BACKGROUND: The effect of glutamine-enriched early enteral nutrition (Gln-EEN) on intestinal mucosal barrier injury after liver transplantation (LT) remains uncertain. METHODS: The Wistar-to-Wistar rat LT model was used to explore the protective effect of Gln-EEN. Morphologic changes of intestinal mucosa, levels of intestinal malondialdehyde and secretory immunoglobulin (sIgA), plasma endotoxin, D-lactic acid, serum tumor necrosis factor-alpha (TNF-alpha), rates of bacterial translocation, and expression of intestinal nuclear factor-kappaB, TNF-alpha, and intercellular adhesion molecule-1 were determined. RESULTS: After LT, intestinal mucosa was damaged seriously. At 12, 24, and 48 hours posttransplantation, levels of intestinal sIgA were decreased; levels of malondialdehyde, endotoxin, D-lactic acid, and TNF-alpha, the ratio of bacterial translocation, and the expression of intestinal nuclear factor-kappaB, TNF-alpha, and intercellular adhesion molecule-1 all were increased. However, changes in earlier-mentioned parameters in recipients treated with Gln-EEN were attenuated remarkably at 24 to 48 hours. CONCLUSIONS: Our data show that Gln-EEN is a potent protectant against intestinal mucosal barrier injury after LT.
BACKGROUND: The effect of glutamine-enriched early enteral nutrition (Gln-EEN) on intestinal mucosal barrier injury after liver transplantation (LT) remains uncertain. METHODS: The Wistar-to-Wistar rat LT model was used to explore the protective effect of Gln-EEN. Morphologic changes of intestinal mucosa, levels of intestinal malondialdehyde and secretory immunoglobulin (sIgA), plasma endotoxin, D-lactic acid, serum tumor necrosis factor-alpha (TNF-alpha), rates of bacterial translocation, and expression of intestinal nuclear factor-kappaB, TNF-alpha, and intercellular adhesion molecule-1 were determined. RESULTS: After LT, intestinal mucosa was damaged seriously. At 12, 24, and 48 hours posttransplantation, levels of intestinal sIgA were decreased; levels of malondialdehyde, endotoxin, D-lactic acid, and TNF-alpha, the ratio of bacterial translocation, and the expression of intestinal nuclear factor-kappaB, TNF-alpha, and intercellular adhesion molecule-1 all were increased. However, changes in earlier-mentioned parameters in recipients treated with Gln-EEN were attenuated remarkably at 24 to 48 hours. CONCLUSIONS: Our data show that Gln-EEN is a potent protectant against intestinal mucosal barrier injury after LT.