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

被引:66
作者
Feng, Yongjia [1 ]
Ralls, Matthew W. [1 ]
Xiao, Weidong [1 ]
Miyasaka, Eiichi [1 ]
Herman, Richard S. [1 ]
Teitelbaum, Daniel H. [1 ]
机构
[1] Univ Michigan, Dept Surg, Pediat Surg Sect, Ann Arbor, MI 48109 USA
来源
BARRIERS AND CHANNELS FORMED BY TIGHT JUNCTION PROTEINS II | 2012年 / 1258卷
关键词
small intestine; p-Akt; parenteral nutrition; epithelial barrier function; TOTAL PARENTERAL-NUTRITION; GAMMA-INDUCED INCREASES; GROWTH-FACTOR; INTRAEPITHELIAL LYMPHOCYTES; POTENTIAL MECHANISM; RECEPTOR ACTIVATION; CELL PROLIFERATION; EGF RECEPTOR; EXPRESSION; GUT;
D O I
10.1111/j.1749-6632.2012.06572.x
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
070301 [无机化学]; 070403 [天体物理学]; 070507 [自然资源与国土空间规划学]; 090105 [作物生产系统与生态工程];
摘要
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.
引用
收藏
页码:71 / 77
页数:7
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