase and phosphoenolpyruvate carboxykinase-1 in intestines; and abundances of claudin-1 and occludin proteins. TLG supplementation decreased mRNA levels for: hepatic hormone-sensitive lipase E, lipoprotein lipase, FASN, insulin-like growth factor-binding protein-3, and SLC27A2; and intestinal lipoprotein lipase, FASN and NADPH oxidase. Furthermore, TLG supplementation enhanced abundances of genus Bifidobacterium, while reducing abundances of family Enterobacteriaceae in ileum, colon and cecum; jejunal caspase-3 protein and diarrhea rate. In conclusion, dietary supplementation with TLG modulated lipid metabolism and alleviated diarrhea by improving intestinal function and regulating intestinal microflora in piglets.

Here, the potential mechanisms of the protective effects of fish oil against LPS-induced liver injury in a piglet model were investigated by using RNA sequencing. Twenty-four piglets were used in a 2 × 2 factorial design, and the main factors included diet (5% corn oil or 5% fish oil) and immunological challenge (LPS or saline, on d 19). All piglets were slaughtered at 4 h after challenge, and liver samples were collected. Fish oil improved liver morphology and reduced TNF-α, IL-1β and IL-6 productions after LPS challenge. RNA sequencing analysis showed fish oil had significant effect on the expressions of genes involved in immune response during LPS-induced inflammation. Selected gene expression changes were validated using quantitative RT-PCR. Fish oil reduced the expressions of pro-inflammatory genes IL1R1, IL1RAP, CEBPB and CRP, and increased that of anti-inflammatory genes IL-18BP, NFKBIA, IFIT1, IFIT2 and ATF3. Moreover, fish oil restored the expressions of some lipid metabolism-related genes, such as ACAA1, ACACA, ACADS and ACADM, which were only decreased in pigs fed a corn oil diet after LPS challenge. Our RNA sequencing reveals novel gene-nutrient interactions following fish oil supplementation and evoked inflammation, which add to the current understanding of the benefits of n-3 polyunsaturated fatty acids against liver injury.

Oleum cinnamomi (OCM) is increasingly used as a feed additive in animal diets. The aim of this study was to investigate the effects of dietary supplementation with coated-OCM (cOCM) on the immunity and intestinal integrity of broiler chickens. A total of 396 one-day-old chicks were randomly assigned into six groups. The basal diets were supplemented with 50 mg/kg of flavomycin (positive control) as well as 0 (control), 50, 100, 200, and 300 mg/kg of cOCM. Compared with the control, both positive control and cOCM treatments did not improve the growth performance. Serum immunoglobulin (Ig) Y levels were decreased by flavomycin and 50 mg/kg of cOCM treatments (p < 0.05). Dietary cOCM decreased ileal secretory IgA contents at d 21 and commonly down-regulated duodenal and ileal mRNA expression of interleukin (IL)-1β and IL-8 at d 42 (p < 0.05). The 300 mg/kg of cOCM increased jejunal ratio of villus height to crypt depth and upregulated intestinal claudin-1 expression (p < 0.05). Jejunal (at d 21) and duodenal (at d 42) mucin-2 expression was up and downregulated by both 50 and 300 mg/kg of cOCM, respectively (p < 0.05). In conclusion, dietary cOCM addition helped to maintain noninflammatory states of humoral and mucosal immunity, and improved the intestinal integrity of broiler chickens., (© 2018 Japanese Society of Animal Science.)

The traditionally classified nutritionally non-essential amino acids are now known to be insufficiently synthesized for maximal growth and optimal health in piglets. This study determined the effects of dietary supplementation with an amino acid blend (AAB; glutamate:glutamine:glycine:arginine:N-acetylcysteine = 5:2:2:1:0.5) on piglet growth performance and intestinal functions. Sixteen piglets (24-day-old) were randomly assigned to a corn and soybean meal-based diet supplemented with 0.99% alanine (isonitrogenous control) or 1% AAB. On day 20 of the trial, blood and intestinal tissue samples were obtained from piglets. Compared with the control, AAB supplementation reduced (P < 0.05) diarrhoea incidence; plasma alanine aminotransferase and diamine oxidase activities; intestinal concentrations of hydrogen peroxide, malondialdehyde, and heat shock protein-70, and intestinal mRNA levels for interleukin-1β, interferon-γ, and chemokine (C-X-C motif) ligand-9; and the numbers of Enterobacterium family, Enterococcus genus and Clostridium coccoides in the colon digesta. Furthermore, AAB supplementation enhanced (P < 0.05): the plasma concentrations of serine, aspartate, glutamate, cysteine, tyrosine, phenylalanine, tryptophan, lysine, arginine, citrulline, ornithine, taurine, and γ-aminobutyric acid; intestinal villus height and surface area, villus height/crypt depth ratio, antioxidative enzyme activities, and mRNA levels for porcine β-defensin-1, sodium-independent amino acid transporters (b 0,+ AT and y + LAT1), aquaporin (AQP) 3, AQP8, AQP10, nuclear factor erythroid 2-related factor 2 and glutathione S-transferase omega-2, and protein abundances of AQP3, AQP4, claudin-1, occludin and myxovirus resistance 1; and the numbers of Bifidobacterium genus and Lactobacillus genus in the colon digesta. Collectively, these comprehensive results indicate that dietary AAB supplementation plays an important role in improving piglet growth and intestinal function.

α-Ketoglutarate (AKG) is an extensively used dietary supplement in human and animal nutrition. The aim of the present study was to investigate effects of dietary AKG supplementation on the energy status and anti-oxidative capacity in liver and intestinal mucosa of Cherry Valley ducks. A total of 80 1-day-old ducks were randomly assigned into four groups, in which ducks were fed basal diets supplemented with 0% (control), 0.5%, 1.0% and 1.5% AKG, respectively. Graded doses of AKG supplementation linearly decreased the ratio of adenosine monophosphate (AMP) to adenosine triphosphate (ATP) in the liver, but increased ATP content and adenylate energy charge (AEC) in a quadratic and linear manner, respectively (P < 0.05). Increasing dietary AKG supplemental levels produced linear positive responses in ATP content and AEC, and negative responses in AMP concentration, the ratio of AMP to ATP and total adenine nucleotide in the ileal mucosa (P < 0.05). All levels of dietary AKG reduced the production of jejunal hydrogen peroxide and hepatic malondialdehyde (P < 0.05). Hepatic and ileal messenger RNA expression of AMP kinase α-1 and hypoxia-inducible factor-1α were linearly up-regulated as dietary AKG supplemental levels increased (P < 0.05). In conclusion, dietary AKG supplementation linearly or quadratically enhanced hepatic and intestinal energy storage and anti-oxidative capacity of Cherry Valley ducks., (© 2017 Japanese Society of Animal Science.)

