Type 2 diabetes represents a progressive disease, primarily characterised by impairment of glycoregulation, despite the application of various therapy modalities. The main problem with type 2 diabetes, is progressive impairment of betacell functioning, and impairment of insulin resistance. There is an ongoing pursuit after adequate therapy modalities aiming at preservation of beta-cell function followed by loss of weight and assurance of good glycoregulation. For mentioned reasons, research has been done recently on the functioning of enteropancreatic axis in type 2 diabetes. It has been noted that oral intake of food or glucose leads to higher increase in secretion of insulin in comparison to the intake of the same quantity of glucose intravenously, resulting in assumption that hormone signals from endocrine cells of intestine released by the intake of food represent potent stimulators of insulin secretion. Such role is played by GLP-1 and GIP, GIT peptide hormons which stimulate secretion of insulin and release themselves into blood when stomach himus penetrates into duodenum, that is before glucose from himus is absorbed into internal body media. Persons with type 2 diabetes have got low level of secreted GLP-1 after meal. Chronic administration of GLP-1 agonists leads to reducing glycemia and HbA1c. The potential of GLP-1 agonists to decelerate progressive decay of beta-cells at diabetics is alluring, but insufficiently documented. DPP-IV inhibitors represent complementary approach for provoking incretin effects, by oral intake of pills.