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Glucagon‐Like Peptide 2 Is an Endogenous Mediator of Postresection Intestinal Adaptation
Author(s) -
Perez Alexander,
Duxbury Mark,
Rocha Flavio G.,
Ramsanahie Anthony P.,
Farivar Robert S.,
Varnholt Heike,
Ito Hiromichi,
Wong Helen,
Rounds Jan,
Zinner Michael J.,
Whang Edward E.,
Ashley Stanley W.
Publication year - 2005
Publication title -
journal of parenteral and enteral nutrition
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.935
H-Index - 98
eISSN - 1941-2444
pISSN - 0148-6071
DOI - 10.1177/014860710502900297
Subject(s) - ileum , endogeny , glucagon like peptide 2 , small intestine , glucagon , mediator , medicine , short bowel syndrome , gastroenterology , glucagon like peptide 1 , gastrointestinal hormone , jejunum , adaptation (eye) , endocrinology , biology , peptide hormone , peptide , hormone , parenteral nutrition , biochemistry , diabetes mellitus , type 2 diabetes , neuroscience
Background: After massive small bowel resection, the remnant intestine undergoes compensatory adaptation. We tested the hypothesis that glucagon‐like peptide‐2 (GLP‐2) is an endogenous mediator of postresection intestinal adaptation. Methods: Rats were allocated to 1 of 4 groups: groups 1 and 2 rats underwent mid‐small bowel transection and reanastomosis; groups 3 and 4 rats underwent 75% mid‐small bowel resection and reanastomosis. Groups 2 and 4 rats were administered 1.8 mg of antirat GLP‐2 antibody twice daily beginning immediately after the surgical procedure; groups 1 and 3 rats were administered rabbit serum (control). Ileal specimens were harvested on postoperative day 7. Results: Ileal mucosa from group 3 animals displayed morphologic and proliferative indices of adaptation. Each of these indices of adaptation was inhibited by GLP‐2 immunoneutralization (group 4). Morphologic and proliferative parameters in the ileum from animals that had undergone transection with reanastomosis were unaffected by GLP‐2 immunoneutralization. Conclusions: These results suggest that GLP‐2 is an endogenous mediator of postresection intestinal adaptation.