Intestinal mucosal adaptation in re-fed mice is dependent on the physiological actions of glucagon-like peptide-2 (GLP-2).
Published: 2004
Language: eng
Number of pages: 86
Description: Our understanding of the intestinotropic actions of GLP-2 is based upon pharmacological studies, However, the physiological role of GLP-2 remains poorly understood. The antagonistic properties of the dipeptidylpeptidase-IV-derived metabolite, GLP-23--33 were determined in BHK-cells transfected with the GLP-2 receptor. To investigate the role of endogenous GLP-2 in gut adaptation, GLP-23--33 was administered to mice that were re-fed for 24hr after 24hr of fasting. Fasting mice exhibited atrophy of the small intestine, with a decrease in weight, crypt-villus height and an increase apoptosis. Adaptive growth in re-fed mice restored small intestinal weight, crypt-villus height, proliferation, and apoptosis to normal control levels. Concomitant treatment of re-fed mice with GLP-23--33 prevented the adaptive changes in small intestinal weight, crypt-villus height, proliferation and apoptosis. Endogenous GLP-2 is therefore a physiological regulator of the dynamic adaptation of the gut mucosal epithelium in response to luminal nutrients, through modulation of crypt cell proliferation and villus apoptosis.
Notes: Thesis (M.Sc.)--University of Toronto, 2004.

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Source: Masters Abstracts International, Volume: 43-03, page: 0764.

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