The aim of this study was to investigate the direct involvement of adiponectin on the atherogenic process. For that purpose, the authors analyzed adiponectin-dependent and –independent effects of chronic peroxisome proliferator-activated receptor (PPAR)-g agonism on atherosclerosis in mouse models that were made adiponectin deficient or overexpressing adiponectin and subsequently crossed into low-density lipoprotein receptor-null (Ldlr -/-). Results showed that adiponectin deficiency did not accelerate the formation of atherosclerosis lesions in lean Ldlr -/- mice. Accordingly, pharmacological induction of adiponectin by PPAR-g agonism did not prevent atherosclerosis in lean mice. Overexpression of adiponectin improved glucose tolerance as well as lipoprotein profile, but had no effect on the formation of lesions. These findings suggest that adiponectin does not contribute directly to atherosclerotic plaque formation in these rodent models.
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