Increased adiponectin synthesis in the visceral adipose tissue in men with coronary artery disease treated with pravastatin: a role of the attenuation of oxidative stress

Pravastatin is reported to increase the adiponectin level in humans, but the mechanism remains unclear. We examined plasma and gene expressions of adiponectin, tumor necrosis factor (TNF)-α, interleukin (IL)-6 and protein carbonyl level, an indicator of oxidative stress, in visceral and subcutaneous adipose tissue from 32 patients with coronary artery disease undergoing coronary artery bypass grafting (CABG). Fourteen patients with serum LDL-cholesterol level >100 mg/dl were treated with pravastatin at 10 mg/day for 2 months before CABG (Statin), and the other 18 with LDL-cholesterol ≤100 mg/dl were not (Control). The plasma adiponectin level was higher in the Statin than the Control group (P < 0.05), but TNF-α and IL-6 levels were not different. Adiponectin gene expression in visceral tissue was 3-fold higher in the Statin than the Control group (P < 0.01), but was not different in subcutaneous tissue. TNF-α and IL-6 gene expressions in each tissue were not different between the 2 groups. Protein carbonyl levels in plasma and visceral tissue were lower in the Statin than the Control group (both, P < 0.05). Thus, adiponectin expression and generation in visceral adipose tissue is increased in men with coronary artery disease treated with pravastatin. Pravastatin-initiated attenuation of oxidative stress could be involved.