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.