One of adipokines involved in the development of insulin resistance is retinol-binding protein 4(RBP4). The physiological role of RBP4 is transport of retinol from the liver to peripheral tissues. One of the first events related to the excessive visceral fat accumulation is the development of inflammation followed by hormonal adipose tissue dysfunction, including excessive RBP4 production. Reduced density of the membrane-type glucose transporter 4 (GLUT4) is considered as a direct cause for the stimulation of RBP4 release to the circulation by adipocytes. Circulating RBP4 inhibits the signal pathways stimulated by insulin in skeletal muscle cells, resulting in the development of insulin resistance. Drugs stimulating receptor peroxisome proliferator-activated gamma (PPARγ) - thiazolidinediones - inhibit the production of RBP4 by adipose tissue and increase the insulin sensitivity of the tissues. Increased secretion of RBP4 stimulates the expression of adhesion molecules in the endothelial cells, promoting development of atherosclerosis and arterial hypertension. Population studies demonstrated an association between serum RBP4 in the circulation, and the severity of atherosclerosis and risk of the cardiovascular events and type 2 diabetes. It also appears that the rbp4 gene functional polymorphisms may influence the risk of metabolic complications of obesity, including vascular injury. Therefore, the concentration of RBP4 in the circulation may be considered both as the causative factor and marker of chronic vascular injury. This article summarizes the current state of knowledge on the potential role of RBP4 in the pathogenesis of cardiovascular diseases, particularly related to insulin resistance.