Background/aims: The aim of this trial was to study the role of glucagon-like peptide-2 in reducing bacterial translocation by virtue of its anti-inflammatory effects and ability to decrease intestinal permeability in rat models of inflammatory bowel diseases. On the basis of our results and those of other recent studies, we suggest a new treatment modality for colitis. To our knowledge, this is the first study of the effectiveness of glucagon-like peptide-2 on bacterial translocation, in treating an. experimental colitis model. Methods: Rats were randomized into 3 groups of 7 rats each-the control group, colitis group, and treatment group. On the 75 day after induction of colitis, the levels of tissue myeloperoxidase, serum tumor necrosis factor-alpha, and plasma endotoxin were measured. Tissue samples were obtained from the liver, spleen, and mesenteric lymph nodes for evaluating bacterial translocation. Results: Bacterial translocation in samples of the liver, spleen, mesenteric lymph nodes, and portal and systemic blood obtained from the treatment group was lower than that in samples obtained from the colitis group (p<0.05). The levels of tissue myeloperoxidase, serum tumor necrosis factor-alpha, and plasma endotoxin in the treatment group were significantly lower than those in the colitis group (p<0.05). Conclusions: In experimental colitis models, which were induced using trinitrobenzene sulfonic acid in ethanol, glucagon-like peptide-2 treatment reduced inflammation and bacterial translocation from the intestinal mucosa. Our results indicate that glucagon-like peptide-2 is a potential agent for treating colitis; however, extensive trials are needed to confirm our results.