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lüll Role of the incretin pathway in the pathogenesis of type 2 diabetes mellitus Freeman JSCleve Clin J Med 2009[Dec]; 76 Suppl 5 (ä): S12-9Nutrient intake stimulates the secretion of the gastrointestinal incretin hormones, glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP), which exert glucose-dependent insulinotropic effects and assist pancreatic insulin and glucagon in maintaining glucose homeostasis. GLP-1 also suppresses glucose-dependent glucagon secretion, slows gastric emptying, increases satiety, and reduces food intake. An impaired incretin system, characterized by decreased responsiveness to GIP and markedly reduced GLP-1 concentration, occurs in individuals with type 2 diabetes mellitus (T2DM). The administration of GLP-1 improves glycemic control, but GLP-1 is rapidly degraded by the enzyme dipeptidyl peptidase-4 (DPP-4). Exenatide, a DPP-4-resistant exendin-4 GLP-1 receptor agonist, exhibits the glucoregulatory actions of GLP-1 and reduces body weight in patients with T2DM. It may possess cardiometabolic actions with the potential to improve the cardiovascular risk profile of patients with T2DM. DPP-4 inhibitors such as sitagliptin and saxagliptin increase endogenous GLP-1 concentration and demonstrate incretin-associated glucoregulatory actions in patients with T2DM. DPP-4 inhibitors are weight neutral. A growing understanding of the roles of incretin hormones in T2DM may further clarify the application of incretin-based treatment strategies.|Adamantane/analogs & derivatives/pharmacology[MESH]|Blood Glucose/metabolism[MESH]|Diabetes Mellitus, Type 2/*etiology/*metabolism[MESH]|Dipeptides/pharmacology[MESH]|Dipeptidyl-Peptidase IV Inhibitors/pharmacology[MESH]|Exenatide[MESH]|Glucagon-Like Peptide 1/metabolism[MESH]|Glutaminase/metabolism[MESH]|Homeostasis[MESH]|Humans[MESH]|Hypoglycemic Agents/pharmacology[MESH]|Incretins/*metabolism[MESH]|Intracellular Signaling Peptides and Proteins/metabolism[MESH]|Peptides/pharmacology[MESH]|Pyrazines/pharmacology[MESH]|Signal Transduction[MESH]|Sitagliptin Phosphate[MESH]|Triazoles/pharmacology[MESH]|Venoms/pharmacology[MESH] |