Administration of a dipeptidyl peptidase IV inhibitor enhances the intestinal adaptation in a mouse model of short bowel syndrome
Research output: Contribution to journal › Journal article › Research › peer-review
Glucagon-like peptide-2 induces small intestine mucosal epithelial cell proliferation and may have benefit for patients who suffer from short bowel syndrome. However, glucagon-like peptide-2 is inactivated rapidly in vivo by dipeptidyl peptidase IV. Therefore, we hypothesized that selectively inhibiting dipeptidyl peptidase IV would prolong the circulating life of glucagon-like peptide-2 and lead to increased intestinal adaptation after development of short bowel syndrome.
Original language | English |
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Journal | Surgery |
Volume | 150 |
Issue number | 2 |
Pages (from-to) | 217-223 |
Number of pages | 7 |
ISSN | 0263-9319 |
DOIs | |
Publication status | Published - Aug 2011 |
- Adaptation, Physiological, Animals, Dipeptidyl-Peptidase IV Inhibitors, Disease Models, Animal, Glucagon-Like Peptide 2, Intestine, Small, Mice, Mice, Inbred C57BL, Short Bowel Syndrome
Research areas
ID: 38433225