Background: Skeletal muscle undergoes rapid loss in response to inflammation. α-Ketoglutarate (AKG) has been reported to enhance muscle growth in piglets, but the underlying mechanisms are largely unknown., Objectives: This study tested the hypothesis that dietary AKG supplementation activates mechanistic target of rapamycin (mTOR) signaling and improves skeletal muscle energy metabolism in lipopolysaccharide (LPS)-challenged piglets., Methods: Forty-eight male piglets (Duroc × Landrace × Yorkshire) were weaned at 21 d of age to a corn- and soybean meal-based diet. After a 3-d period of adaptation, piglets with a mean weight of 7.21 kg were randomly assigned to control, LPS (intraperitoneal administration of 80 μg LPS/kg body weight on days 10, 12, 14, and 16), or LPS plus 1% dietary AKG (LPS+AKG) groups. On day 16, blood samples were collected from 8 piglets/group 3 h after LPS administration. On day 17, piglets were killed to obtain gastrocnemius muscle from 8 piglets/group for biochemical analysis., Results: Compared with the control group, LPS administration increased (P < 0.05) plasma concentrations of globulin (by 14%) and tumor necrosis factor α (by 59%) and the intramuscular ratio of AMP to ATP (by 93%) and abundance of phosphorylated acetyl-coenzyme A carboxylase (ACC) β protein (by 64%). Compared with the control group, LPS administration reduced (P < 0.05) weight gain (by 15%); plasma concentrations of glutamine (by 20%), glucose (by 23%), insulin, insulin-like growth factor I, and epidermal growth factor; intramuscular concentrations of glutamine (by 27%), ATP (by 12%), ADP (by 22%), and total adenine nucleotides; and intramuscular ratios of phosphorylated mTOR to total mTOR (by 38%) and of phosphorylated 70-kDa ribosomal protein S6 kinase (p70S6K) to total p70S6K (by 39%). These adverse effects of LPS were ameliorated (P < 0.05) by AKG supplementation., Conclusions: Dietary AKG supplementation activated mTOR signaling, inhibited ACC-β, and improved energy status in skeletal muscle of LPS-challenged piglets. These results provide a biochemical basis for the use of AKG to enhance piglet growth under inflammatory or practical postweaning conditions., (© 2016 American Society for Nutrition.)

L-arginine (Arg) is utilized via multiple pathways to synthesize protein and low-molecular-weight bioactive substances (e.g., nitric oxide, creatine, and polyamines) with enormous physiological importance. Furthermore, Arg regulates cell signaling pathways and gene expression to improve cardiovascular function, augment insulin sensitivity, enhance lean tissue mass, and reduce obesity in humans. Despite its versatile roles, the use of Arg as a dietary supplement is limited due to the lack of data to address concerns over its safety in humans. Data from animal studies are reviewed to assess arginine catabolism and the safety of long-term Arg supplementation. The arginase pathway was responsible for catabolism of 76-85 and 81-96 % Arg in extraintestinal tissues of pigs and rats, respectively. Dietary supplementation with Arg-HCl or the Arg base [315- and 630-mg Arg/(kg BW d) for 91 d] had no adverse effects on male or female pigs. Similarly, no safety issues were observed for male or female rats receiving supplementation with 1.8- and 3.6-g Arg/(kg BW d) for at least 91 d. Intravenous administration of Arg-HCl to gestating sheep at 81 and 180 mg Arg/(kg BW d) is safe for at least 82 and 40 d, respectively. Animals fed conventional diets can well tolerate large amounts of supplemental Arg [up to 630-mg Arg/(kg BW d) in pigs or 3.6-g Arg/(kg BW d) in rats] for 91 d, which are equivalent to 573-mg Arg/(kg BW d) for humans. Collectively, these results can help guide studies to determine the safety of long-term oral administration of Arg in humans.

Recent studies suggest an important role for L-homoarginine in cardiovascular, hepatic and neurological functions, as well as the regulation of glucose metabolism. However, little is known about whole-body L-homoarginine synthesis or its response to dietary L-arginine intake in animals. Four series of experiments were conducted to determine L-homoarginine synthesis and catabolism in pigs and rats. In Experiment 1, male and female pigs were fed a corn- and soybean meal-based diet supplemented with 0.0-2.42 % L-arginine-HCl. In Experiment 2, male and female rats were fed a casein-based diet, while receiving drinking water containing supplemental L-arginine-HCl to provide 0.0-3.6 g L-arginine/kg body-weight/day. In both experiments, urine collected from the animals for 24 h was analyzed for L-homoarginine and related metabolites. In Experiment 3, pigs and rats received a single oral dose of 1 or 10 mg L-homoarginine/kg body-weight, respectively, and their urine was collected for 24 h for analyses of L-homoarginine and related substances. In Experiment 4, slices of pig and rat tissues (including liver, brain, kidney, heart, and skeletal-muscle) were incubated for 1 h in Krebs-bicarbonate buffer containing 5 or 50 µM L-homoarginine. Our results indicated that: (a) animal tissues did not degrade L-homoarginine in the presence of physiological concentrations of other amino-acids; (b) 95-96 % of orally administered L-homoarginine was recovered in urine; (c) L-homoarginine was quantitatively a minor product of L-arginineg catabolism in the body; and (d) dietary L-arginine supplementation dose-dependently increased whole-body L-homoarginine synthesis. These novel findings provide a new framework for future studies of L-homoarginine metabolism and physiology in animals and humans.

Cinnamon is a traditional herb used for treatment of many human diseases. The most important chemical compounds of the essential oil are cinnamaldehyde and eugenol. Oleum cinnamomi (OCM, cinnamon oil) is increasingly used as a feed additive to animal diets. Beneficial effects of OCM in protecting tissues from inflammation and injury by endogenous and exogenous agents (such as hydrogen peroxide and lipopolysaccharide (LPS)) may result, in part, from its action on regulating amino acid metabolism in cells to favor the synthesis of glutathione (a major low-molecular-weight antioxidant) from cysteine, glycine and glutamate. In support of this notion, results of recent studies indicate that supplementing OCM (50 mg/kg diet) to a corn- and soybean meal-based diet for piglets weaned at 21 days of age enhances intestinal anti-oxidative capacity and reduces the incidence of diarrhea. Additionally, dietary supplementation with OCM ameliorates LPS-induced mucosal barrier dysfunction and mucosal damage in the small intestine. OCM holds great promise for protecting the gut from injury under conditions of inflammation, infections, and oxidative stress.

This study was conducted to determine effects of dietary supplementation with 1 % L-glutamine for 14 days on the abundance of intestinal bacteria and the activation of intestinal innate immunity in mice. The measured variables included (1) the abundance of Bacteroidetes, Firmicutes, Lactobacillus, Streptococcus and Bifidobacterium in the lumen of the small intestine; (2) the expression of toll-like receptors (TLRs), pro-inflammatory cytokines, and antibacterial substances secreted by Paneth cells and goblet cells in the jejunum, ileum and colon; and (3) the activation of TLR4-nuclear factor kappa B (NF-κB), mitogen-activated protein kinases (MAPK), and phosphoinositide-3-kinases (PI3K)/PI3K-protein kinase B (Akt) signaling pathways in the jejunum and ileum. In the jejunum, glutamine supplementation decreased the abundance of Firmicutes, while increased mRNA levels for antibacterial substances in association with the activation of NF-κB and PI3K-Akt pathways. In the ileum, glutamine supplementation induced a shift in the Firmicutes:Bacteroidetes ratio in favor of Bacteroidetes, and enhanced mRNA levels for Tlr4, pro-inflammatory cytokines, and antibacterial substances participating in NF-κB and JNK signaling pathways. These results indicate that the effects of glutamine on the intestine vary with its segments and compartments. Collectively, dietary glutamine supplementation of mice beneficially alters intestinal bacterial community and activates the innate immunity in the small intestine through NF-κB, MAPK and PI3K-Akt signaling pathways.

