Peanut ingestion increases rectal proliferation in individuals with mucosal expression of peanut lectin receptor

Abstract

Background & Aims: The Thomsen–Friedenreich blood group antigen (galactose β1,3- N-acetyl galactosamine α-) acts as an oncofetal antigen in the colonic epithelium, with low expression in normal adult epithelia but increasing to fetal levels of expression in hyperplasia or malignancy. Peanut lectin is one of the commonest dietary lectins that binds this antigen. The aim of this study was to determine whether peanut ingestion can alter rectal epithelial proliferation. Methods: Thirty-six patients with normal colonic mucosa consumed 100 g of peanuts each day for 5 days. Rectal mitotic index was measured before and after ingestion, and changes in proliferation were correlated with immunohistochemical detection of lectin receptor expression by colonocytes and fecal lectin activity as measured by hemagglutination assay. Results: Peanut ingestion caused a 41% increase in rectal mucosal proliferation in individuals with macroscopically normal mucosa who express TF antigen in their rectal mucosae (10 of 36 patients studied). The proliferative response correlated with fecal hemagglutinating activity, and peanut lectin could be shown immunohistochemically within the rectal mucosa. Conclusions: The common expression of galactose β1,3- N-acetyl galactosamine α- by hyperplastic and neoplastic epithelia may therefore be functionally important because it allows interaction with mitogenic dietary lectins. This could be an important mechanism for the association between diet and colorectal cancer. GASTROENTEROLOGY 1998;114:44-49