It has been shown in the rat that insulin affects expression of the rat equilibrative nucleoside transporter (rENT)2 and rat concentrative nucleoside transporter (rCNT)1 and 2 in cardiac fibroblasts (1) and adenosine uptake by cardiac myocytes (2). The aim of this study was to explore the effects of streptozotocin(STZ)-induced diabetes in rat on the expression of rENT1 and 2 and rCNT1, 2 and 3 in the heart. Diabetes was induced in Sprague-Dawley rats by an i.p. injection of STZ (60 mg/kg); controls were treated with vehicle. Diabetes was confirmed by plasma glucose >17 mM. Rats were sacrificed after 4 weeks, cardiac muscle samples were carefully collected and frozen in liquid nitrogen. Real time polymerase chain reaction was used to estimate the threshold cycles for target amplification (Ct) values. The difference between the Ct values for ENTs and CNTs and the Ct values for the housekeeping gene beta actin was calculated (ΔCt) and the difference between diabetic group and control group tested for significance as explained earlier (3). Data are presented as mean±S.D., n=3. Results revealed that the Ct value of beta actin did not differ significantly between the diabetic group (19.6±0.48) and control group (19.58±0.09, p>0.05), so, this gene was used as the endogenous control for the subsequent quantification of rENT1, rENT2, rCNT1, rCNT2 and rCNT3 gene expression. In the control group, the mRNA for rCNT2 and for rENT2 was abundant, with the ΔCt 2.4±0.4 and 4.3±0.3.7, respectively. The mRNA for rENT1 and the mRNA for rCNT1 were less abundant (ΔCt 7.4±0.6 and 8.1±0.1, respectively), while the mRNA for rCNT3 was either absent or of very low abundance. Four-week diabetes has caused significant decrease in the amount of mRNA for rCNT1 (ΔCt 9.19±0.31, p<0.05 vs control), while the ΔCt values for other nucleoside transporters did not change significantly. The observed changes in rCNT1 mRNA amount may indicate a decrease in the amount of this pyrimidine-preferable transporter in the plasma-membrane, which in turn could reduce uptake of pyrimidines by cardiac muscle in diabetes.