The metabolic syndrome associates obesity, inflammation and arterial stiffness. We characterized the coagulation phenotype in 25 and 80 week old Zucker rats, that mimics human metabolic syndrome. We adapted a calibrated automated thrombography technique which follows thrombin activity after in vitro stimulation by tissue factor. The endogenous thrombin potential (ETP) which represents the area under the curve of thrombin generation was higher in 25 week old obese rats than in control lean rats of the same age (428 ± 29 nM.min versus 328 ± 27 nM.min) and still higher at 80 weeks (422 ± 30 versus 306 ± 11 nM.min). The most striking finding was an increase in thrombin generation characterized by a widening of the area under the curve associated with an increase in plasma fibrinogen. This hypercoagulability was corroborated by F1+2 test in vivo at 25 weeks and did not depend on platelets because it was observed in platelet free plasma. Endothelial dysfunction was shown by a high plasma concentration of von Willebrand factor and inflammation by an increase in several cytokines in a cytokine array and in metalloproteinase activity by zymography. In contrast, there was no increase in thrombin generation in vitro with ageing whatever the strain. To conclude, we have shown that thrombin generation increased in vitro with obesity, independently of platelet activation as early as 25 weeks of age. We suggest an implication of fibrinogen whereby thrombin interacting with fibrinogen is protected from its inhibition by antithrombin.