Glucagon-like peptide 2 is a potent growth factor for small intestine and colon |
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Authors: | Litvak David A Hellmich Mark R Evers B Mark Banker Nitesh A Townsend Courtney M |
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Institution: | (1) Department of Surgery, The University of Texas Medical Branch, 301 University Blvd., 77555-0527 Galveston, TX |
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Abstract: | Factors that stimulate gut mucosal proliferation may be beneficial during periods of gut disuse or atrophy. Recently glucagon-like
peptide 2 (GLP-2) has been shown to stimulate small bowel growth. The purpose of our study was to compare the trophic effects
of GLP-2 with those of neurotensin (NT), a potent gut trophic factor. Mice were randomized to receive either GLP-2, NT, or
saline solution (control) for 10 days. The mice were killed on day 11, at which time the jejunum, ileum, and colon were removed,
weighed, and DNA and protein content measured. Mice treated with GLP-2 showed a significant increase in the weight of the
jejunum, ileum, and colon compared to both control and NT-treated mice. DNA content, a marker of cellular hyperplasia, was
significantly increased in the small bowel and colon by treatment with GLP-2 and NT compared to control tissues. Small intestinal
protein content, an indicator of cellular hypertrophy, was significantly increased by GLP-2 compared to both NT and control;
protein content of the colon was greater in each of the treatment groups compared with control mice. We have demonstrated,
for the first time, that GLP-2 stimulates colonic growth. In addition, GLP-2 is a potent trophic factor of normal small intestine
with proliferative effects that are equal to or greater than those of NT Administration of GLP-2 may be useful clinically
to enhance small intestinal regeneration and adaptation during periods of disease and in the early phases of the short bowel
syndrome.
Supported by grants from the National Institutes of Health (PO1 DK35608, ROl AG10885, and T32-DK07633).
Presented at the Thirty-Eighth Annual Meeting of The Society for Surgery of the Alimentary Tract, Washington, D.C., May 11–14,
1997, and published as an abstract in Gastroenterology 112:A1455, 1997. |
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