Besides impeding the oxidation of nLDL, shown in our present study, several further modes of action have been reported rendering metformin an antiatherosclerotic drug, namely, the regulation of oxLDL-provoked endothelial dysfunction through upregulation of sirtuin 1 expression [55], protection of the vasculature by activation of endothelial nitric oxide synthase [56], and decreased inflammatory activity in patients taking metformin [57]. This evidence concerns the gene SIRT1 and endothelial dysfunction.