4.3 Article

Effects of glutamine supplementation on the immune status in weaning piglets with intrauterine growth retardation

期刊

ARCHIVES OF ANIMAL NUTRITION
卷 66, 期 5, 页码 347-356

出版社

TAYLOR & FRANCIS LTD
DOI: 10.1080/1745039X.2012.683325

关键词

cytokines; glutamine; heat shock proteins; piglets; growth retardation; immune responses; immune globulins

资金

  1. National Natural Science Foundation of China [30972116]
  2. Foundation of Nanjing Agricultural University [KJ2011010]
  3. Specialized Research Fund for the Doctoral Program of Higher Education of China [20110097120033]
  4. Priority Academic Program Development of Jiangsu Higher Education Institutions

向作者/读者索取更多资源

Neonates with intrauterine growth retardation (IUGR) often suffer from impaired cellular immunity, and weaning may further aggravate adverse effects of IUGR on development and function of the immune system. In this study, we investigated effects of glutamine supplementation on immune status in the intestines of weaning pigs with IUGR, focusing on molecular mechanisms underlying altered immune response. Piglets with IUGR were weaned at 21 days of age and received orally 1.22 g alanine or 1 g glutamine per kg body weight every 12 h. Weight gain and intestinal weight of weaning piglets were increased by glutamine supplementation. Levels of serum IgG in piglets supplemented with glutamine were increased compared with Control piglets. The production of IL-1 and IL-8 in the serum and jejunum was decreased by glutamine supplementation, whereas the levels of IL-4 in the serum and the concentrations of IL-4 and IL-10 in the jejunum were increased. The expression of heat shock protein 70 (Hsp70) in the jejunum was increased by glutamine supplementation, but the degradation of inhibitor kappa B and the activity of nuclear factor-kappa B (NF-kappa B) were decreased. In conclusion, glutamine supplementation enhanced immune response in weaning piglets with IUGR. The effects of glutamine in IUGR are associated with increased Hsp70 expression and suppression of NF-kappa B activation.

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