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Clinical Models of Intestinal Adaptation
Author(s) -
SCHULZKE JÖRGDIETER,
SCHMITZ HEINS,
FROMM MICHAEL,
BENTZEL CARL J.,
RIECKEN ERNST OTTO
Publication year - 1998
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.1749-6632.1998.tb11117.x
Subject(s) - tight junction , cotransporter , downregulation and upregulation , jejunum , intestinal mucosa , microbiology and biotechnology , chemistry , barrier function , adaptation (eye) , hyperplasia , endocrinology , biophysics , medicine , biology , biochemistry , neuroscience , gene , organic chemistry , sodium
ABSTRACT: Mucosal adaptation of the small intestine is morphologically restricted to only three different patterns, namely, atrophy , hyperplasia , and hyperregeneration . The hyperplastic mucosa in the experimental short bowel syndrome exhibits unchanged epithelial barrier properties and a differential functional adaptation with a 150% increase in Na‐glucose cotransport but no change in electroneutral NaCl cotransport. In the hyperregeneratively transformed mucosa of the self‐filling blind loop of rat jejunum, absorption is seriously impaired, as indicated by the 80% decrease in Na‐glucose cotransport. To compensate for this, epithelial barrier function is upregulated by an increase in tight junction complexity to prevent leak flux of ions and substrates. In contrast, the hyperregeneratively transformed mucosa in celiac sprue shows reduced tight junction complexity. Possible candidates responsible for the heterogeneity of tight junction adaptation in these conditions could be cytokines, because tumor necrosis factor‐a can specifically downregulate the tight junction, as indicated in the intestinal HT‐29/B6 cell model.