Pro-inflammatory cytokines play a critical role in many models of liver injury. In addition, aspartate (Asp) plays an important role in many biological and physiological processes including liver physiology. We hypothesized that Asp could alleviate lipopolysaccharide (LPS)-induced liver injury. Forty-eight weanling pigs were assigned to four treatments including: (1) non-challenged control; (2) LPS challenged control; (3) LPS+0.5% Asp; (4) LPS+1.0% Asp. After 20-d feeding with control (0% Asp), 0.5% or 1.0% Asp supplemented diets, pigs were injected with saline or LPS. At 4 (early phase) and 24 h (late phase) post-injection, blood and liver samples were obtained. Asp attenuated liver injury indicated by reduced serum aspartate aminotransferase activity and increased ratio of serum alanine aminotransferase and aspartate aminotransferase at 24 h, and less severe histological liver damage induced by LPS challenge at 4 or 24 h. In addition, Asp supplementation to LPS challenged pigs decreased mRNA expressions of tumor necrosis factor (TNF)-α and cyclooxygenase-2 linearly and quadratically at 4 h, and increased mRNA expressions of these pro-inflammatory mediators linearly and quadratically at 24 h. Finally, Asp decreased mRNA expression of toll-like receptor 4 (TLR4) signaling related genes (TLR4, myeloid differentiation factor 88, IL-1 receptor-associated kinase 1, TNF-α receptor-associated factor (6), nucleotide-binding oligomerization domain protein (NOD) signaling related genes (NOD1, NOD2 and receptor-interacting serine/threonine-protein kinase 2) and nuclear factor-κB p65 linearly or quadratically at 4 h. However, Asp increased mRNA expressions of these signaling molecules linearly or quadratically at 24 h. These results indicate that, at early and late phases of LPS challenge, Asp exerts opposite regulatory effects on mRNA expression of hepatic pro-inflammatory cytokines and TLR4 and NOD signalling related genes, and improves liver integrity., (Copyright © 2014 Elsevier Inc. All rights reserved.)

The present study was carried out to determine whether N-acetylcysteine (NAC) could modulate liver injury in a lipopolysaccharide (LPS)-challenged piglet model. For this purpose, eighteen piglets were randomly assigned to the control, LPS or NAC group. Piglets in the control and LPS groups were fed a basal diet, whereas those in the NAC group were fed the basal diet supplemented with 500 mg/kg NAC. On days 10, 13 and 20 of the trial, the LPS- and NAC-treated piglets were intraperitoneally administered LPS (100 μg/kg body weight), while the control group was administered the same volume of saline. On day 20 of the trial, blood samples were obtained 3 h after LPS or saline injection. On day 21, the piglets were killed to collect liver samples. Dietary NAC supplementation attenuated LPS-induced liver histomorphological abnormalities. Compared with the control group, in the LPS-challenged piglets, the activities of alanine aminotransferase and aspartate aminotransferase and the concentrations of H2O2, TNF-α, IL-6 and PGE2 were dramatically increased in the plasma and the activity of superoxide dismutase in the plasma and that of glutathione peroxidase in the liver were significantly decreased. The LPS challenge also increased the concentration of AMP and the ratio of AMP:ATP, but decreased adenylate energy charges and the levels of ATP and ADP. These adverse effects of the LPS challenge were ameliorated by NAC supplementation. Moreover, NAC inhibited the LPS-induced increases in the abundance of liver heat shock protein 70 and NF-κB proteins. In conclusion, these results suggest that dietary NAC supplementation alleviates LPS-induced liver injury by reducing the secretion of pro-inflammatory cytokines, increasing the antioxidative capacity and improving energy metabolism.

This study determined whether N-acetylcysteine (NAC) could affect intestinal redox status, proinflammatory cytokines, epidermal growth factor (EGF), EGF receptor (EGFR), Toll-like receptor-4 (TLR4), and aquaporin-8 in a lipopolysaccharide (LPS)-challenged piglet model. Eighteen piglets (35-day-old) were randomly allocated into one of the three treatments (control, LPS and NAC). The control and LPS groups were fed a basal diet, and the NAC group received the basal diet +500 mg/kg NAC. On days 10, 13, and 20 of the trial, the LPS- and NAC-treated piglets received intraperitoneal administration of LPS (100 μg/kg BW), whereas the control group received the same volume of saline. On days 10 and 20, venous blood samples were obtained at 3 h post LPS or saline injection. On day 21 of the trial, piglets were killed to obtain the intestinal mucosa for analysis. Compared with the control group, LPS challenge reduced (P < 0.05) the activities of superoxide dismutase, catalase, and glutathione peroxidase in jejunal mucosae, while increasing (P < 0.05) the concentrations of malondialdehyde, H2O2, O2 (·-) and the ratio of oxidized to reduced glutathione in jejunal mucosae, and concentrations of TNF-α, cortisol, interleukin-6, and prostaglandin E2 in both plasma and intestinal mucosae. These adverse effects of LPS were attenuated (P < 0.05) by NAC supplementation. Moreover, NAC prevented LPS-induced increases in abundances of intestinal HSP70 and NF-κB p65 proteins and TLR4 mRNA. NAC supplementation enhanced plasma EGF concentration and intestinal EGFR mRNA levels. Collectively, these results indicate that dietary NAC supplementation alleviates LPS-induced intestinal inflammation via regulating redox, EGF, and TLR4 signaling.

This study was conducted to determine the immunostimulatory effect of L-proline on inactivated vaccine immunized mice. Ninety-five female KM mice were randomly divided into five groups: (1) mice received dietary supplementation with 0.4% L-proline and immunized with inactivated vaccine (V-P group); (2) mice received dietary supplementation with 0.3% L-alanine (isonitrogenous control) and immunized with inactivated vaccine (V-A group, negative control); (3) mice were immunized with inactivated vaccine with oil adjuvant (V-O group, positive control); (4) mice were immunized with inactivated vaccine with aluminum hydroxide adjuvant (V-H group, positive control); (5) mice immunized with phosphate-buffered saline (control group). All mice were dead in the control group between 36 and 48 h post infection. Mice in the V-P group showed 100% protection after challenge with P. multocida serotype A (CQ2) at dose of 4.4 × 10(5) CFU (2LD50). Meanwhile, serum antibody titers in the V-P group were higher than those in the V-A group before infection and those in the V-A and V-O groups at 36 h post infection. Moreover, serum IL-1β levels in the V-P group were lower than those in V-O group. Furthermore, serum GSH-PX levels in the V-P group were higher than those in the V-A and V-O groups. Collectively, dietary proline supplementation confers beneficial immunostimulatory effects in inactivated P. multocida vaccine immunized mice.

