4.7 Article Book Chapter

Loss of enteral nutrition in a mouse model results in intestinal epithelial barrier dysfunction

出版社

BLACKWELL SCIENCE PUBL
DOI: 10.1111/j.1749-6632.2012.06572.x

关键词

small intestine; p-Akt; parenteral nutrition; epithelial barrier function

资金

  1. NIAID NIH HHS [R01 AI044076-13, R01 AI-4407-12, R01 AI-4407-11, R01 AI044076, R01 AI044076-12] Funding Source: Medline

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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-alpha and IFN-gamma. 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.

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