Pravastatin increases the plasma adiponectin level. We examined whether this is a statins' class effect or specific to pravastatin. Of 50 patients undergoing cardiac surgery for coronary artery disease (CAD, n = 36) and valvular heart disease (VHD, n = 14), 23 with CAD and serum LDL-cholesterol level >100 mg/dL were randomized to pravastatin at 10 mg/day (PRAVA, n = 12) or rosuvastatin at 2.5 mg/day (ROSUVA, n = 11) for 2 months, and the other 13 with CAD and LDL-cholesterol ≤100 mg/dL were not treated with statin (Non-statin, n = 13). Patients with VHD did not have CAD and were not treated with statin. Blood was sampled at baseline and surgery. Visceral (VIS) and subcutaneous (SC) adipose tissues were harvested during surgery. At baseline, the plasma adiponectin level was low in patients with CAD compared with that of patients with VHD. At surgery, adiponectin level in PRAVA was increased to the level in VHD, whereas those in ROSUVA and Non-statin were unchanged. VIS contents and gene expressions of adiponectin in PRAVA and VHD were similar to each other and were both higher than those in Non-statin and ROSUVA. SC content and gene expression of adiponectin were similar among 4 groups. Protein carbonyl (PC) level, an indicator of oxidative stress, in VIS was lower in PRAVA and VHD than in ROSUVA and Non-statin. There was a negative correlation between the plasma adiponectin and VIS PC levels (r = -0.41, P < 0.05). Thus, pravastatin increases adiponectin generation, whereas rosuvastatin does not.
