This study was conducted to investigate the protective effects of l-threonine (l-Thr) supplementation on growth performance, inflammatory responses and intestinal barrier function of young broilers challenged with lipopolysaccharide (LPS). A total of 144 1-d-old male chicks were allocated to one of three treatments: non-challenged broilers fed a basal diet (control group), LPS-challenged broilers fed a basal diet without l-Thr supplementation and LPS-challenged broilers fed a basal diet supplemented with 3·0 g/kg l-Thr. LPS challenge was performed intraperitoneally at 17, 19 and 21 d of age, whereas the control group received physiological saline injection. Compared with the control group, LPS challenge impaired growth performance of broilers, and l-Thr administration reversed LPS-induced increase in feed/gain ratio. LPS challenge elevated blood cell counts related to inflammation, and pro-inflammatory cytokine concentrations in serum (IL-1β and TNF-α), spleen (IL-1β and TNF-α) and intestinal mucosa (jejunal interferon-γ (IFN-γ) and ileal IL-1β). The concentrations of intestinal cytokines in LPS-challenged broilers were reduced by l-Thr supplementation. LPS administration increased circulating d-lactic acid concentration, whereas it reduced villus height, the ratio between villus height and crypt depth and goblet density in both jejunum and ileum. LPS-induced decreases in jejunal villus height, intestinal villus height:crypt depth ratio and ileal goblet cell density were reversed with l-Thr supplementation. Similarly, LPS-induced alterations in the intestinal mRNA abundances of genes related to intestinal inflammation and barrier function (jejunal toll-like receptor 4, IFN- γ and claudin-3, and ileal IL-1 β and zonula occludens-1) were normalised with l-Thr administration. It can be concluded that l-Thr supplementation could attenuate LPS-induced inflammatory responses and intestinal barrier damage of young broilers.

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The aim of this study was to investigate effects of L-threonine (L-Thr) supplementation on the growth performance, immunity, antioxidant status, and intestinal health of broilers at the early age. One hundred and forty-four 1-day-old male broiler chicks (Arbor Acres Plus) were allocated into 3 treatments with 6 replicates of 8 birds each, and fed a basal diet (analyzed Thr content, 7.87 g/kg) supplemented with 0 (control diet), 1 and 3 g/kg L-Thr for 21 d, respectively. Treatments did not alter growth performance of broilers. Compared with control, 1 g/kg Thr supplementation increased relative weight of spleen (P = 0.013). A higher level of Thr (3 g/kg) increased relative weight of thymus (P = 0.003). The supplementation of 3 g/kg Thr reduced Escherichia coli (P = 0.040) and Salmonella colonies (P = 0.015), whereas increased Lactobacillus colonies (P < 0.001) in the cecal contents. Thr supplementation increased intestinal villus height (P < 0.05), and the ratio of villus height to crypt depth (P < 0.001), and the values for these parameters were intermediate with 1 g/kg Thr. Goblet cell density was increased by Thr supplementation (P < 0.001). The jejunal immunoglobulin G content was increased by the inclusion of Thr (P = 0.002). Broilers fed diet supplemented with 1 g/kg Thr exhibited increased concentrations of jejunal immunoglobulin M (P = 0.037) and secretory immunoglobulin A (P = 0.018). Likewise, 3 g/kg Thr inclusion increased ileal secretory immunoglobulin A content (P = 0.023). The jejunal malondialdehyde accumulation was reduced by Thr inclusion (P = 0.012). A higher level of Thr inclusion also reduced malondialdehyde content in the serum (P = 0.029). The high level of Thr inclusion (3 g/kg) upregulated mucin-2 mRNA expression (P = 0.034), whereas downregulated the mRNA abundances of interferon-γ (P = 0.036) and interleukin-1β (P = 0.031) in the ileum. In conclusion, L-Thr supplementation can improve immunity, antioxidant capacity, and intestinal health of broilers at an early age.

This study aimed to investigate the effects of chitooligosaccharide (COS) inclusion as an alternative to antibiotics on growth performance, intestinal morphology, barrier function, antioxidant capacity, and immunity in broilers. In total, 144 one-day-old Arbor Acres broiler chicks were randomly assigned into 3 groups and fed a basal diet free from antibiotics (control group) or the same basal diet further supplemented with either chlortetracycline (antibiotic group) or COS, for 21 days. Compared with the control group, inclusion of COS reduced the feed to gain ratio, the jejunal crypt depth, the plasma diamine oxidase activity, and the endotoxin concentration, as well as jejunal and ileal malondialdehyde contents, whereas increased duodenal villus height, duodenal and jejunal ratio of villus height to crypt depth, intestinal immunoglobulin G, and jejunal immunoglobulin M (IgM) contents were observed, with the values of these parameters being similar or better to that of the antibiotic group. Additionally, supplementation with COS enhanced the superoxide dismutase activity and IgM content of the duodenum and up-regulated the mRNA level of claudin three in the jejunum and ileum, when compared with the control and antibiotic groups. In conclusion, dietary COS inclusion (30 mg/kg), as an alternative to antibiotics, exerts beneficial effects on growth performance, intestinal morphology, barrier function, antioxidant capacity, and immunity in broilers.

Dietary synbiotic supplementation into the diet of broilers may be an effective method for improving growth performance and carcass compositions, resulting in the production of meat with a favorable quality and oxidative stability. © 2017 Society of Chemical Industry.

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Diabetic peripheral neuropathy (DPN) is the most common complication in both type 1 and type 2 diabetes, but any treatment toward the development of DPN is not yet available. Axon degeneration is an early feature of many peripheral neuropathies, including DPN. Delay of axon degeneration has beneficial effects on various neurodegenerative diseases, but its effect on DPN is yet to be elucidated. Deficiency of Sarm1 significantly attenuates axon degeneration in several models, but the effect of Sarm1 deficiency on DPN is still unclear. In this study, we show that Sarm1 knockout mice exhibit normal glucose metabolism and pain sensitivity, and deletion of the Sarm1 gene alleviates hypoalgesia in streptozotocin-induced diabetic mice. Moreover, Sarm1 gene deficiency attenuates intraepidermal nerve fiber loss in footpad skin; alleviates axon degeneration, the change of g-ratio in sciatic nerves, and NAD + decrease; and relieves axonal outgrowth retardation of dorsal root ganglia from diabetic mice. In addition, Sarm1 gene deficiency markedly diminishes the changes of gene expression profile induced by streptozotocin in the sciatic nerve, especially some abundant genes involved in neurodegenerative diseases. These findings demonstrate that Sarm1 gene deficiency attenuates DPN in mice and suggest that slowing down axon degeneration is a potential promising strategy to combat DPN.