Lectins are
proteins or
glycoproteins of nonimmune origin, which bind specifically to
carbohydrate structures. They are widespread in the human diet, and many are resistant to digestion. High doses of
lectins have been shown to stimulate intestinal and pancreatic growth. The aim of the present study was to investigate the long-term actions of low doses of
lectins on the rat intestine and pancreas. A long-term
carcinogenesis study was performed using low levels (40 micro g/rat/day) of peanut (PNA) or mushroom
lectin (ABA) which bind to O-linked (
mucin-type)
oligosaccharides in the gut. While this was primarily designed as a colon
carcinogenesis study, the pancreas was also investigated. No significant changes in colon
carcinogenesis were seen, however, the colons were slightly heavier in the
lectin treated groups. The weight of the pancreas was significantly greater (by 18 and 23%) in both
lectin treated groups (P < 0.03/0.001). The weights of the acini and septal tissue were also increased by 39-46% in PNA and ABA fed animals, respectively (P < 0.002); there was no significant change in the endocrine pancreas. In conclusion, long-term feeding of low doses of
lectin can influence pancreatic growth, and this trophic action may have potential adverse implications for the development of
pancreatic cancer in humans.