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Updated: Jan 13, 2026
Mucin Agarose Gel Electrophoresis: Western Blotting for High-molecular-weight Glycoproteins
Published on: June 14, 2016
Liraglutide upregulates the Cftr gene and regulates the mucus transcriptome profile in Brunner's glands in mice
Louise Marie Voetmann1,2, Bidda Rolin2, Rikke Kaae Kirk2
1Department of Veterinary and Animal Sciences, Faculty of Health and Medical Sciences, University of Copenhagen, Frederiksberg, Denmark.
Background:
The metabolic syndrome encompasses a state of inflammation and metabolic dysfunction, possibly mediated via a disturbed intestinal barrier. Glucagon-like peptide-1 receptor agonists (GLP-1RAs), such as liraglutide, have shown promising anti-inflammatory effects beyond glucose lowering and weight loss, but the underlying mechanism remains to be elucidated. We hypothesised that GLP-1RAs improve the intestinal barrier function and overall inflammatory status by direct gene activation in mucus-secreting Brunner's glands in the mouse duodenum, known for their high density of glucagon-like peptide-1 receptors (GLP-1Rs).
Methods:
Using bulk RNA sequencing, in situ hybridisation, and immunohistochemistry, we analysed the change in the genetic phenotype of mouse Brunner's gland cells following GLP-1R activation by liraglutide.
Results:
We show that liraglutide induces a novel and robust upregulation of the gene for the Cystic fibrosis transmembrane conductance regulator, Cftr, in Brunner's glands as a part of an overall genetic phenotype involved in ion channel activity, mucus secretion, and hydration via GLP-1R activation. Additionally, we found a robust upregulation of the genes Muc5b, Il33, Ren1, and Vldlr in Brunner's glands.
Conclusion:
Collectively, our results imply an enhanced mucus response from Brunner's glands following GLP-1R activation, which might play a role in the effect of GLP-1.
