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
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.