Administration of a dipeptidyl peptidase IV inhibitor enhances the intestinal adaptation in a mouse model of short bowel syndrome
Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › fagfællebedømt
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.
Originalsprog | Engelsk |
---|---|
Tidsskrift | Surgery |
Vol/bind | 150 |
Udgave nummer | 2 |
Sider (fra-til) | 217-223 |
Antal sider | 7 |
ISSN | 0263-9319 |
DOI | |
Status | Udgivet - aug. 2011 |
ID: 38433225