Modulation of the GLP-1 receptor has attracted much attention as a means of improving glycaemic control in type 2 diabetes patients. Such treatments have the advantage of minimizing the risk of hypoglycaemia, since the actions of GLP-1 are glucose-dependent and diminish as blood glucose levels are normalized. As GLP-1 is rapidly rendered inactive by the dipeptidyl peptidase IV enzyme, current approaches fall into two classes: (a) injection of an ‘incretin mimetic’, that is, a peptidic GLP-1 receptor agonist resistant to degradation by dipeptidyl peptidase IV and (b) inhibition of dipeptidyl peptidase IV to preserve endogenous GLP-1 in its active form.