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Luminal glucose protects against ischemia/reperfusion‐induced intestinal epithelial barrier defects in rats
Author(s) -
Huang ChingYing,
Hsiao JongKai,
Lu YenZhen,
Yu Linda C.H.
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.1120.11
Subject(s) - mannitol , intestinal permeability , medicine , jejunum , endocrinology , ischemia , superior mesenteric artery , chemistry , in vivo , pathology , biology , biochemistry , microbiology and biotechnology
Intestinal ischemia/reperfusion (I/R) results in mucosal barrier disruption and enteric bacterial translocation (BT). Previous study showed that enhanced sodium‐dependent glucose transport inhibits the LPS‐induced increase of epithelial permeability. The aim was to evaluate whether luminal glucose protects against I/R‐induced intestinal epithelial barrier defects in rats. A 10 cm jejunal loops was created containing Krebs buffer without or with 25 mM of sugar (glucose or mannitol). Rats then received sham operation or I/R challenge by occlusion of superior mesenteric artery for 20 min and reperfusion for 1 hr. Histological evidence exhibited shortened villi and denuded tips in the jejunum, and heightened bacterial colony forming units were seen in liver and spleen of I/R rats. A novel technique utilizing magnetic resonance imaging (MRI) was developed for the detection of real‐time in vivo intestinal permeability changes. A contrast probe gadodiamide was injected into the jejunal loop, and the increase of MRI signals in the liver, kidney and plasma were five fold higher in I/R rats compared to sham controls. The I/R‐induced jejunal mucosal damages, increased epithelial permeability and BT were reduced by administration of luminal glucose, but not of mannitol. These findings suggest that glucose plays a protective role against the intestinal barrier dysfunction induced by I/R.