Effect of atorvastatin and fenofibric acid on adipokine release from visceral and subcutaneous adipose tissue of patients with mixed dyslipidemia and normolipidemic subjects

Because of methodological limitations and conflicting results of studies conducted thus far, the possible involvement of human adipose tissue in pleiotropic effects of statins and fibrates requires better understanding. Samples of visceral and subcutaneous adipose tissue obtained from 23 mixed dyslipidemic patients and 23 normolipidemic subjects were treated in vitro for 48 h with atorvastatin, fenofibric acid or both these agents. Visceral and subcutaneous fat of mixed dyslipidemic patients released more leptin, resistin, interleukin-6, tumor necrosis factor α (TNFα) and plasminogen activator inhibitor-1 (PAI-1), and less adiponectin than respective adipose tissue of patients without lipid abnormalities. In both groups of patients, visceral and subcutaneous tissue varied in the amount of secreted adipokines. In dyslipidemic patients both drugs administered alone affected adipose tissue adiponectin and resistin secretion. Additionally, atorvastatin decreased PAI-1 while fenofibric acid reduced leptin release. A combined administration of atorvastatin and fenofibric acid changed the release of all studied markers by visceral fat but did not affect interleukin-6 and TNFα release by subcutaneous tissue. In normolipidemic subjects the effect on adipokine release was more pronounced in visceral fat, in which it was strongest if the drugs were given together. Adipose tissue hormonal activity differs between mixed dyslipidemic and normolipidemic patients and between visceral and subcutaneous adipose tissue. Atorvastatin and fenofibrate exhibit their pleiotropic effects in part by changing the adipokine release by human adipose tissue, regardless of its origin. These effects are stronger in patients with mixed dyslipidemia and are particularly pronounced if atorvastatin and fenofibric acid are given together.