Abstract
The incretin effect, mediated by glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP), plays an important role in the regulation of insulin secretion in response to oral glucose. The discovery of deficiencies in incretin pathways associated with development of type 2 diabetes mellitus has propelled the growth of incretin-based therapies in patients with this disease. The basic rationale for incretin-based therapies, including both GLP-1-receptor agonists and dipeptidyl peptidase-4 (DPP-4) inhibitors is reviewed, focusing on their roles in glucose regulation and potential therapeutic benefits. Increased awareness of the differences among incretin mimetics, GLP-1 analogs, and DPP-4 inhibitors, including their structures, half-lives, dosages, hemoglobin A(1c)-lowering capacities, effects on weight, and adverse events will help shape the future of these therapeutic agents. Improved understanding of the mechanism of action and clinical effects of incretin-based therapies will help advance their appropriate use within clinical practice.
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