The incretin effect, defined by a significantly greater insulin stimulatory effect evoked after an oral glucose load than that evoked from an intravenous glucose infusion when plasma glucose concentrations are matched, was first described in the 1960’s.10 Although other hormones may take part in the incretin effect, the majority of the effect is thought to be due to glucose-dependent insulinotropic peptide (GIP) and glucagon like peptide-1 (GLP-1).11-15 The physiological importance of GIP and GLP-1 in overall glucose metabolism has been demonstrated using receptor-knockout animal models,11-14 as well as with the use of receptor antagonists.15-17 Patients with type 2 diabetes have a significant reduction of the incretin effect, implying that these patients either have decreased concentration of the incretin hormones, or a resistance to their effects. GLP-1 concentrations are reduced in patients with type 2 diabetes in response to a meal, while GIP concentrations are either normal or increased, suggesting a resistance to the actions of GIP thus making GLP-1 a more logical target for therapeutic intervention.18,19