The glucagon-like peptide-1 receptor responds to the peptide (GLP-1), mediating a range of physiological processes, including insulin secretion, that make it a key therapeutic target for the treatment of diabetes. However, due to its short half-life in vivo GLP-1 cannot be administered therapeutically and more stable peptide mimetics of GLP-1 are used clinically. However, results from clinical studies reveal that these mimetics have different physiological outcomes than GLP-1. The results of this thesis suggest that these differences may be due to the peptides differentially altering the specific localisation of the receptor and key signalling molecules in pancreatic cells.