Effects of fish meal and sodium butyrate on growth performance, gut development and glucagon-like peptide-2 secretion in weanling piglets

The experiment was conducted to study the effects of fish meal and sodium butyrate on growth performance, gut development and GLP-2 secretion in weanling piglets. A 2×2 factorial design was used with two fish meal levels （0, 5%）, and two sodium butyrate levels （0, 0.3%）. There were 4 dietary treatments： control diet （CD）; control diet supplemented with fish meal （CF）, control diet supplemented with sodium butyrate （CB）, control diet supplemented with fish meal and sodium butyrate （FB）. A total of 44 28-days-old Large White×Landrace weanling piglets were randomly allotted into 4 treatment averagely. The experiment period was 14 days. The results showed that sodium butyrate＇s addition increased average diary gain （ADG）, average diary feed intake （ADFI） and gain to feed intake ratio （G：F） of weanling piglets （all P〈0,05）, improved gut morphology （mucosa thickness, ratio of villous height to crypt depth） and sucrase activity, and fish meal＇s addition increased maltase activity （all P〈0.05）. Either sodium butyrate or fish meal addition decreased cecum colibacillus quantity, sodium butyrate increaded ratio of cecum lactobacilli to colibacillus （P〈0.05）. Consequently, diarrhea was reduced in diet supplemented with fish meal （P=-0.08） and diet supplemented with sodium butyrate （P=0.15） through 14 days of experiment, significant reduction of diarrhea rate was observed in diet supplemented with fish meal through the first 7 days （P〈0.05）. In addition, sodium butyrate and fish meal addition in diets tended to increase plasma GLP-2 concentration, however, GLP-2 concentration on the 4th day was consistently decreased in diet supplemented with fish meal relative to that on day 0 （P=0.08）. Overall, it could be concluded that both sodium butyrate and fish meal addition improve intestinal development and sodium butyrate addition significantly increase growth performance. The gut trophic response to sodium butyrate or may be in agreement with development. peptide GLP-2 increases in fish meal addition in diet and the alteration of intestinal

Injection of pGRF Gene Plasmid May Relieve Growth Depression Induced by Lipopolysaccharide in Weanling Piglets

The purpose of this study was to evaluate the effect and the potential mechanism of administering a pGRF gene plasmid on the growth and immunological function of weanling piglets subjected to immune-stress.Eighteen weanling(Duroc×Landrace×Large White) piglets aged 35 d±2 d and initial BW of 7.86 kg±0.59 kg were randomly assigned to three treatments according to gender and BW by using a single factor design.The three treatments were injections of a pGRF gene plasmid,pGRF gene plasmid followed by challenge with lipopolysaccharide(LPS),and LPS to piglets not receiving the plasmid.Each treatment group consisted of six piglets.The results were as follows:piglets in the pGRF gene plasmid plus LPS treatment had a better growth performance than those only receiving LPS(P【0.05), and F/G of piglets in the pGRF gene plasmid plus LPS group were very slightly lower(P】0.05) than those in the LPS group;serum levels of IGF-1 in the pGRF gene plasmid plus LPS group were significantly higher than those in the LPS group(P【0.05 or P【0.01);serum levels of IgG in the pGRF gene plasmid plus LPS group were higher than those in the LPS group(P【0.05);serum levels of IL-1 and IL-6 in the pGRF gene plasmid plus LPS group were significantly lower than those in the LPS group(P【0.05 or P【0.01).

Dietary ellagic acid supplementation attenuates intestinal damage and oxidative stress by regulating gut microbiota in weanling piglets

Intestinal oxidative stress triggers gut microbiota dysbiosis,which is involved in the etiology of postweaning diarrhea and enteric infections.Ellagic acid(EA)can potentially serve as an antioxidant supplement to facilitate weaning transition by improving intestinal oxidative stress and gut microbiota dysbiosis.Therefore,we aimed to investigate the effects of dietary EA supplementation on the attenuation of intestinal damage,oxidative stress,and dysbiosis of gut microbiota in weanling piglets.A total of126 piglets were randomly assigned into 3 groups and treated with a basal diet and 2 m L saline orally(Ctrl group),or the basal diet supplemented with 0.1%EA and 2 m L saline orally(EA group),or the basal diet and 2 m L fecal microbiota suspension from the EA group orally(FEA group),respectively,for 14 d.Compared with the Ctrl group,EA group improved growth performance by increasing average daily feed intake and average daily weight gain(P<0.05)and decreasing fecal scores(P<0.05).EA group also alleviated intestinal damage by increasing the tight junction protein occludin(P<0.05),villus height,and villus height-to-crypt depth ratio(P<0.05),while decreasing intestinal epithelial apoptosis(P<0.05).Additionally,EA group enhanced the jejunum antioxidant capacity by increasing the total antioxidant capacity(P<0.01),catalase(P<0.05),and glutathione/oxidized glutathione(P<0.05),but decreased the oxidative metabolite malondialdehyde(P<0.05)compared to the Ctrl group.Compared with the Ctrl group,EA and FEA groups increased alpha diversity(P<0.05),enriched beneficial bacteria(Ruminococcaceae and Clostridium ramosum),and increased metabolites short-chain fatty acids(P<0.05).Correspondingly,FEA group gained effects comparable to those of EA group on growth performance,intestinal damage,and intestinal antioxidant capacity.In addition,the relative abundance of bacteria shifted in EA and FEA groups was significantly related to the examined indices(P<0.05).Overall,dietary EA supplementation could improve growth performance and attenuate intestinal damage and oxidative stress by regulating the gut microbiota in weanling piglets.

Dietary supplement of selenium-rich yeast may relieve lipopolysaccharide-induced growth depression in piglets via improving immune and antioxidant status

Selenium protects cells from oxidative damage and reduces lipopolysaccharide （LPS）-induced expression of inflammatory cytokines. Because inflammatory cytokines induce growth depression, we hypothesized that selenium-rich yeast （SeY） would inhibit growth depression caused by LPS. Twenty Meishan weanling pigs [28 （s.d. 2 d）, 7.6 （s.d. 0.3 kg） body weight （BW）] were used in a 2×2 factorial design （n=5）. The main factors were dietary Se sources [selenium-rich yeast （SeY） vs. sodium selenite （SSe）] with supplement level at 0.3 mg Se/kg, and immunological stress （LPS vs. saline）. The experiment lasted for 28 d. On d 14 and d 21, half of pigs in each dietary treatment were intramuscularly injected with either 50 μg/kg BW LPS or an equivalent amount of sterile saline. Blood samples were collected at 3 h post-injection. There were no interactions between dietary Se sources and immunological stress on growth performance. LPS depressed average daily gain （ADG） （d 14-21, P〈0.05; d 21-28, P〈 0.01）, and elevated feed to gain ratio （F/G） （d 21-28, P〈0.05）, while SeY elevated ADG （d 0-14, P〈0.05; d 21-28 and d 0-28, P〈0.01）, and decreased F/G （P〈0.01）. Interactions were observed on interleukin-1β（IL-1β） and interleukin-6 （IL-6） from serum samples of d 14 and d 21 （P〈0.01）, as well as superoxide dismutase （SOD） and insulin like growth factor （IGF-1） of d 21 （P〈0.05）. In conclusion, SeY relieved the growth depression of piglets immunologically stressed by LPS, which maybe resulted from the decreased externalization of inflammatory cytokines and improved antioxidant status.