Effects of creep feeding and supplemental glutamine or glutamine plus glutamate (Aminogut) on pre- and post-weaning growth performance and intestinal health of piglets

Background： Creep feeding is used to stimulate piglet post-weaning feed consumption.L-Glutamine（GLN） is an important source of fuel for intestinal epithelial cells.The objective of this study was to determine the impact of creep feeding and adding GLN or AminoGut（AG;containing glutamine ＋ glutamate） to pre-and post-weaning diets on pig performance and intestinal health.Litters（N = 120） were allotted to four treatments during 14–21 d of lactation： 1） No creep feed（NC,n = 45）;2） creep fed control diet（CFCD,n = 45）;3） creep fed 1% GLN（CFGLN,n = 15）;4） creep fed.88% AG（CFAG,n = 15）.After weaning,the NC and CFCD groups were sub-divided into three groups（n = 15 each）,receiving either a control nursery diet（NC-CD,CFCD-CD） or a diet supplemented with either GLN（NC-GLN,CFCD-GLN） or with AG（NC-AG,CFCD-AG）.Litters that were creep fed with diets containing GLN or AG also were supplemented with those amino acids in the nursery diets（CFGLN-GLN,CFAG-AG）.Glutamine was added at 1% in all three post-weaning diet phases and AG was added at.88% in phase 1 and 2 and at.66% in phase 3.Results： Feed conversion（feed/gain） showed means among treatment means close to significance（P = 0.056） and Tukey＇s test for pairwise mean comparisons showed that Pigs in the CFGLN-GLN group had the best feed conversion（feed/gain） in the first three-week period post-weaning,exceeding（P = 0.044） controls（CFCD-CD） by 34%.The NC-AG group had（P = 0.02） the greatest feed intake in the last three week of the study,exceeding controls（CFCD-CD） by 12%.CFGLN-GLN,CFCD-GLN and sow reared（SR） pigs had the greatest（P = 0.049） villi height exceeding the CFCD-AG group by 18%,20% and 19% respectively.The CFAG-AG group had the deepest（P = 0.001） crypts among all treatments.CFGLN-GLN,CFCD-GLN and SR groups had the greatest（P = 0.001） number of cells proliferating（PCNA） exceeding those in the NC-CD group by 43%,54% and 63% respectively.Sow reared pigs showed the greatest（P = 0.001） intestinal absorption capacity for xylose and mannitol.Conclusion： Supplementation of creep feed and nursery diets with GLN and/or AminoGut in the first three week improved feed conversion possibly due to improved intestinal health.

The health benefits of selenium in food animals:a review

Selenium is an essential trace mineral important for the maintenance of homeostasis in animals and humans.It evinces a strong antioxidant,anti-inflammatory and potential antimicrobial capacity.Selenium biological function is primarily achieved by its presence in selenoproteins as a form of selenocysteine.Selenium deficiency may result in an array of health disorders,affecting many organs and systems;to prevent this,dietary supplementation,mainly in the forms of organic(i.e.,selenomethionine and selenocysteine)inorganic(i.e.,selenate and selenite)sources is used.In pigs as well as other food animals,dietary selenium supplementation has been used for improving growth performance,immune function,and meat quality.A substantial body of knowledge demonstrates that dietary selenium supplementation is positively associated with overall animal health especially due to its immunomodulatory activity and protection from oxidative damage.Selenium also possesses potential antiviral activity and this is achieved by protecting immune cells against oxidative damage and decreasing viral replication.In this review we endeavor to combine established and novel knowledge on the beneficial effects of dietary selenium supplementation,its antioxidant and immunomodulatory actions,and the putative antimicrobial effect thereof.Furthermore,our review demonstrates the gaps in knowledge pertaining to the use of selenium as an antiviral,underscoring the need for further in vivo and in vitro studies,particularly in pigs.

Acute effects of rotavirus and malnutrition on intestinal barrier function in neonatal piglets

