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. 2026 Aug 14;63:e26028. doi: 10.1590/S0004-2803.24612026-028

TABLE 3. Level of evidence and main clinical findings of the included studies.

Citation Level of evidence Main clinical findings
Liu et al., 2025 11 VI - Weak Treatment with the peptide 1907B (a dual agonist of GCGR/GLP1R) restores signaling at the receptors of these enzymes; reduces glycolysis and lactate production in epithelial cells; decreases H3K9 lactylation, inhibiting the activation of pro-fibrotic genes; and reduces intestinal fibrosis histologically.
Wang, Zhang, Zhang 2023 12 III - Strong Mice treated with GLP-1 analogs showed improvement in ulcerative colitis at the histological level; in these tissues, they obtained a reduction in the expression of inflammatory cytokines, such as IL-1β, IL-6 and TNF-α; modulation of the intestinal microbiota favoring the presence of beneficial microorganisms.
Zatorski et al., 2019 8 V - Moderate GLP-1 has suppressive effects on inflammatory cytokines in intestinal tissues, improves the intestinal barrier function by aiding in the integrity of the epithelium, assists in the remission of IBD, and reduces the severity and activity of IBD. GLP-2 stimulates the proliferation of intestinal epithelial cells and reduces permeability, stimulates the regeneration of the intestinal mucosa, and alters the intestinal bacterial flora.
El-Jamal et al., 2014 15 III - Strong The expression of GLP-2 receptors: was found in extraintestinal media, mainly in the liver; its expression was reduced by up to 60% in tissues extensively affected by inflammation. The use of GLP-2 analogs aided in liver regeneration in mice after partial hepatectomy, with histological evidence.
Villumsen et al., 2021 4 IV - Moderate The use of GLP-1 analogs did not increase IBD activity in participants, with typical gastrointestinal symptoms occurring, but without flare-ups of the underlying disease. This medication is linked to a lower risk of hospitalizations and surgeries, in addition to enabling the control of inflammation, avoiding the escalation of immunosuppressive drugs. GLP-1 reduces the expression of inflammatory cytokines (TNF-α, IL-6, IL-1β), aids in the integrity of the intestinal mucosa, and modulates the intestinal microbiota with an increase in beneficial microorganisms.
Pizzoferrato et al., 2022 16 V - Moderate The use of teduglutide in patients with Crohn’s disease after multiple surgical procedures and nutritional deficiencies has proven viable in reducing or even eliminating the need for parenteral nutrition in these patients. It presents only mild to moderate side effects, such as nausea or mild abdominal pain.
Buchman et al,. 2010 17 II - Strong Teduglutide is potentially effective in inducing remission and mucosal healing in patients with moderate to severe active Crohn’s disease.
Xiao et al,. 2000 18 IV - Moderate Serum GLP-2 levels were found in patients with IBD that were higher than in control patients, being 229% higher in ulcerative colitis and 317% higher in Crohn’s disease. Similarly, the active form of GLP-2 was higher in IBD patients, and the DPP-IV enzyme that degrades GLP-2 was lower in these patients. Therefore, the elevated GLP-2 levels in these patients are linked to an adaptive response to intestinal inflammation.
St-Pierre et al., 2024 13 IV - Moderate GLP-1 analogs, such as semaglutide and tirrizepatide, can effectively reduce weight and BMI in non-diabetic patients with IBD, with manageable side effects.
Belinchon et al., 2025 14 IV - Moderate The use of GLP-1 agonists was effective in reducing weight by 6.2% in 6 months, showing a good safety profile in IBD. The most frequent adverse event was nausea. Commonly, GLP-1 agonists cause mild gastrointestinal symptoms such as nausea, vomiting, and diarrhea. The improved course of IBD may be explained by the reduction of intestinal inflammation through the interaction between GLP-1 agonists and intestinal intraepithelial lymphocytes. Treatment with GLP-1-SSM reduced the expression of the pro-inflammatory cytokine IL-1β, increased goblet cells, and preserved the intestinal epithelial architecture in a colitis model.

IBD: inflammatory bowel disease. UC: ulcerative colitis. CD: crohn‘s disease.