[Pathophysiological background for incretin therapy: is it capable of more than we think?]

Incretin-based therapy functions through the increase of endogenous glucagon-like peptide-1 (GLP-1) levels due to inhibition of dipeptidyl peptidase-4--an enzyme degrading GLP-1 (gliptins) or through the administration of drugs activating GLP-1 receptor (GLP-1 agonists). Both approaches increase insulin and decrease glucagon secretion leading to improved diabetes compensation. The advantages of gliptins include little side effects, body weight neutrality and potential protective effects on pancreatic beta cells. GLP-1 agonists on the top of that consistently decrease body weight and blood pressure and their effects on diabetes compensation and likelihood of protective effects on beta cells is somewhat higher than those of gliptins. Another advantage of both approaches includes their safety with respect to induction of hypoglycemia. In addition to well-known metabolic effects, other potentially benefitial consequences of incretin based therapy in both type 2 diabetic and non-diabetic patients are anticipated. Direct positive effects of incretin-based therapy on myocardial metabolism and function as well as its positive influence on endothelial dysfunction and neuroprotective effects are intensively studied. The possible indications for GLP-1 agonists could be in future further widened to obese patients with type 1 diabetes and obese patients without diabetes. The aim of this review is to summarize both metabolic and extrapancreatic effects of incretin-based therapies and to outline perspectives of potential wider use of this treatment approach.