AIM: To investigate the effect of protein-energy malnutrition on intestinal barrier function during rotavirus enteritis in a piglet model.METHODS: Newborn piglets were allotted at day 4 of age to the following treatments:(1) full-strength formula(FSF)/noninfected;(2) FSF/rotavirus infected;(3) half-strength formula(HSF)/noninfected;or(4) HSF/rotavirus infected.After one day of adjustment to the feeding rates,pigs were infected with rotavirus and acute effects on growth and diarrhea were monitored for 3 d and jejunal samples were collected for Ussingchamber analyses.RESULTS: Piglets that were malnourished or infected had lower body weights on days 2 and 3 post-infection(P < 0.05).Three days post-infection,marked diarrhea and weight loss were accompanied by sharp reductions in villus height(59%) and lactase activity(91%) and increased crypt depth(21%) in infected compared with non-infected pigs(P < 0.05).Malnutrition also increased crypt depth(21%) compared to full-fed piglets.Villus:crypt ratio was reduced(67%) with viral infection.There was a trend for reduction in transepithelial electrical resistance with rotavirus infection and malnutrition(P = 0.1).3H-mannitol flux was significantly increased(50%;P < 0.001) in rotavirus-infected piglets compared to non-infected piglets,but there was no effect of nutritional status.Furthermore,rotavirus infection reduced localization of the tight junction protein,occludin,in the cell membrane and increased localization in the cytosol.CONCLUSION: Overall,malnutrition had no additive effects to rotavirus infection on intestinal barrier function at day 3 post-infection in a neonatal piglet model.

Influence of birth order, birth weight, colostrum and serum immunoglobulin G on neonatal piglet survival

Background： Intake of colostrum after birth is essential to stimulate intestinal growth and function, and to provide systemic immunological protection via absorption of Immunoglobulin G （IgG）. The birth order and weight of 745 piglets （from 75 litters） were recorded during a one-week period of farrowing. Only pigs weighing greater than 0.68 kg birth weight were chosen for the trial. Sow colostrum was collected during parturition, and piglets were bled between 48 and 72 hours post-birth. Piglet serum IgG and colostral IgG concentrations were determined by radial immunodiffusion. Results： Sow parity had a significant （P 〈 0.001） effect on sow colostral IgG concentration, being 5% higher in multiparous females. Sow colostral IgG concentration explained 6% and piglet birth order accounted for another 4% of the variation observed in piglet serum IgG concentration （P 〈 0.05）; however, birth weight had no detectable effect. Piglet serum IgG concentration had both a linear （P 〈 0.05） and quadratic effect （P 〈 0.05） on % survival. Piglets with 1,000 mg/dl serum IgG or less （n=24） had a 67% survival; whereas, piglets with IgG concentrations between 2250 to 2500 mg/dl （n=247） had a 91% survival. Birth order had no detectable effect on survival, but birth weight had a positive linear effect （P 〈 0.05）. Piglets weighing 0.9 kg （n = 107） at birth had a 68% survival rate, and those weighing 1.6 kg （n = 158） had an 89% survival. Conclusion： We found that the combination of sow colostrum IgG concentration and birth order can account for 10% of the variation of piglet serum IgG concentration and that piglets with less than 1,000 mg/dl IgG serum concentration and weight of 0.9 kg at birth had low survival rate when compared to their larger siblings. The effective management of colostrum uptake in neonatal piglets in the first 24 hrs post-birth may potentially improve survival from birth to weaning.

Optimizing dietary lipid use to improve essential fatty acid status and reproductive performance of the modern lactating sow:a review

Dietary lipid supplementation benefits the prolific and high-producing modern lactating sow. A comprehensive review of recent studies showed that lipid supplementation increases average daily energy intake, which is partitioned for lactation as indicated by greater milk fat output and improved litter growth rate. Recent compelling findings showed that addition of particular lipids during lactation improved the subsequent reproductive outcome of sows. Such benefits were related to the level of dietary essential fatty acids（EFA, linoleic acid, C18：2n-6; and α-linolenic acid, C18：3n-3） during lactation. Lactation diets without supplemental EFA resulted in a pronounced negative balance（intake minus milk output） of linoleic（-25.49 g/d） and α-linolenic acid（-2.75 g/d）; which compromised sow fertility（farrowing rate 〈 75 % and culling rates 〉 25 % of weaned sows）. This phenomenon seems to be increasingly important with advancing sow age because of a progressive reduction of body EFA pool over successive lactations. The net effect of supplemental EFA during lactation was to create a positive EFA balance, which improved the subsequent reproduction of sows. Adequate linoleic acid intake improved the proportion of sows that farrowed in the subsequent cycle（Farrowing rate（%） = [（-1.5 × 10^-3× linoleic acid intake（g/d）^2） ＋（0.53 × linoleic acid intake（g/d）） ＋（45.2）]; quadratic P = 0.002, R^2= 0.997, RMSE = 0.031）. In addition, increasing linoleic acid intake increased the number of pigs born in the subsequent cycle（total pigs born（n） = [（9.4 × 10^-5× linoleic acid intake（g/d）^2） ＋（0.04 × linoleic acid intake（g/d）） ＋（10.94）]; quadratic P = 0.002, R^2= 0.997, RMSE = 0.031）. Supplemental α-linolenic acid resulted in a rapid return to estrus（sows bred： sows weaned = 94.2 %; wean-to-estrus interval = 4.0 d） and achieved a high retention of pregnancy（sows pregnant： sows bred = 98 %）. Collectively, we conclude that a minimum dietary intake of10 g/d of α-linolenic acid, simultaneous with a minimum of 125 g/d of linoleic acid should be provided to ≥ 95 % of the sows; thereby, achieving a maximum sow reproductive efficiency through multiple mechanisms that include rapid return to estrus, high maintenance of pregnancy and large subsequent litter size in mature sows, that appear to be susceptible to EFA deficiency.

