Gastrointestinal responses to a panel of lectins in rats maintained on total parenteral nutrition

Total parenteral nutrition (TPN) causes atrophy of gastrointestinal epithel ia, so we asked whether lectins that stimulate epithelial proliferation can reverse this effect of TPN. Two lectins stimulate pancreatic proliferation by releasing CCK, so we asked whether lectins that stimulate gastrointesti nal proliferation also release hormones that might mediate their effects. S ix rats per group received continuous infusion of TPN and a once daily bolu s dose of purified lectin (25 mg . rat(-1) . day(-1)) or vehicle alone (con trol group) for 4 days via an intragastric cannula. Proliferation rates wer e estimated by metaphase arrest, and hormones were measured by RIAs. Phytoh emagglutinin (PHA) increased proliferation by 90% in the gastric fundus (P < 0.05), doubled proliferation in the small intestine (P < 0.001), and had a small effect in the midcolon (P < 0.05). Peanut agglutinin (PNA) had a mi nor trophic effect in the proximal small intestine (P < 0.05) and increased proliferation by 166% in the proximal colon (P < 0.001) and by 40% in the midcolon (P < 0.001). PNA elevated circulating gastrin and CCK by 97 (P < 0 .05) and 81% (P < 0.01), respectively, and PHA elevated plasma enteroglucag on by 69% and CCK by 60% (both P < 0.05). Only wheat germ agglutinin increa sed the release of glucagon-like peptide-1 by 100% (P < 0.05). PHA and PNA consistently reverse the fall in gastrointestinal and pancreatic growth ass ociated with TPN in rats. Both lectins stimulated the release of specific h ormones that may have been responsible for the trophic effects. It is sugge sted that lectins could be used to prevent gastrointestinal atrophy during TPN. Their hormone-releasing effects might be involved.