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Effects of Lipid-Lowering Drugs on Adiponectin

[ Vol. 8 , Issue. 6 ]


Apostolos Perelas, Anna Tsoulkani and Despina Perrea   Pages 836 - 848 ( 13 )


Adiponectin has been implicated in the pathogenesis of coronary heart disease. We review the literature describing the effect of lipid-lowering agents on adiponectin bioavailability. Statins exert variable effects that can be influenced by patient-dependent characteristics (i.e. diabetes or insulin resistance). Fibrates and especially niacin can raise adiponectin levels. The impact of plant sterols, ezetimibe and ω-3 fish oils on adiponectin in humans remains to be defined.There was no literature on whether resins can alter adiponectin levels.

As far as mechanisms are concerned, statins enhance peroxisome proliferator-activator receptor (PPAR)-γ activation and have antioxidant or anti-inflammatory potential. Niacin, ω-3 fatty acids, plant sterols and bezafibrate primarily act by increasing PPAR-γ activity and possibly by reducing oxidative stress or inflammation. Both fibrates and ω-3 fish oils act as synthetic ligands for PPAR-α.

Hypolipidaemic drugs can affect adiponectin bioavailability, although the impact depends on the individual drug administered and patient characteristics. However, with the exception of niacin, the results observed are not conclusive.


Adiponectin, hypolipidaemic drugs, statins, omega-3 fish oils, niacin, fibrates, sterols, ezetimibe, Lipid-Lowering Drugs, coronary heart disease, diabetes, insulin resistance, plant sterols, peroxisome proliferator-activator receptor, omega-3 fatty acids, bezafibrate primarily, coronary artery disease, bile acids sequestrants, probucol, nitric oxide, reactive oxygen species, fibrinolysis, adipoQ, GBP28, atorvastatin, pitavastatin, flu-vastatin, simvastatin, pravastatin, rosuvastatin, fibrates, fenofibrate, bezafibrate, gemfibrozil, ciprofibrate, nicotinic acid, stanols, T-cadherin, Hypoadiponect-inaemia, dyslipidaemia, hyperadiponectinaemia, leptin, resistin, apelin, visfatin, vaspin, hepcidine, chemerin, omentin, plasminogen activator inhibitor, tumour necrosis factor, vascular remodelling, West of Scotland Coronary Prevention Study, athero-genesis, proliferated-activator receptor gamma 2, phospholipase 2, 15-deoxy-delta 12, 14-prostaglandin J2, Oxidative Stress


Laboratory for ExperimentalSurgery and Surgical Research, ‘N. S. Christeas’ School of Medicine, National and Kapodistrian University of Athens, 15 B Ag. Thoma Street, 11527, Athens, Greece.

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