This study was conducted to evaluate whether dietary supplementation with L-arginine (Arg) could attenuate Escherichia coli LPS-induced liver injury through the TLR4 signaling pathway in weaned pigs. Eighteen weaned pigs were allotted to three treatments: non-challenged control, LPS challenged control and LPS + 0.5% Arg. On d 18, pigs were injected with LPS at 100 µg/kg of body weight (BW) or sterile saline. Blood samples were obtained at 4 h post-injection. Pigs were then sacrificed for the collection of liver samples. Arg supplementation (0.5%) alleviated liver morphological impairment, including hepatocyte caryolysis, karyopycnosis and fibroblast proliferation induced by LPS challenge; it mitigated the increase of serum aspartate aminotransferase and alkaline phosphatase activities induced by LPS (P < 0.05); it prevented the increase of hepatic TNF-α, malondialdehyde contents and mast cell number induced by LPS administration (P < 0.05); and it attenuated the elevation of hepatic NF-κB and TLR4-positive cell percentages (P < 0.05). These results indicate that Arg supplementation has beneficial effects in attenuating hepatic morphological and functional injury induced by LPS challenge in piglets. Additionally, it is possible that the protective effects of Arg on the liver are associated with a decreased release of liver pro-inflammatory cytokines and free radicals through inhibiting TLR4 signaling.

Recent studies indicate extensive catabolism of amino acids (AA) by the portal-drained viscera (PDV) of pigs and humans. Because of ethical concerns over invasive surgical procedures on infants or adults, in vivo investigations are often performed with the pig which is both an agriculturally important livestock species and a widely used animal model for nutritional and physiological studies in humans. Here, we described a new technique for implanting chronic catheters into the portal vein, ileal mesenteric vein, and carotid artery to study AA metabolism in the PDV of young pigs. This method allowed for the reduction of surgery time by 1 h and measurements of the entry of dietary AA into the portal circulation. Using such an approach, we found that dietary supplementation with 100 mg/kg chitosan (a prebiotic and a polysaccharide not digested by animal cells) reduced oxygen consumption, as well as the net absorption of dietary AA into the portal vein, thereby enhancing their bioavailability for extraintestinal tissues. In contrast, opposite results were obtained with dietary supplementation of 12% pea-hull (containing 95% of fermentable nonstarch polysaccharide). Thus, this improved technique is useful to quantify in vivo absorption and metabolism of dietary AA in young pigs.

This study determined effects of dietary supplementation with L-arginine (Arg) or N-carbamylglutamate (NCG) on intestinal health and growth in early-weaned pigs. Eighty-four Landrace x Yorkshire pigs (average body weight of 5.56+/-0.07 kg; weaned at 21 days of age) were fed for 7 days one of the three isonitrogenous diets: (1) a corn- and soybean meal-based diet (CSM), (2) CSM+0.08% NCG (0.08%), and (3) CSM+0.6% Arg. There were four pens of pigs per diet (7 pigs/pen). At the end of a 7-day feeding period, six piglets were randomly selected from each treatment for tissue collections. Compared with the control group, Arg or NCG supplementation increased (P<0.05): (1) Arg concentrations in plasma, (2) small-intestinal growth, (3) villus height in duodenum, jejunum and ileum, (4) crypt depth in jejunum and ileum, (5) goblet cell counts in intestinal mucosae, and (6) whole-body weight gain in pigs. Real-time polymerase chain reaction and western blotting analyses revealed that both mRNA and protein levels for heat shock protein-70 (HSP70) were higher (P<0.05) in the intestinal mucosae of Arg- or NCG-supplemented pigs than in the control group. Furthermore, the incidence of diarrhea in the NCG group was 18% lower (P<0.01) than that in the control group. Collectively, these results indicate that dietary supplementation with 0.6% Arg or 0.08% NCG enhances intestinal HSP70 gene expression, intestinal growth and integrity, and the availability of dietary nutrients for whole-body weight gain in postweaning pigs fed a CSM-based diet. Thus, Arg or NCG is a functional ingredient in the weaning diet to improve nutrition, health, and growth performance of these neonates.

Two experiments were conducted to evaluate the effects of dietary supplementation with Astragalus polysaccharide (APS) on growth performance, apparent ileal digestibilities (AID) of amino acids (AA), and their serum concentrations in early weaned piglets. In Exp. 1, 60 pigs were weaned at 21 days of age (BW 7.35 +/- 0.23 kg) and allocated to three treatments (20 pigs/treatment), representing supplementing 0.0% (control), 0.02% colistin (antibiotic), or 0.1% APS to a corn- and soybean meal-based diet. Average daily gain (ADG), average daily feed intake (ADFI), and feed/gain ratio (F/G) were measured weekly. Blood samples were obtained from five pigs selected randomly from each treatment for the measurement of serum free AA concentrations on days 7, 14, and 28. In Exp. 2, 12 pigs were weaned at 21 day of age (BW 7.64 +/- 0.71 kg), assigned to three treatment groups as in Exp. 1, and surgically fitted with a simple T-cannula at the terminal ileum. Ileal digesta samples were obtained for the measurement of AID of AA on days 7, 14 and 28. Dietary APS did not affect ADFI, but enhanced (P < 0.05) ADG by 11 and 4.4%, and improved F/G by 5.6 and 8.4%, respectively, compared with the control and antibiotic groups. Addition of APS to the diet increased AID and serum concentrations of most nutritionally essential and non-essential AA (including arginine, proline, glutamate, lysine, methionine, tryptophan, and threonine) on days 14 and 28. Circulating levels of total AA were affected by the age of pigs and treatment x time interaction. Collectively, these findings indicate that APS may ameliorate the digestive and absorptive function and regulate AA metabolism to beneficially increase the entry of dietary AA into the systemic circulation, which provide a mechanism to explain the growth-promoting effect of APS in early weaned piglets.

The aim of this study was to investigate the effects of dietary l-glutamine (Gln) supplementation on the morphology and function of the intestine and the growth of muscle in piglets. In this study, sixteen 21-day-old piglets were randomly divided into two groups: the Control group (fed a basal diet) and the Gln group (fed a basal diet supplemented with 0.81% Gln). Blood, gut, and muscle samples were collected from all piglets on Day 20 of the trial. Compared with the Control group, the supplementation of Gln increased (p < 0.05) the villus height, villus width, villus surface area, and villus height/crypt depth ratio of the small intestine. Furthermore, the supplementation of Gln increased (p < 0.05) total protein, total protein/DNA, and RNA/DNA in both the jejunum and ileum. It also increased (p < 0.05) the concentrations of carnosine and citrulline in the jejunal mucosa, as well as citrulline and cysteine concentrations in the ileum. Conversely, Gln supplementation decreased (p < 0.05) Gln concentrations in both the jejunum and ileum, along with β-aminoisobutyric acid and 1-Methylhistidine concentrations, specifically in the ileum. Subsequent research revealed that Gln supplementation increased (p < 0.05) the mRNA levels for glutathione-S-transferase omega 2 and interferon-β in the duodenum. In addition, Gln supplementation led to an increase (p < 0.05) in the number of Lactobacillus genus in the colon, but a decrease (p < 0.05) in the level of HSP70 in the jejunum and the activity of diamine oxidase in plasma. Also, Gln supplementation reduced (p < 0.05) the mRNA levels of glutathione-S-transferase omega 2 and interferon stimulated genes, such as MX1, OAS1, IFIT1, IFIT2, IFIT3, and IFIT5 in both the jejunum and ileum, and the numbers of Clostridium coccoides, Enterococcus genus, and Enterobacterium family in the colon. Moreover, Gln supplementation enhanced (p < 0.05) the concentrations of total protein, RNA/DNA, and total protein/DNA ratio in the longissimus dorsi muscle, the concentrations of citrulline, ornithine, arginine, and hydroxyproline, and the mRNA level of peptide transporter 1, while reducing the contents of hydrogen peroxide and malondialdehyde and the mRNA level of glutathione-S-transferase omega 2 in the longissimus dorsi muscle. In conclusion, dietary Gln supplementation can improve the intestinal function of piglets and promote the growth of the longissimus dorsi muscle. [ABSTRACT FROM AUTHOR]

