Background: The metabolic syndrome (MetS) has been found to be closely related with thrombotic diseases. The mechanism, however, is far from elucidated.
Aim: This study was designed to investigate the relationship between endogenous resistin and thrombosis mediating factors, as well as its potential effects on the gene expression of cardiovascular disease biomarkers.
Methods: Ninety patients satisfied the MetS criteria, and 55 healthy subjects were recruited as part of a single-center clinical study. Plasma levels of resistin, tissue factor (TF), tissue factor pathway inhibitor (TFPI), tissue plasminogen activator (tPA), plasminogen activator inhibitor-1 (PAI-1) were measured by enzymelinked immunosorbent assays. The effect of resistin on the expression of cardiovascular disease biomarkers in human umbilical vein endothelial cells (HUVEC) was assayed by gene microarray.
Results: 1) The average levels of resistin in MetS patients with or without acute myocardial or cerebral infarction were significantly higher than those of the controls. 2) The TF and TFPI increase was higher in MetS with infarction patients than in MetS patients. 3) In MetS with infarction patients, resistin was positively correlated with TF and PAI-1 (r=0.313, p=0.008; r=0.401, p=0.002, respectively). 4) In HUVEC, the microarray showed that apolipoprotein C-I, ACE, tumor necrosis factor receptor superfamily member 1A (TNFRSF1A) and member 5 (CD40) genes expression were dramatically increased by resistin.
Conclusion: In patients with MetS, resistin is strongly associated with hypercoagulative and hypofibrinolitic activities. Moreover, resistin may induce thrombotic complications via mediating the lipoprotein metabolism and stimulating inflammation.