The modern therapeutic approach to treatment of diabetes type 2 is focused at increasing levels of incretin hormones in the circulation. The incretins are endogenous regulatory peptides secreted by cells of the intestine, and their purpose is to stimulate insulin release, inhibite glucagon secretion and gluconeogenesis in the liver, and in opposite to other drugs it leads to slow gastric emptying, decrease appetite, increase satiety and reduced food intake leading to reduction in body weight. In diabetes mellitus type 2 their secretion or action is disturbed. Human body has two main incretins: glucagon-like peptide-1 (GLP-1) which is secreted from the L-cells of the distal gut (ileum and colon) and glucose-dependent insulinotropic poypeptide (GIP) which is secreted from the K-cells of the small intestine (duodenum and proximal jejunum). Quick degradation by the enzyme DPP-4 limits the effect of GLP-1 and GIP on glucose homeostasis. Although GIP and GLP-1 have expressed insulinotropic effect, only GLP-1 is considered as a potential candidate for therapeutic treatment of diabetes mellitus type 2. There are two therapeutic options based on incretins: incretin analogues resistant to DPP-4 and incretin enhancers, substances which prevent degradation of endogenous incretins by inhibiting dipeptidyl peptidase - 4 (DPP-4) which breaks them down. Both groups of drugs represent an effective alternative to the currently available hypoglycaemic drugs. Due to their glucose-dependent effect, the risk of hypoglycaemia is very low. GLP-1 has numerous extrapancreatic metabolic effects. It is known that receptors for the GLP-1 are found in other organs and today numerous effects of GLP-1 in organism are being investigated.