Abstract
Several experimental studies and some clinical experience have shown that metabolic syndrome and caloric restriction exert opposite effects on thrombosis, because these two nourishing conditions are at extreme ends of the same spectrum. The antithrombotic action induced by caloric restriction happens through Sirtuin 1 (SIRT1), a gene/protein activated by the reduction of calorie intake lower than is typical. The antithrombotic effect is due to the activation of SIRT1 acting through an increase of insulin sensitivity, which reduces endothelial dysfunction. Sirtuins have been implicated in several processes, including genomic stability, DNA repair, apoptosis, and adipogenesis. In addition, they have been shown to promote longevity in simple eukaryotes. Some compounds, such as resveratrol, mimic the action of SIRT1 and seem able to correct the prothrombotic state induced by metabolic syndrome. To confirm this, we demonstrated that resveratrol improved the left ventricular function of type 2 diabetics who suffered recent acute myocardial infarction (AMI) when a moderate red wine amount (containing resveratrol) was taken daily by patients receiving conventional antiischemic therapy, in comparison with another group treated with antiischemic compounds alone.