Vnitr Lek 2011, 57(11):897-902
Pathophysiological background for incretin therapy: is it capable of more than we think?
- 1 III. interní klinika 1. lékařské fakulty UK a VFN Praha, přednosta prof. MUDr. Štěpán Svačina, DrSc., MBA
- 2 Ústav tělovýchovného lékařství 1. lékařské fakulty UK a VFN Praha, přednosta doc. MUDr. Zdeněk Vilikus, CSc.
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 β 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 β 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.
Keywords: type 2 diabetes mellitus; incretin-based therapy; cardiovascular complications; hypoglycemia
Received: September 21, 2011; Published: November 1, 2011 Show citation
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