Dietary arachidonate in milk replacer triggers dual benefits of PGE2 signaling in LPS-challenged piglet alveolar macrophages

Background: Respiratory infections challenge the swine industry, despite common medicinal practices. The dual signaling nature of PGE2(supporting both inflammation and resolution) makes it a potent regulator of immune cell function. Therefore, the use of dietary long chain n-6 PUFA to enhance PGE2 effects merits investigation.Methods: Day-old pigs(n = 60) were allotted to one of three dietary groups for 21 d(n = 20/diet), and received either a control diet(CON, arachidonate = 0.5% of total fatty acids), an arachidonate(ARA)-enriched diet(LC n-6,ARA = 2.2%), or an eicosapentaenoic(EPA)-enriched diet(LC n-3, EPA = 3.0%). Alveolar macrophages and lung parenchymal tissue were collected for fatty acid analysis. Isolated alveolar macrophages were stimulated with LPS in situ for 24 h, and m RNA was isolated to assess markers associated with inflammation and eicosanoid production.Culture media were collected to assess PGE2 secretion. Oxidative burst in macrophages was measured by: 1)oxygen consumption and extracellular acidification(via Seahorse), 2) cytoplasmic oxidation and 3) nitric oxide production following 4, 18, and 24 h of LPS stimulation.Results: Concentration of ARA(% of fatty acids, w/w) in macrophages from pigs fed LC n-6 was 86% higher than CON and 18% lower in pigs fed LC n-3(P < 0.01). Following LPS stimulation, abundance of COX-2 and TNF-α mRNA(P < 0.0001), and PGE2 secretion(P < 0. 01) were higher in LC n-6 PAM vs. CON. However, ALOX5 abundance was1.6-fold lower than CON. Macrophages from CON and LC n-6 groups were 4-fold higher in ALOX12/15 abundance(P < 0.0001) compared to LC n-3. Oxygen consumption and extracellular acidification rates increased over 4 h following LPS stimulation(P < 0.05) regardless of treatment. Similarly, increases in cytoplasmic oxidation(P < 0.001)and nitric oxide production(P < 0.002) were observed after 18 h of LPS stimulation but were unaffected by diet.Conclusions: We infer that enriching diets with arachidonic acid may be an effective means to enhance a stronger innate immunologic response to respiratory challenges in neonatal pigs. However, further work is needed to examine long-term safety, clinical efficacy and economic viability.

Transplacental induction of fatty acid oxidation in term fetal pigs by the peroxisome proliferator-activated receptor alpha agonist clofibrate

Background： To induce peroxisomal proliferator-activated receptor α（PPARα） expression and increase milk fat utilization in pigs at birth, the effect of maternal feeding of the PPARα agonist, clofibrate（2-（4-chlorophenoxy）-2-methyl-propanoic acid, ethyl ester）, on fatty acid oxidation was examined at ful-term delivery（0 h） and 24 h after delivery in this study.Each group of pigs（n = 10） was delivered from pregnant sows fed a commercial diet with or without 0.8% clofibrate for the last 7 d of gestation. Blood samples were col ected from the utero-ovarian artery of the sows and the umbilical cords of the pigs as they were removed from the sows by C-section on day 113 of gestation.Results： HPLC analysis identified that clofibric acid was present in the plasma of the clofibrate-fed sow（~4.2 μg/m L）and its offspring（~1.5 μg/m L）. Furthermore, the maternal-fed clofibrate had no impact on the liver weight of the pigs at 0 h and 24 h, but hepatic fatty acid oxidation examined in fresh homogenates showed that clofibrate increased（P 〈 0.01）^14C-accumulation in CO2 and acid soluble products 2.9-fold from [1-^14C]-oleic acid and 1.6-fold from[1-^14C]-lignoceric acid respectively. Correspondingly, clofibrate increased fetal hepatic carnitine palmitoyltransferase（CPT）and acyl-Co A oxidase（ACO） activities by 36% and 42% over controls（P 〈 0.036）. The m RNA abundance of CPT I was 20-fold higher in pigs exposed to clofibrate（P 〈 0.0001） but no differences were detected for ACO and PPARα m RNA between the two groups.Conclusion： These data demonstrate that dietary clofibrate is absorbed by the sow, crosses the placental membrane, and enters fetal circulation to induce hepatic fatty acid oxidation by increasing the CPT and ACO activities of the newborn.

