Abstract
Incretins are hormones secreted by intestinal cells in response to a prandial stimulus. The main mechanisms by which glucose homeostasis is affected are glycemic-dependent insulin secretion, postprandial suppression of glucagon secretion, and gastric evacuation.
The most clinically important is glucagon-like peptide 1 (GLP 1). It has a very short half-life (2-7 minutes), is degraded by the ubiquitously present enzyme dipeptidyl peptidase IV (DPP IV).
The potential of incretins is used therapeutically either in the form of so-called incretin mimetics (exenatide, has the same effect but is resistant to enzymatic degradation, is injected) or by inhibiting DPP IV (gliptins, ultimately increasing the level of endogenous GLP 1). Published clinical studies demonstrate the beneficial effect of both treatment modalities in terms of the basic parameter - improved compensation evaluated by HbA.