Background: Ingested peanut agglutinin stimulates colonic proliferation in
humans. In rats, ingested peanut agglutinin stimulates hormone release and
proliferation in the small and large intestines. Peanut agglutinin is absor
bed into the circulation but little is known about the systemic effect of t
his lectin. Therefore, we studied the effect of intravenous peanut agglutin
in on hormone release and intestinal growth.
Methods: Six rats per group received peanut agglutinin infusion at 0, 2, 20
or 200 mu g/rat/day for 6 days via the right jugular vein. Organ weights w
ere measured, pancreatic enzymes, DNA, RNA and protein levels were analysed
. Plasma hormones were measured by radioimmunoassay. All tissues were exami
ned histologically. Small intestinal and colonic proliferation rates were e
stimated by metaphase arrest.
Results: High-dose peanut agglutinin significantly reduced the wet weight o
f the stomach by 7% (P < 0.05) and large intestine by 10% (P < 0.05). Peanu
t agglutinin dose-dependently released enteroglucagon; low-, medium- and hi
gh-dose by 64%, 126% (P < 0.01) and 180% (P < 0.01), respectively, and gluc
agon-like peptide-1 by 127% (P < 0.01), 169% (P < 0.01) and 315% (P < 0.001
), respectively. Peanut agglutinin had no effect on cholesystokinin, gastri
n or insulin levels. Peanut agglutinin, low-, medium- and high-dose stimula
ted proliferation in the mid colon by 42% (P < 0.01), 30% and 38%, respecti
vely. Only high-dose peanut agglutinin stimulated proliferation in the dist
al colon by 54% (P < 0.01). No histological changes were evident in any tis
sue.
Conclusion: Intravenous peanut agglutinin released hormones and stimulated
colonic proliferation. Proliferation of the small intestine seen after inge
stion of peanut agglutinin in previous studies appears to require luminal c
ontact between enterocytes and the lectin. Possible clinical applications i
nclude reversal of atrophy during total parenteral nutrition, anastomotic h
ealing after surgery and restoration of mucosa integrity in colitis.