Red kidney bean lectin is a potent cholecystokinin releasing stimulus in the rat inducing pancreatic growth

Abstract

Background-Lectins are proteins capable of specific binding to carbohydrates 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 the ligand. Oral administration of phytohaemagglutinin (PHA) in rats dose dependently induces growth of the small intestine and the pancreas by an unknown mechanism. Aims-To investigate the mechanism of PHA induced intestinal and pancreatic growth. Methods-Thirty day old male rats were pairfed for 10 days with lactalbumin as a control diet or lactalbumin plus PHA or purified soybean trypsin inhibitor (STI) as a positive control (42 mg/rat/day) with or without 20 µg of the cholecystokinin A (CCK-A) antagonist MK 329. To investigate further the eVect of PHA on CCK release intestinal mucosal cells were isolated from rats which were continuously perfused in a perfusion apparatus. CCK release into the medium was assayed. Results-PHA and STI significantly stimulated growth of the pancreas and the small intestine. MK 329 blocked this growth eVect in the pancreas but not in 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 addition, in vitro PHA dose dependently stimulated CCK release with a maximal eVect at 100 ng/ml. Conclusion-In vivo and in vitro PHA is a potent stimulus for CCK release in the rat, thereby inducing pancreatic growth, whereas intestinal growth is stimulated by a CCK independent mechanism.

The influence of lectins isolated from pea and soyabean seeds on performance and pancreatic enzyme activity in rats

“…According to Liener (1994) and Rådberg et al (2001) lectins can modulate hormone secretion (insulin, CCK, gastrin). At high doses, lectin intake can lead to intestinal and pancreatic overgrowth (Jordinson et al, 1996;Herzig et al, 1997;Grant et al, 2000;Kelsall et al, 2002). Our results showed that the applied doses of PSA and SBA did not result in significant pancreatic overgrowth, which is in agreement with Li et al (2003a,b) and our previous study (Czerwiński et al, 2005).…”

“…Many authors have shown that lectins interacting with brush border membrane can modulate CCK secretion by intestinal endocrine cells (Jordinson et al, 1996;Herzig et al, 1997;Li et al, 2003a,b). Moreover, absorbed lectins can immediately interact with pancreatic cells Kelsall et al, 2002).…”

“…Finally, they can influence the secretion and activity of enzymes. At high doses, lectins can stimulate intestinal and pancreatic overgrowth (Jordinson et al, 1996;Herzig et al, 1997;Grant et al, 2000;Kelsall et al, 2002), diminish enzyme activity (protease, disaccharidase), disturb lipid absorption in the small intestine and modulate insulin, CCK and gastrin secretion (Liener, 1994;Bardocz et al, 1999).…”

TRPA1 channel activation induces cholecystokinin release via extracellular calcium

“…CCK is released from enteroendocrine I-cells in the mucosa of duodenum and proximal jejunum in the intestinal phase of digestion in response to fatty acids and proteins in the intestinal lumen [25] and other duodenal peptides [26]. CCK activates the CCK1 receptors in the afferent fibers of the vagus nerve which in addition to the elevated plasma CCK levels mediates the digestive effects of CCK by stimulating exocrine pancreatic secretion and gallbladder contraction.…”

The effect of early-life kidney bean lectin administration on pig performance in the peri-weaning period – a safety study

“…The higher levels of glucose in the blood of piglets receiving kidney bean lectin extract in our study may be a sign of high reactivity of the exocrine pancreas in these animals as compared with the control group. These binding results in the stimulation of the release of cholecystokinin and glucagon-like peptides (Herzig et al, 1997;Rådberg et al, 2001), two hormones known to stimulate exo-and endocrine pancreas function. According to Grant et al (1987), a high lectin content induces glycogen catabolism and as a result of this process, serum glucose levels increase.…”