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.