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Glucagon-Like Peptide 2 Is an Endogenous Mediator of Postresection Intestinal Adaptation

Alexander Perez, MD^*, Mark Duxbury, MA, MRCS^*, Flavio G. Rocha, MD^*, Anthony P. Ramsanahie, FRCS^*, Robert S. Farivar, MD, PhD^*, Heike Varnholt, MD, Hiromichi Ito, MD^*, Helen Wong, MD, Jan Rounds, BSc^*, Michael J. Zinner, MD^*, Edward E. Whang, MD^* and Stanley W. Ashley, MD^*

From the ^* Department of Surgery, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts; Department of Pathology, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts; and CURE: Digestive Disease Research Center, University of California, Los Angeles, California

Correspondence: Stanley W. Ashley, MD, Department of Surgery, Brigham and Women's Hospital, 75 Francis Street, Boston, MA 02115. Electronic mail may be sent to sashley{at}partners.org.

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.

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