Background and aims: Cardiovascular Diseases (CVD) are the most common causes of mortality and morbidity among patients with type 2 diabetes. Poorly controlled postprandial hyperglycemia contributes to the development of atherosclerosis. Fluctuations of the postprandial glucose levels bring changes in the coagulation system and propensity to thrombosis. Our aim was to determine the change of plasma coagulation parameters like D-Dimer, P-Selectin, Plasminogen activator inhibitor-1 (PAI-1), Prothrombin fragments 1-2 (PTF 1-2) in comparison to the fasting levels in 15 healthy controls and type 2 diabetic patients under treatment of various agents (metformin, insulin secretagog agents and insulin). Materials and methods: Blood samples were withdrawn after 12 h of fasting (min 0) and following breakfast composed of foods proper for each person, at 60th, 90th and 120th minutes. Fasting and 60th, 90th, and 120th minute measurements of glucose, insulin, triglyceride, D-Dimer, P-Selectin, PAI-1, PTF 1-2 had been performed. HA1C and fructosamine were measured also. Results: Some coagulation parameters tend to be changed at the postprandial phase in diabetics as well as in healthy controls. At the postprandial phase, PAI-1 increased significantly in both healthy controls and in all groups of diabetics. The fasting levels of fibrinogen, D-Dimer and P-Selectin were high in diabetics in comparison to healthy controls. An increase in the levels of P-Selectin, PAI-1 and PTF 1-2 at the postprandial phase was observed in healthy persons. Patients receiving insulin secretagog therapy showed an increase in the postprandial levels of PAI-1 like healthy controls. Patients receiving metformin showed an increase in the postprandial levels of PAI-1 and PTF 1-2. Postprandial phase changes in patients receiving metformin were similar to healthy controls. Poorly controlled, older patients with longer diabetes duration had been receiving insulin and these mentioned patients' levels of fibrinogen, D-Dimer and P-Selectin were high in the fasting state and showed an increase in PAI-1 at the postprandial phase. Postprandial levels of PTF 1-2 and D-Dimer were high in insulin treated patients. Levels of fibrinogen and D-Dimer were higher in patients with retinopathy. HA1C and fructosamine were correlated with the coagulation parameters like P-selectin, PAI-1 and PTF 1-2 levels. Correlations showed us that not only postprandial hyperglycemia but also accompanying diabetes, obesity, dyslipidemia and hypertension can aggravate this coagulation tendency at the postprandial phase. Conclusion: Postprandial phase changes can trigger postprandial coagulation cascade in diabetics as well as healthy persons.