The effect of 5-aminoimidazole-4-carboxamide ribonucleoside (AICAR) on fatty acid oxidation in hepatocytes isolated from neonatal piglets

In the present study, the effect of 5-aminoimidazole-4-carboxamide ribonucleoside （AICAR） on long-chain fatty acid oxidation by hepatocytes isolated from suckled neonatal pig liver （a low ketogenic and lipogenic tissue） was tested Incubation of hepatocytes with AICAR （0.5 raM） in the presence of ] mM of carnitine and 10 mM of glucose for 1 hour at 37℃ had no significant effect on total [1-14C]-palrnitate （0.5 mM） oxidation （14CO2 and 14C-Acid soluble products （ASP））. Consistent with the fatty acid oxidation, carnitine palmitoyltransferase I activity and inhibition of its activity by malonyI-CoA （10 MM） assayed in cell homogenate also remained constant. However, addition of AICAR to the hepatocytes decreased 14CO2 production by 18% compared to control （p 〈 0.06）. The reduction of labeled carboxylic carbon accumulated in C02 caused a significant difference in distribution of oxidative products between 14C02 and 14C-ASP （p 〈 0.03） compared with the control. It was also noticed that acetyI-CoA carboxylase （ACC） was increased by AICAR （p 〈 0.03）, indicating that ACC might drive acetyI-CoA toward fatty acid synthesis pathway and induce an increase in distribution of fatty acid carbon to 14C-ASP. Addition of insulin to hepatocyte incubations with AICAR did not change the oxidative product distribution between CO2 and ASP, but further promoted ACC activity. The increased ACC activity was 70% higher than in the control group when citrate was absent in the reaction medium and was 30% higher when citrate was present in the medium. Our results suggest that AICAR may affect the distribution of metabolic products from fatty acid oxidation by changing ACC activity in hepatocyte isolated from suckled neonatal piglets; however, the basis for the increase in ACC activity elicited by AICAR is not apparent.

Effects of medium chain triglycerides on hepatic fatty acid oxidation in clofibrate-fed newborn piglets

To investigate whether increasing tricarboxylic acid(TCA)cycle activity and ketogenic capacity would augment fatty acid(FA)oxidation induced by the peroxisome proliferator-activated receptor-alpha(PPARα)agonist clofibrate,suckling newborn piglets(n=54)were assigned to 8 groups following a 2(±clofibrate)×4(glycerol succinate[SUC],triglycerides of 2-methylpentanoic acid[T2M],valeric acid[TC5]and hexanoic acid[TC6])factorial design.Each group was fed an isocaloric milk formula containing either 0%or 0.35%clofibrate(wt/wt,dry matter basis)with 5%SUC,T2M,TC5 or TC6 for 5 d.Another 6 pigs served as newborn controls.Fatty acid oxidation was examined in fresh homogenates of liver collected on d 6 using[1-^(14)C]palmitic acid(1 mM)as a substrate(0.265μCi/μmol).Measurements were performed in the absence or presence of L-carnitine(1 mM)or inhibitors of 3-hydroxy-3-methylglutaryl-CoA synthase(L659699,1.6μM)or acetoacetate-CoA deacylase(iodoacetamide,50μM).Without clofibrate stimulation,^(14)C accumulation in CO_(2) was higher from piglets fed diets containing T2M and TC5 than SUC,but similar to those fed TC6.Under clofibrate stimulation,accumulation also was higher in homogenates from piglets fed TC5 than all other dietary treatments.Interactions between clofibrate and carnitine or the inhibitors were observed(P=0.0004)for acid soluble products(ASP).In vitro addition of carnitine increased^(14)C-ASP(P<0.0001)above all other treatments,regardless of clofibrate treatment.The percentage of^(14)C in CO_(2) was higher(P=0.0023)in TC5 than in the control group.From these results we suggest that dietary supplementation of anaplerotic and ketogenic FA could impact FA oxidation and modify the metabolism of acetyl-CoA(product ofβ-oxidation)via alteration of TCA cycle activity,but the modification has no significant impact on the hepatic FA oxidative capacity induced by PPARα.In addition,the availability of carnitine is a critical element to maintain FA oxidation during the neonatal period.