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Glucagon-Like Peptide 1 Receptor Agonists (GLP1-RA) and the Clinical Outcomes of Inflammatory Bowel Disease (IBD): A Systematic Review and Meta-analysis
To confirm that the observed effects were mediated through direct GLP-1R activation, or indeed, that they are not secondary autocrine effects of insulin, we performed 2-NBDG uptake experiments in the presence of the GLP1R antagonist Exendin (939) and the potassium channel opener, diazoxide
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