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1 Gastrointestinal Research Group, University of Calgary, Calgary, Alberta, Canada
2 The Panum Institute, Department of Medical Physiology, University of Copenhagen, Copenhagen, Denmark
3 NPS Pharmaceuticals, Mississauga, Ontario, Canada
* To whom correspondence should be addressed. E-mail: marting{at}ucalgary.ca.
Glucagon-like peptide-2 (GLP-2) is an enteroendocrine peptide that is released in response to luminal nutrients and has unique trophic actions in the gastrointestinal tract. These features suggest GLP-2 may be important in controlling intestinal adaptation. We examined the relationship over time of GLP-2 production and adaptation to intestinal resection, the effects of resection-induced malabsorption on GLP-2 production, and the correlation of endogenous serum GLP-2 levels with adaptation as measured by crypt cell proliferation (CCP). We initially examined the effect of nutrient malabsorption, induced by a 90% resection of the proximal intestine studied on day 4, on the time course and levels of GLP-2 release. Secondly, the degree of malabsorption was varied by performing intestinal transection or 50, 75, or 90 % resection of proximal small intestine. Lastly, the relationship of GLP-2 levels over time with adaptation to a 90% resection was examined by determining GLP-2 levels on days 7, 14, and 28, and correlating this with intestinal adaptation, as assessed by morphology and CCP rate. 90% resection significantly increased basal and post-prandial GLP-2 levels, with a net increase in nutrient stimulated exposure over 90 minutes: GLP-2 exposure (integrated levels versus time) increased 12.7 fold in resected animals (p<0.001). Basal and post-prandial GLP-2 levels significantly correlated with the magnitude of intestinal resection (r2=0.71; p<0.001), CCP (r2=0.48; p<0.005), and nutrient malabsorption (protein p<0.001; fat p<0.005). The increase in CCP was maintained to 28 days following small bowel resection and was associated with an ongoing elevation in GLP-2 release. These findings suggest that GLP-2 is important in initiating and maintaining the small intestinal adaptive response to resection.
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