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
Manabu Okawada, Jens Juul Holst, Daniel H Teitelbaum
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.
|Number of pages||7|
|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