RED KIDNEY BEAN LECTIN IS A POTENT CHOLECYSTOKININ RELEASING STIMULUSIN THE RAT INDUCING PANCREATIC GROWTH

Citation
Kh. Herzig et al., RED KIDNEY BEAN LECTIN IS A POTENT CHOLECYSTOKININ RELEASING STIMULUSIN THE RAT INDUCING PANCREATIC GROWTH, Gut, 41(3), 1997, pp. 333-338
Citations number
57
Categorie Soggetti
Gastroenterology & Hepatology
Journal title
GutACNP
ISSN journal
00175749
Volume
41
Issue
3
Year of publication
1997
Pages
333 - 338
Database
ISI
SICI code
0017-5749(1997)41:3<333:RKBLIA>2.0.ZU;2-Z
Abstract
Background-Lectins are proteins capable of specific binding to carbohy drates without altering their covalent structure. As an essential part of plants they are ingested in our daily diet. By binding to glycosyl side chains of receptors lectins can mimic or inhibit the action of t he ligand. Oral administration of phytohaemagglutinin (PHH) in rats do se dependently induces growth of the small intestine and the pancreas by an unknown mechanism. Aims-To investigate the mechanism of PHA indu ced intestinal and pancreatic growth. Methods-Thirty day old male rats were pairfed for 10 days with lactalbumin as a control diet or lactal bumin plus PHA or purified soybean trypsin inhibitor (STI) as a positi ve control (42 mg/rat/day) with or without 20 mu g of the cholecystoki nin A (CCK-A) antagonist MK 329. To investigate further the effect of PHA on CCK release intestinal mucosal cells were isolated from rats wh ich were continuously perfused in a perfusion apparatus. CCK release i nto the medium was assayed. Results-PHA and STI significantly stimulat ed growth of the pancreas and the small intestine. MK 329 blocked this growth effect in the pancreas but not in Germany the small intestine. In vivo, PHA significantly increased CCK plasma levels from 0.75 to 6 .67 (SEM 2.23) compared with 2.3 (0.35) pM in the control group. In ad dition, in vitro PHA dose dependently stimulated CCK release with a ma ximal effect at 100 ng/ml. Conclusion-In vivo and in vitro PHA is a po tent stimulus for CCK release in the rat, thereby inducing pancreatic growth, whereas intestinal growth is stimulated by a CCK independent m echanism.