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Loss of enteral nutrition in a mouse model results in intestinal epithelial barrier dysfunction
Author(s) -
Feng Yongjia,
Ralls Matthew W.,
Xiao Weidong,
Miyasaka Eiichi,
Herman Richard S.,
Teitelbaum Daniel H.
Publication year - 2012
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1111/j.1749-6632.2012.06572.x
Subject(s) - glutamine , parenteral nutrition , proinflammatory cytokine , barrier function , enteral administration , cytokine , tight junction , biology , medicine , immunology , inflammation , microbiology and biotechnology , biochemistry , amino acid
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.