Simple Summary: The aim of this study was to investigate the effect of puerarin supplementation on the growth performance and intestinal function of piglets challenged with enterotoxigenic Escherichia coli (ETEC) K88, which provided a theoretical basis for its practical application as a new feed additive. Dietary supplementation with 5 mg/kg puerarin alleviated intestinal injury and improved the intestinal function of piglets challenged with ETEC K88 by increasing the number of Bifidobacterium in the colon and Lactobacillus in the jejunum, cecum and colon; decreasing the number of Escherichia coli in the jejunum and cecum; reducing the hydrogen peroxide content in the jejunum and myeloperoxidase activity in the jejunum and ileum; and increasing the activities of catalase and superoxide dismutase in the jejunum and ileum. These results provide important insights into the development of an effective treatment for ETEC K88 infection and other enteric diseases. The objective of this study was to investigate the effect of puerarin supplementation on the growth performance and intestinal function of piglets challenged with enterotoxigenic Escherichia coli (ETEC) K88. Twenty-four ternary crossbred piglets were randomly assigned to three treatment groups: control group, ETEC group (challenged with ETEC K88 on day 8), and ETEC + Puerarin group (supplemented with 5 mg/kg puerarin and challenged with ETEC K88 on day 8). All piglets were orally administered D-xylose (0.1 g/kg body weight) on day 10, and blood samples were collected after 1 h. Subsequently, piglets were killed and intestinal samples were collected for further analysis. The results showed that puerarin supplementation significantly decreased the adverse effects of ETEC K88-challenged piglets; significantly improved growth performance; increased the number of Bifidobacterium in the colon and Lactobacillus in the jejunum, cecum and colon; decreased the number of Escherichia coli in the jejunum and cecum; reduced the hydrogen peroxide content in the jejunum and myeloperoxidase activity in the jejunum and ileum; and increased the activities of catalase and superoxide dismutase in the jejunum and ileum. In addition, puerarin supplementation alleviated ETEC K88-induced intestinal injury in piglets, significantly downregulated the mRNA level of Interleukin-1β and upregulated the mRNA levels of intercellular cell adhesion molecule-1, myxovirus resistance protein 1, myxovirus resistance protein 2, and guanylate-binding protein-1 in the small intestine of piglets. In conclusion, dietary supplementation with puerarin could attenuate ETEC K88-induced intestinal injury by increasing the antioxidant and anti-inflammatory capacity and the number of beneficial intestinal bacteria in piglets. [ABSTRACT FROM AUTHOR]

Simple Summary: The aim of this study is to investigate the effects of mono-lactate glyceride on growth performance and the morphology and function of the intestine in weaned piglets, which provided a theoretical basis for its practical application as a new feed additive. Dietary supplementation with 0.6% mono-lactate glyceride (LG) essentially decreased diarrhea rate and the contents of malondialdehyde (MDA) and hydrogen peroxide (H2O2) in the ileum and jejunum, increased the expression of intestinal tight junction protein (Occludin) and the activities of superoxide dismutase (SOD) and catalase (CAT) in the ileum and colon, and improved the intestinal morphologic structure. In addition, mono-lactate glyceride supplementation could enhance intestinal mucosal growth, promote intestinal mucosal water and nutrient transport and lipid metabolism, and enhance antiviral and immune function and antioxidant capacity. Overall, these results suggested that dietary supplementation with mono-lactate glyceride could decrease the diarrhea rate. Mono-lactate glyceride (LG) is a short-chain fatty acid ester. It has been shown that short-chain fatty acid esters play an important role in maintaining intestinal structure and function. The aim of this study is to investigate the effects of mono-lactate glyceride on growth performance and intestinal morphology and function in weaned piglets. Sixteen 21-day-old weaned piglets of similar weight were distributed arbitrarily to two treatments: The control group (basal diet) and the LG group (basal diet + 0.6% mono-lactate glyceride). The experiment lasted for 21 days. On day 21 of the trial, piglets were weighed, and blood and intestinal samples were collected for further analysis. Results showed that dietary supplementation with 0.6% mono-lactate glyceride decreased (p < 0.05) the diarrhea rate and the contents of malondialdehyde and hydrogen peroxide in the ileum and jejunum and increased (p < 0.05) the expression of intestinal tight junction protein (Occludin) and the activities of superoxide dismutase and catalase in the ileum and colon. In addition, mono-lactate glyceride supplementation could enhance intestinal mucosal growth by increasing (p < 0.05) the mRNA levels of extracellular regulated protein kinases, promote intestinal mucosal water and nutrient transport and lipid metabolism by increasing (p < 0.05) the mRNA levels of b0,+ amino acid transporter, aquaporin 3, aquaporin 10, gap junction protein alpha 1, intestinal fatty acid-binding protein, and lipoprotein lipase, enhance antiviral and immune function by increasing (p < 0.05) the mRNA levels of nuclear factor kappa-B, interferon-β, mucovirus resistance protein II, 2'-5'-oligoadenylate synthetase-like, interferon-γ, C-C motif chemokine ligand 2, and toll-like receptor 4, and enhance antioxidant capacity by increasing (p < 0.05) the mRNA levels of NF-E2-related factor 2 and glutathione S-transferase omega 2 and decreasing (p < 0.05) the mRNA level of NADPH oxidase 2. These results suggested that dietary supplementation with mono-lactate glyceride could decrease the diarrhea rate by improving intestinal antioxidant capacity, intestinal mucosal barrier, intestinal immune defense function, and intestinal mucosal water and nutrient transport. Collectively, dietary supplementation with 0.6% mono-lactate glyceride improved the intestinal function of weaned piglets. [ABSTRACT FROM AUTHOR]

