Loss of enteral nutrition in a mouse model results in intestinal epithelial barrier dysfunction
Version of Record online: 25 JUN 2012
© 2012 New York Academy of Sciences.
Annals of the New York Academy of Sciences
Volume 1258, Barriers and Channels Formed by Tight Junction Proteins II pages 71–77, July 2012
How to Cite
Feng, Y., Ralls, M. W., Xiao, W., Miyasaka, E., Herman, R. S. and Teitelbaum, D. H. (2012), Loss of enteral nutrition in a mouse model results in intestinal epithelial barrier dysfunction. Annals of the New York Academy of Sciences, 1258: 71–77. doi: 10.1111/j.1749-6632.2012.06572.x
- Issue online: 25 JUN 2012
- Version of Record online: 25 JUN 2012
- small intestine;
- parenteral nutrition;
- epithelial barrier function
Total parenteral nutrition (TPN) administration in a mouse model leads to a local mucosal inflammatory response, resulting in a loss of epithelial barrier function (EBF). Although, the underlying mechanisms are unknown, a major contributing factor is a loss of growth factors and subsequent critical downstream signaling. An important component of these is the p-Akt pathway. An additional contributing factor to the loss of EBF with TPN is an increase in proinflammatory cytokine abundance within the mucosal epithelium, including TNF-α and IFN-γ. Loss of critical nutrients, including glutamine and glutamate, may affect EBF, contributing to the loss of tight junction proteins. Finding protective modalities for the small intestine during TPN administration may have important clinical applications. Supplemental glutamine and glutamate may be examples of such agents.