Statin treatment improves insulin resistance in skeletal muscle. Thus, this study assessed whether statin may affect the myocardial expression levels of AdipoR1 and R2, receptors of adiponectin that enhances insulin sensitivity, and whether statin may improve insulin resistance in cardiomyocytes. Myocardial infarction (MI) was created by the ligation of the left coronary artery in male mice. Expression levels of mRNA and protein levels of AdipoR1 but not AdipoR2 protein levels were significantly decreased in the remote area as well as the healed infarcted area in the left ventricles 4 weeks after MI. Oral administration of pravastatin (50 mg/kg/day for 4 weeks after MI) reversed the decrease in myocardial expression levels of AdipoR1 independently of changes in serum lipid profiles and insulin levels. Using cultured cardiomyocytes, incubation with tumor necrosis factor-alpha (TNF), a mediator of post-infarction myocardial dysfunction, inhibited AdipoR1 mRNA and protein expression levels. Co-incubation of the cells with pravastatin reversed the inhibitory effects of TNF on AdipoR1 expression. In parallel, pravastatin reversed the TNF-induced decrease in globular adiponectin-induced 2-deoxy-d-[³H] glucose uptake in insulin-treated cultured cells. Moreover, this effect of pravastatin was inhibited by the suppression of AdipoR1 expression by siRNA specific for AdipoR1. Incubation with H₂O₂ reduced adipoR1 expression in cultured cardiomyocytes that was attenuated by NAC or pravastatin. Pravastatin suppressed TNF-induced increase in intracellular oxidants in cultured cardiomyocytes. In conclusion, pravastatin reversed the reduction of AdipoR1 expression in post-infarction mouse myocardium and in TNF-treated cardiomyocytes partly through an anti-oxidative mechanism in association with improved glucose uptake.