Background: The purpose of this research is to determine the effects of sodium gluconate (SG) on the growth performance and intestinal function in weaned pigs challenged with a recombinant Escherichia coli strain expressing heat-stable type I toxin (STa). Results: Pigs (n = 24, 21 days of age) were randomly allocated to three treatments: Control group (pigs were fed basal diet), STa group (pigs were fed basal diet and challenged with a recombinant E. coli strain expressing STa), and SG group (pigs were fed basal diet supplemented with 2500 mg/kg sodium gluconate and challenged with a recombinant E. coli strain expressing STa). The trial period lasted for 15 days. On days 12 and 13, pigs in the STa and SG groups were orally administered with the recombinant Escherichia coli strain, while those in the control group were orally administered with normal saline at the same volume. On day 15, blood, intestinal tissues and colonic contents were collected for further analysis. Results showed that dietary SG supplementation had a tendency to increase average daily gain, and reduced (P < 0.05) feed to gain ratio, plasma glucose concentration, and mean corpuscular hemoglobin concentration as compared with control group on days 0-10 of trial. Additionally, dietary SG supplementation attenuated(P < 0.05) the morphological abnormalities of small intestinal and the increase of the number of eosinophils in blood of pigs challenged with the recombinant Escherichia coli strain on day 15 of trial. Compared with control group, diarrhea rate and the number of eosinophils in blood and the concentrations of malondialdehyde in the jejunum were increased (P < 0.05). The height, width and surface area of the villi of the duodenum, the width and surface area of villi of jejunum and the height and width of villi of ileum were decreased (P < 0.05) in pigs challenged with the recombinant Escherichia coli strain in the STa group compared with those in control group on day 15 of trial. However, these adverse effects were ameliorated (P < 0.05) by SG supplementation in the SG group on day 15 of trial. Furthermore, dietary SG supplementation could reduce (P < 0.05) the total bacterial abundance in the colon, but SG did not restore the recombinant Escherichia coli-induced microbiota imbalance in colon. Conclusions: In conclusion, dietary supplementation with SG could improve piglet growth performance and alleviate the recombinant Escherichia coli-induced intestinal injury, suggesting that SG may be a promising feed additive for swine. [ABSTRACT FROM AUTHOR]

L-Glutamate (Glu) has traditionally not been considered as a nutrient needed in diets for humans and other animals (including swine) due to the unsubstantiated assumption that animals can synthesize sufficient amounts of Glu to meet their needs. The lack of knowledge about Glu nutrition has contributed to suboptimal efficiency of global livestock production. Over the past 25 years, there has been growing interest in Glu metabolism in the pig, which is an agriculturally important species and also a useful model for studying human biology. Because of analytical advances in its analysis, Glu is now known to be a highly abundant free amino acid in milk and intracellular fluid, a major constituent of food and tissue proteins, and a key regulator of gene expression, cell signaling, and anti-oxidative reactions. Emerging evidence shows that dietary supplementation with 2% Glu maintains gut health and prevents intestinal dysfunction in weanling piglets, while enhancing their growth performance and survival. In addition, the inclusion of 2% Glu is required for dietary arginine to maximize the growth performance and feed efficiency in growing pigs, whereas dietary supplementation with 2% Glu reduces the loss of skeletal muscle mass in endotoxin-challenged pigs. Furthermore, supplementing 2% Glu to a corn- and soybean-meal-based diet promotes milk production by lactating sows. Thus, an adequate amount of dietary Glu as a quantitatively major nutrient is necessary to support maximum growth, development, and production performance of swine. These results also have important implications for improving the nutrition and health of humans and other animals. [ABSTRACT FROM AUTHOR]

Porcine epidemic diarrhea virus (PEDV) infects the intestine of young pigs, but effective measures for prevention and treatment are lacking. N-Acetylcysteine (NAC) has been shown to reduce endotoxin-induced intestinal dysfunction. This study was conducted with the PEDV-infected neonatal piglet model to determine the effect of NAC supplementation on intestinal function. Thirty-two 7-day-old piglets were randomly allocated to one of four treatments in a 2 × 2 factorial design consisting of two liquid diets (0 or 50 mg/kg BW NAC supplementation) and oral administration of 0 or 10 TCID (50% tissue culture infectious dose) PEDV. On day 7 of the trial, half of the pigs ( n = 8) in each dietary treatment received either sterile saline or PEDV (Yunnan province strain) solution at 10 TCID per pig. On day 10 of the trial, d-xylose (0.1 g/kg BW) was orally administrated to all pigs. One hour later, jugular vein blood samples were collected, and then all pigs were killed to obtain the small intestine. PEDV infection increased diarrhea incidence, while reducing ADG. PEDV infection also decreased plasma d-xylose concentration, small intestinal villus height, mucosal I-FABP and villin mRNA levels but increased mucosal MX1 and GCNT3 mRNA levels ( P < 0.05). Dietary NAC supplementation ameliorated the PEDV-induced abnormal changes in all the measured variables. Moreover, NAC reduced oxidative stress, as indicated by decreases in plasma and mucosal HO levels. Collectively, these novel results indicate that dietary supplementation with NAC alleviates intestinal mucosal damage and improves the absorptive function of the small intestine in PEDV-infected piglets. [ABSTRACT FROM AUTHOR]

Background: Skeletal muscle undergoes rapid loss in response to inflammation. α-Ketoglutarate (AKG) has been reported to enhance muscle growth in piglets, but the underlying mechanisms are largely unknown.Objectives: This study tested the hypothesis that dietary AKG supplementation activates mechanistic target of rapamycin (mTOR) signaling and improves skeletal muscle energy metabolism in lipopolysaccharide (LPS)-challenged piglets.Methods: Forty-eight male piglets (Duroc × Landrace × Yorkshire) were weaned at 21 d of age to a corn- and soybean meal-based diet. After a 3-d period of adaptation, piglets with a mean weight of 7.21 kg were randomly assigned to control, LPS (intraperitoneal administration of 80 μg LPS/kg body weight on days 10, 12, 14, and 16), or LPS plus 1% dietary AKG (LPS+AKG) groups. On day 16, blood samples were collected from 8 piglets/group 3 h after LPS administration. On day 17, piglets were killed to obtain gastrocnemius muscle from 8 piglets/group for biochemical analysis.Results: Compared with the control group, LPS administration increased (P < 0.05) plasma concentrations of globulin (by 14%) and tumor necrosis factor α (by 59%) and the intramuscular ratio of AMP to ATP (by 93%) and abundance of phosphorylated acetyl-coenzyme A carboxylase (ACC) β protein (by 64%). Compared with the control group, LPS administration reduced (P < 0.05) weight gain (by 15%); plasma concentrations of glutamine (by 20%), glucose (by 23%), insulin, insulin-like growth factor I, and epidermal growth factor; intramuscular concentrations of glutamine (by 27%), ATP (by 12%), ADP (by 22%), and total adenine nucleotides; and intramuscular ratios of phosphorylated mTOR to total mTOR (by 38%) and of phosphorylated 70-kDa ribosomal protein S6 kinase (p70S6K) to total p70S6K (by 39%). These adverse effects of LPS were ameliorated (P < 0.05) by AKG supplementation.Conclusions: Dietary AKG supplementation activated mTOR signaling, inhibited ACC-β, and improved energy status in skeletal muscle of LPS-challenged piglets. These results provide a biochemical basis for the use of AKG to enhance piglet growth under inflammatory or practical postweaning conditions. [ABSTRACT FROM AUTHOR]

