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Seventy-two crossbred pigs (Duroc x Large White x Landrace) weaned at age 21± 1 d (5.78 ± 0.26 kg), were balanced for initial body weight and ancestry across four treatment groups. Pigs were allotted to four treatments including: (1) non-challenged control; (2) LPS-challenged control; (3) LPS + 0.5% Arg; (4) LPS + 1.0% Arg. On day 16, pigs were injected with LPS or sterile saline. At 6 h post-injection, one pig per pen was killed for evaluation of intestinal morphology and gene expression of pro-inflammatory cytokines and PPARg. The remaining pigs per pen were provided feed until 08.00 hours of day 18. Body weight and feed intake were measured on days 0, 16 and 18.
Within 48 h of challenge, 0.5% Arg alleviated the weight loss induced by LPS challenge (P=0.025). In all three intestinal segments, 0.5 or 1.0% Arg mitigated intestinal morphology impairment (e.g. lower villus height and higher crypt depth) induced by LPS challenge (P<0.05), and alleviated the decrease of crypt cell proliferation and the increase of villus cell apoptosis after LPS challenge (P<0.01). The 0.5% Arg prevented the elevation of jejunal IL-6 mRNA abundance (P=0.082), and jejunal (P=0.030) and ileal (P=0.039) TNF-a mRNA abundance induced by LPS challenge. The 1.0% Arg alleviated the elevation of jejunal IL-6 mRNA abundance (P=0.053) and jejunal TNF-a mRNA abundance (P=0.003) induced by LPS challenge. The 0•5% Arg increased PPARg mRNA abundance in all three intestinal segments (P<0.10), and 1.0% Arg increased duodenal PPARg mRNA abundance (P=0.094).
It is concluded that Arg supplementation has beneficial effects in alleviating gut mucosal injury induced by LPS challenge. Additionally, it is possible that the protective effects of Arg on the intestine are associated with decreasing the expression of intestinal proinflammatory cytokines through activating PPARg expression.
Y Liu, J Huang, Y Hou, H Zhu, S Zhao, B Ding, Y Yin, G Yi, J Shi and W Fan. 2008. British Journal of Nutrition. 100:552-560.
