Enteral supplementation with glycyl-glutamine improves intestinal barrier function after liver transplantation in rats

BackgroundMost patients after liver transplantation (LT) suffer from intestinal barrier dysfunction. Glycyl-glutamine (Gly-Gln) by parenteral supplementation is hydrolyzed to release glutamine, which improves intestinal barrier function in intestinal injury. This study aimed to investigate the effect of Gly-Gln by enterai supplementation on intestinal barrier function in rats after allogenetic LT under immunosuppressive therapy.MethodsTwelve inbred Lewis rats were selected randomly as donors, and 24 inbred Brown Norway (BN) rats as recipients of allogenetic LT. The recipients were divided into a control group (Ala, n=12) and an experimental group (Gly-Gln, n=12). In each group, 6 normal BN rats were sampled for normal parameters on preoperative day 3. The 6 recipients in the control group received alanine (Ala) daily by gastric perfusion for 3 preoperative days and 7 postoperative days, and the 6 recipients in the experimental group were given Gly-Gln in the same manner. The 12 BN recipients underwent orthotopic LT under sterile conditions after a 3-day fast and were given immunosuppressive therapy for 7 days. They were harvested for sampling on postoperative day 8. The following parameters were assessed: intestinal mucosal protein content, mucosal ultrastructure, ileocecal slgA content, portal plasma levels of endotoxin and TNF-α, and bacterial translocation.ResultsAll recipients were alive after LT. On preoperative day 3, all parameters were similar in the two groups. On postoperative day 8, all parameters in the two groups were remarkably changed from those on preoperative day 3. However, compared to the Ala group, supplementation with Gly-Gln increased the levels of intestinal mucosal protein and ileocecal slgA, improved mucosal microvilli, and decreased portal plasma levels of endotoxin and TNF-α as well as bacterial translocation.ConclusionEnterai supplementation with Gly-Gln improved intestinal barrier function after allogenetic LT in rats.