Administration of a dipeptidyl peptidase IV inhibitor enhances the intestinal adaptation in a mouse model of short bowel syndrome

Research output: Contribution to journalJournal articleResearchpeer-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.
Original languageEnglish
Issue number2
Pages (from-to)217-223
Number of pages7
Publication statusPublished - Aug 2011

    Research areas

  • Adaptation, Physiological, Animals, Dipeptidyl-Peptidase IV Inhibitors, Disease Models, Animal, Glucagon-Like Peptide 2, Intestine, Small, Mice, Mice, Inbred C57BL, Short Bowel Syndrome

ID: 38433225