Background. Insulin therapy is associated with the risk of hypoglycemia, high variability of glycemia. Therefore, therapy with analogues GLP1 becomes relevant for patients with myocardial infarction and diabetes mellitus type 2. These drugs can reduce glycemic variability and risk of hypoglycemia. Objective. The effects of combination therapy analogue GLP1 and insulin should be studied in rats with experimental myocardial infarction and the impact of such therapy should be studied on the level of markers of myocardial damage, BNP, dynamics of the echocardiographic parameters and level of glycemia in patients with diabetes mellitus type 2 and myocardial infarction. Design and methods . Neonatal streptozotocin diabetes mellitus was modeled in an experiment in rats. Groups of animals were formed depending on the time of the beginning of insulin therapy, analogue GLP1(exenatide) or a combination of these drugs — before or after experimental myocardial infarction. Morphological assessment of ischemia and necrosis areas was carried out and glycemic variability was assessed. Two groups of patients with type 2 diabetes mellitus and myocardial infarction were formed in the clinical part. The first group received standard insulin therapy, the second group received combination therapy with insulin and exenatide. Parameters of glycemia, markers of myocardial damage, BNP, dynamics of echocardiography were evaluated. Results. The decrease of the area of necrosis, was observed in the combination therapy group in the experiment. Troponin I and CPK MV levels did not differ initially in all groups of patients. Reducing glycemic variability, a positive trend of level BNP, and EF was noted in patients with exenatide. Conclusion. Exenatide has the most pronounced positive effect on the course of myocardial infarction at the introduction before the start of reperfusion. Exenatide had no effect on the dynamics of markers of myocardial damage, but reduced the glycemic variability, improved the dynamics of laboratory parameters in patients.