The intestine requires a high amount of energy to maintain its health and function; thus, energy deficits in intestinal mucosa may lead to intestinal damage. Asparagine (Asn) is a precursor for many other amino acids such as aspartate, glutamine and glutamate, which can be used to supply energy to enterocytes. In the present study, we hypothesise that dietary supplementation of Asn could alleviate bacterial lipopolysaccharide (LPS)-induced intestinal injury via improvement of intestinal energy status. A total of twenty-four weaned piglets were assigned to one of four treatments: (1) non-challenged control; (2) LPS+0 % Asn; (3) LPS+0·5 % Asn; (4) LPS+1·0 % Asn. On day 19, piglets were injected with LPS or saline. At 24 h post-injection, piglets were slaughtered and intestinal samples were collected. Asn supplementation improved intestinal morphology, indicated by higher villus height and villus height:crypt depth ratio, and lower crypt depth. Asn supplementation also increased the ratios of RNA:DNA and protein:DNA as well as disaccharidase activities in intestinal mucosa. In addition, Asn supplementation attenuated bacterial LPS-induced intestinal energy deficits, indicated by increased ATP and adenylate energy charge levels, and decreased AMP:ATP ratio. Moreover, Asn administration increased the activities of key enzymes involved in the tricarboxylic acid cycle, including citrate synthase, isocitrate dehydrogenase and α-ketoglutarate dehydrogenase complex. Finally, Asn administration decreased the mRNA abundance of intestinal AMP-activated protein kinase-α1 (AMPKα1), AMPKα2, silent information regulator 1 (SIRT1) and PPARγ coactivator-1α (PGC1α), and reduced intestinal AMPKα phosphorylation. Collectively, these results indicate that Asn supplementation alleviates bacterial LPS-induced intestinal injury by modulating the AMPK signalling pathway and improving energy status. [ABSTRACT FROM PUBLISHER]

There is growing interest in glutamate as a functional amino acid in nutrition and health. This study was conducted to determine whether glutamate precursor α-ketoglutarate (AKG) could alleviate lipopolysaccharide (LPS)-induced liver injury in young pigs. Twenty-four piglets were randomly assigned to the control, LPS, or LPS + AKG group. Piglets in the control and LPS groups were fed a basal diet, whereas piglets in the NAC group were fed the basal diet supplemented with 1 % AKG. On days 10, 12, 14, and 16 of the trial, piglets in the LPS and LPS + AKG groups received intraperitoneal administration of LPS (80 μg/kg BW), whereas piglets in the control group received the same volume of saline. On day 16 of the trial, blood samples were collected 3 h after LPS or saline injection. Twenty-four hours post-administration of LPS or saline (on day 17 of the trial), piglets were killed to obtain liver for analysis. Dietary AKG supplementation alleviated LPS-induced histomorphological abnormalities and mitigated LPS-induced increases in aspartate aminotransferase (AST) activity and AST/ALT ratio ( P < 0.05). Compared with the LPS group, dietary supplementation with AKG decreased plasma glutamate concentration, while increasing hepatic concentrations of glutamate, glutamine, leucine, asparagine, lysine, alanine, serine, threonine, valine, and phenylalanine ( P < 0.05). LPS challenge dramatically increased concentrations of malondialdehyde and decreased glutathione peroxidase activity in the liver. Additionally, LPS challenge enhanced concentrations of AMP and total protein, as well as RNA/DNA and total protein/DNA ratios, while decreasing hepatic ADP concentrations. These adverse effects of LPS challenge were ameliorated by AKG supplementation. Collectively, dietary AKG supplementation provides a new means to ameliorate LPS-induced liver injury by increasing anti-oxidative capacity and improving energy metabolism in young pigs. [ABSTRACT FROM AUTHOR]

Purpose: This study was conducted to investigate whether aspartate (Asp) could improve liver energy status in the lipopolysaccharide (LPS)-challenged pigs. Methods: Twenty-four weaned pigs were assigned to four treatments: (1) nonchallenged control (control diet and saline-treated); (2) LPS-challenged control (the same control diet and LPS-challenged); (3) LPS + 0.5 % Asp treatment (0.5 % Asp diet and LPS-challenged); and (4) LPS + 1.0 % Asp treatment (a 1.0 % Asp diet and LPS-challenged). On d 19, the pigs were injected intraperitoneally with Escherichia coli LPS at 100 μg/kg body weight, and the same volume of 0.9 % NaCl solution, respectively. All pigs were slaughtered at 24 h after LPS or saline injection, and the liver was collected for further analysis. Results: Dietary supplementation with Asp improved liver energy status evidenced by the increased ATP concentration and adenylate energy charges, and the decreased AMP concentration and AMP/ATP ratio ( p < 0.05). Asp supplementation increased the mRNA expression of key enzymes in hepatic glycolysis and tricarboxylic acid (TCA) cycle, including pyruvate kinase and citrate synthase ( p < 0.05), and had a tendency to increase hepatic pyruvate dehydrogenase and isocitrate dehydrogenase β mRNA expression ( p < 0.10). In addition, Asp increased the mRNA expressions of hepatic AMP-activated protein kinase (AMPK) α1, AMPKα2, silent information regulator (Sirt1), and proliferator-activated receptor-γ coactivator 1α (PGC1α) ( p < 0.05). Moreover, Asp increased AMPKα phosphorylation ( p < 0.05). Conclusions: These results indicated that dietary supplementation of Asp could improve energy status in LPS-injured liver, which might result from motivating the metabolism pathway of TCA cycle and glycolysis and stimulating the AMPK signaling pathway. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM PUBLISHER]

The objective of this study was to evaluate effects of dietary l-lysine on the intestinal mucosa and expression of cationic amino acid transporters (CAT) in weaned piglets. Twenty-eight piglets weaned at 21 days of age (Duroc × Landrace × Yorkshire; 6.51 ± 0.65 kg body weight) were assigned randomly into one of the four groups: Zein + LYS (zein-based diet + 1.35 % supplemental lysine), Zein − LYS (zein-based diet), NF (nitrogen-free diet), and CON (basal diet). The experiment lasted for 3 weeks, during which food intake and body weight were recorded. At the end of the trial, blood was collected from the jugular vein of all pigs, followed by their euthanasia. Dietary supplementation with lysine enhanced villus height and crypt depth in the jejunum ( P < 0.05). Jejunal mRNA levels for the b-AT, yLAT1 and CAT1 genes were greater ( P < 0.05) in the Zein + LYS group than in the control, and the opposite was observed for CAT1. Dietary content of lysine differentially affected intestinal CAT expression to modulate absorption of lysine and other basic amino acids. Thus, transport of these nutrients is a key regulatory step in utilization of dietary protein by growing pigs and lysine in the diet influences the expression of amino acid transporters in the small intestine. [ABSTRACT FROM AUTHOR]

Simple Summary: The biological characteristics of E. faecium R1 and the effect of dietary supplementation with E. faecium R1 on the growth performance of weaned piglets were studied. The results showed that E. faecium R1 had the characteristics of effective bacteriostatic activity, acid resistance, bile salt resistance, and high-temperature resistance. Dietary supplementation with E. faecium R1 (6.5 × 106 CFU/g) improved intestinal function of weaning piglets by decreasing diarrhea incidence. Further research found that dietary supplementation with E. faecium R1 (6.5 × 106 CFU/g) attenuated intestinal and liver injury in piglets challenged by lipopolysaccharide. In this study, a strain of E. faecium R1 with effective bacteriostatic activity, acid resistance, bile salt resistance, high-temperature resistance was screened. To study the effect of E. faecium R1 on lipopolysaccharide (LPS)-induced intestinal and liver injury in piglets, twenty-four weaned female piglets were randomly assigned into one of three groups (8 piglets per group). Piglets in the control group and LPS group were fed a basal diet, piglets in the E. faecium group were fed the basal diet supplemented with E. faecium R1 (6.5 × 106 CFU/g). On day 21 of the trial, piglets in the LPS group and E. faecium group were intraperitoneally administered LPS (100 μg/kg), piglets in the control group were administered the same volume of saline. Subsequently, blood samples were collected at 3 h, and intestinal, liver, and pancreas samples were collected at 6 h. Results showed that E. faecium R1 supplementation significantly decreased the diarrhea rate and feed to gain ratio, and dramatically reduced LPS-induced intestinal and liver injury in piglets. Compared with the LPS group, E. faecium R1 supplementation significantly increased the content of glucagon in plasma and IL-1β in the liver, and the mRNA levels of villin in jejunum and ileum and Bcl-xL and pBD-L in the ileum, and significantly decreased the contents of prostaglandin 2 and malondialdehyde in the liver and the activities of myeloperoxidase and aspartate aminotransferase in plasma in piglets. Moreover, E. faecium R1 improved the pancreatic antioxidant capacity in piglets, which was indicated by a significant increase in catalase activity and a decrease in total nitric oxide synthase activity. In summary, dietary supplementation with E. faecium R1 alleviates intestinal and liver injury in LPS-challenged piglets. [ABSTRACT FROM AUTHOR]

