Conflict of interest statement: C. D. has received lecture fees from Merck & Co, Novo Nordisk and Prosidion; has served on advisory boards; and has acted as a consultant for Novo Nordisk and Dainippon Sumimoto Pharma Co Ltd. This article is based on a presentation given by Dr D. J. Drucker at a stand-alone symposium entitled, ‘Islet enhancement through DPP-4 inhibition as a treatment strategy in prediabetes,’ which was held during the Second International Congress on ‘Prediabetes’ and the metabolic syndrome in Barcelona.
Incretin-based treatment of type 2 diabetes: glucagon-like peptide-1 receptor agonists and dipeptidyl peptidase-4 inhibitors*
Article first published online: 15 SEP 2007
2007 Blackwell Publishing Ltd
Diabetes, Obesity and Metabolism
Special Issue: Rationale for Islet Enhancement through DPP-4 Inhibition as a Treatment Stratergy in Prediabetes
Volume 9, Issue Supplement s1, pages 23–31, September 2007
How to Cite
Deacon, C. F. (2007), Incretin-based treatment of type 2 diabetes: glucagon-like peptide-1 receptor agonists and dipeptidyl peptidase-4 inhibitors. Diabetes, Obesity and Metabolism, 9: 23–31. doi: 10.1111/j.1463-1326.2007.00765.x
- Issue published online: 15 SEP 2007
- Article first published online: 15 SEP 2007
- Received 2 July 2007; accepted 16 July 2007
- dipeptidyl peptidase-4;
- glucagon-like peptide-1;
- glucose-dependent insulinotropic peptide;
Incretins are gut peptides that potentiate nutrient-stimulated insulin secretion following meal ingestion. Activities of the dominant incretins, glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic peptide, include glucose-dependent stimulation of insulin secretion and, in preclinical models, improvement in islet β-cell mass. GLP-1 additionally reduces glucagon secretion, inhibits gastric emptying and promotes satiety. Patients with type 2 diabetes mellitus (T2DM) exhibit reduced total and intact GLP-1 levels, and exogenous administration of the hormone via continuous infusion results in glucose profiles similar to those in non-diabetic subjects. Incretins are rapidly degraded by dipeptidyl peptidase-4 (DPP-4). Thus, strategies to enhance incretin activity have included development of GLP-1 receptor agonists resistant to the action of DPP-4 (e.g. exenatide and liraglutide) and DPP-4 inhibitors that act to increase concentrations of endogenous intact incretins (e.g. sitagliptin and vildagliptin). Clinical trials of these incretin-based therapies have shown them to be effective in improving glycaemic control in patients with T2DM.