Diabetes is one of the major public healthcare concerns of the 21st century. Within the UK alone, the number of people diagnosed with type 2 diabetes has recently exceeded 2 million people,1 and there is believed to be another million people who remain undiagnosed. The picture is similar on a global scale with the number of people with diabetes in 2003 estimated at 194 million, a number expected to double by 2025.2 The increasing prevalence of diabetes, and more specifically, type 2 diabetes, makes it not only an increasing healthcare problem, but also a political and social challenge. Current therapeutic approaches to the treatment of type 2 diabetes advocate the initial use of lifestyle changes, including diet modification, adopting a regular exercise regimen, and alteration of alcohol consumption.3 If these prove to be ineffective at achieving or maintaining blood glucose target levels (defined here as glycated haemoglobin (HbA1c) levels of 6.5–7.5 per cent4), then current guidelines recommend the use of pharmacological therapy with oral metformin as the initial first-line agent.3,4 Failure to reach glycaemic targets with oral monotherapy leads to the use of additional drugs, such as the sulphonylureas and the thiazolidinediones (TZDs). The gradual failure of oral hypoglycaemic agents (OHAs) to keep patients’ glucose levels at target, due to the progressive nature of type 2 diabetes and the inexorable decline in beta cell function, means that many patients with type 2 diabetes eventually require insulin therapy3. The recognised importance of managing the growing number of people with type 2 diabetes has led to an explosion in the research and development of diabetes treatments. A number of these new treatments function by improving, either directly or indirectly, endogenous insulin secretion. The incretin hormone, glucagon like peptide-1 (GLP-1), stimulates glucose-dependent insulin release and inhibits glucagon release from pancreatic islet cells. In type 2 diabetes, GLP-1 secretion is decreased,5 and so agents that restore the action of GLP-1 may be effective future therapies. There are several GLP-1 analogues in development, the most advanced of which are exenatide, D I S E A S E M A N A G E M E N T