Trihexanoin is a short-chain triglyceride (SCT). Many studies have reported that SCTs play important roles in the maintenance of intestinal epithelial structure and function. The present work was to investigate the effects of trihexanoin on growth performance, carbohydrate and fat metabolism, as well as intestinal morphology and function in weaned piglets. Twenty weaned piglets (21 ± 2 d) were randomly allocated to one of two treatment groups: The control group (basal diet supplemented with 0.5% soya oil); the TH group (basal diet supplemented with 0.5% trihexanoin). Dietary trihexanoin supplementation significantly reduced diarrhea rate; increased the concentrations of LDL, HDL and total protein in plasma; decreased cholesterol concentrations and glutamyl transpeptidase activity in plasma; improved intestinal morphologic structure; altered the mRNA levels and abundances of proteins related to glycogen and fat metabolism, mucosal barrier function, antioxidant capacity and water transport capacity; and altered the community of intestinal microflora. These results indicate that dietary trihexanoin supplementation could reduce diarrhea, regulate carbohydrate and fat metabolism, exert beneficial effects on the intestinal mucosal barrier, protect the intestinal mucosa from injuries, improve intestinal transport and absorption, and enhance antioxidant capacity. In conclusion, dietary supplementation with 0.5% trihexanoin improves the intestinal function and health of weaned piglets. [ABSTRACT FROM AUTHOR]

The present study was to determine the efficacy of dietary supplementation with oleum cinnamomi (OCM) on growth performance and intestinal functions in piglets. Sixteen piglets (24-day-old) were randomly assigned to the control or OCM groups. Piglets in the control group were fed a basal diet, whereas piglets in the OCM group were fed the basal diet supplemented with 50 mg/kg OCM. On day 20 of the trial, blood samples and intestinal tissues were obtained from piglets. Compared with the control group, dietary OCM supplementation increased (p < 0.05) average daily feed intake, plasma insulin levels, villus width and villous surface area in the duodenum and jejunum, DNA levels and RNA/DNA ratios in the ileum, the abundance of Enterococcus genus and Lactobacillus genus in caecum digesta, mRNA levels for epithelial growth factor receptor (EGFR), Ras, extracellular signal-regulated kinase 1/2 (Erk1/2), b-cell lymphoma-extra large (Bcl-xL), villin, junctional adhesion molecule A (JAM-A), myxovirus resistance (MX) 1, MX2 and regenerating islet-derived protein 3 gamma (REG3G), and protein abundances of Ras and claudin-1, but decreased (p < 0.05) diarrhoea incidence; the abundances of Enterobacteriaceae family, Enterococcus genus, Lactobacillus genus, Bifidobacterium genus, and Clostrium coccoides in the colon digesta, and AMP-activated protein kinase (AMPK) mRNA levels and caspase-3 protein abundance in the jejunal mucosa of piglets. Taken together, these data indicate that dietary OCM supplementation modulates intestinal microbiota and improves intestinal function in weanling pigs. OCM is an effective feed additive and alternative to feed antibiotics for improving intestinal health in swine. [ABSTRACT FROM AUTHOR]

Oleum cinnamomi (OCM, cinnamon oil), which is produced by aromatic cinnamon plants, is increasingly used as a feed additive to animal diets. OCM is a natural product rich in polyphenolic compounds that exhibit strong antioxidative property. However, the direct addition of OCM to the feed is questionable due to several limiting physical–chemical factors such as the high hydrophobicity, volatility, odor, fast decomposition, and poor availability in the lower gastrointestinal tract of animals. Therefore, the coated form of OCM (cOCM) is one of the ways to solve these concerns. We have demonstrated that dietary cOCM supplementation did not improve the growth performance of broiler chickens, but it showed beneficial effects on immunity and intestinal integrity. In the current study, we further investigated the intestinal cinnamaldehyde release and antioxidative capacity of chickens fed cOCM-supplemented diets. As cinnamaldehyde is a major constituent of OCM, we evaluated the release of cOCM in the intestine of birds by determining the contents of cinnamaldehyde in the digesta of small intestine and cecum. The increased availability of OCM in the lower intestine supplied a foundation for exerting its antioxidative effects. The activities of antioxidative enzymes were increased and superoxide levels were decreased in the plasma and intestinal mucosa of birds fed cOCM-supplemented diets. The improvement of antioxidative capacity was achieved by modulating the gene expression of nuclear factor erythroid 2-related factor 2 and downstream antioxidative enzymes. [ABSTRACT FROM AUTHOR]

Abstract: The intestine has a high requirement for ATP to support its integrity, function and health, and thus, energy deficits in the intestinal mucosa may play a critical role in intestinal injury. Aspartate (Asp) is one of the major sources of ATP in mammalian enterocytes via mitochondrial oxidation. We hypothesized that dietary supplementation of Asp could attenuate lipopolysaccharide (LPS)-induced intestinal damage via modulation of intestinal energy status. Twenty-four weanling piglets were allotted to one of four treatments: (1) nonchallenged control, (2) LPS-challenged control, (3) LPS+0.5% Asp treatment, and (4) LPS+1.0% Asp treatment. On day 19, pigs were injected with saline or LPS. At 24 h postinjection, pigs were killed and intestinal samples were obtained. Asp attenuated LPS-induced intestinal damage indicated by greater villus height and villus height/crypt depth ratio as well as higher RNA/DNA and protein/DNA ratios. Asp improved intestinal function indicated by increased intestinal mucosal disaccharidase activities. Asp also improved intestinal energy status indicated by increased ATP, ADP and total adenine nucleotide contents, adenylate energy charge and decreased AMP/ATP ratio. In addition, Asp increased the activities of tricarboxylic acid cycle key enzymes including citrate synthase, isocitrate dehydrogenase and alpha-oxoglutarate dehydrogenase complex. Moreover, Asp down-regulated mRNA expression of intestinal AMP-activated protein kinase α1 (AMPKα1), AMPKα2, silent information regulator 1 (SIRT1) and peroxisome proliferator–activated receptor gamma coactivator-1α (PGC1α) and decreased intestinal AMPKα phosphorylation. These results indicate that Asp may alleviate LPS-induced intestinal damage and improve intestinal energy status. [Copyright &y& Elsevier]