GLP‑1 Agonists Linked to Higher Remission Rates in Ulcerative Colitis: Real‑World Evidence

GLP‑1 receptor agonists were associated with improved remission rates in patients with ulcerative colitis, a retrospective cohort study indicated.

• Previous research has suggested that GLP-1 receptor agonists may offer benefits in inflammatory bowel disease.
• In a retrospective cohort study of patients with ulcerative colitis, use of liraglutide or semaglutide was associated with higher remission rates compared with no use at 12 weeks.
• Weight loss was not independently associated with remission.

Among 300 ulcerative colitis patients, 150 received a GLP‑1 drug (liraglutide 46.7% or semaglutide 53.3%) and 150 served as controls. At 4, 8, and 12 weeks, remission (partial Mayo score ≤2) was significantly higher in the treatment group versus controls (34.7% vs 15.3%, P=0.001; 54.7% vs 18%, P<0.001; 66.7% vs 25.3%, P<0.001). After adjustment for age, sex, baseline partial Mayo score, obesity, diabetes status, and concomitant biologic therapy, GLP‑1 use remained strongly predictive of remission (adjusted OR 5.90, 95% CI 3.52–9.86, P<0.001).

Semaglutide showed a modest advantage over liraglutide at 12 weeks (remission 72.5% vs 60%; OR 1.77, 95% CI 1.02–3.25, P=0.04). Clinical improvement preceded meaningful weight loss, suggesting an anti‑inflammatory effect independent of weight reduction.

Exploratory endoscopic data indicated that 58% of GLP‑1 users achieved endoscopic remission versus 38% of controls, and 69% versus 47% showed endoscopic improvement.

Mean weight loss in the GLP‑1 group was 8.2% at 12 weeks, but multivariable analysis demonstrated no independent association between weight loss and remission (adjusted OR 1.03 per 1% loss, P=0.41). Adverse events were mild; approximately 30% reported transient nausea and 10% occasional vomiting, with no discontinuations or IBD‑specific safety signals.

The findings add to preclinical evidence that GLP‑1 signaling reduces pro‑inflammatory cytokines, enhances epithelial barrier function, and promotes mucosal healing in IBD models.

Authors note limitations inherent to the retrospective design and potential residual confounding despite matching and adjustment.

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