In the present study the effect of high glucose concentrations, insulin, PPARγ activators (rosiglitazone) and NHE-1 inhibitors (cariporide) in atherosclerosis-related functions of human monocytes was investigated. Monocyte adhesion to laminin-1, collagen type IV and endothelial cells, as well as monocyte migration through the same substrates were studied. Incubation of the monocyte suspension with high glucose concentrations, insulin and rosiglitazone induced all the studied atherosclerosis-related functions of the monocytes. In all these functions the addition of cariporide counteracted the activity of glucose, insulin and rosiglitazone. The use of antigen for β1 integrin also counteracted the activity of the above in monocyte adhesion in all three substrates. The data of the present study suggests that PPARγ activation in monocytes induces atherosclerosis, and that NHE-1 and β1 integrin play an important role in the beginning of atherosclerosis.