In addition, fenofibrate has been reported to inhibit vascular inflammation in experimental animals and to improve endothelial function and arterial stiffness in obese glucose tolerant men. Our results showed that fructose administration to rats in drinking water for 12 weeks induced the classic symptoms of the MS. Rats showed significant increase in weight gain compared to the control group. They also had significantly higher levels of blood glucose, serum insulin, total cholesterol, triglycerides, higher SBP, DBP and MAP compared the control rats that did not receive fructose. In addition, fructose induced insulin resistance as evidenced by the significant increase in HOMA-IR index. Together, these alterations confirm the proper induction of MS in our study, which is in agreement with previous reports. Our results showed that fructose administration resulted in hyperuricemia, which is consistent with other previous reports. Fructose-induced hyperuricemia might be attributed to the stimulation of AMP deaminase activity triggered by fructose metabolism resulting in increased formation of uric acid. High level of uric acid during fructose consumption has been suggested as an important causative factor in the development of MS. This is supported by previous findings demonstrating that reducing uric acid level, using XO inhibitors or uricosuric agents, could prevent the development of MS signs in fructose-fed rats. Hyperuricemia plays a pivotal role in the development of insulin resistance and hypertension during MS through uric acid-induced endothelial Bucetin dysfunction. Nakagawa and coworkers showed that uric acid can block acetylcholine-mediated arterial dilation in a dose-dependent Hexylene glycol manner suggesting that uric acid can impair endothelial function. Furthermore, it has been shown that uric acid can reduce endothelial NO bioavailability in both cell culture and in experimental animal models. In this context, our results show that fructose-induced hyperuricemia is associated with a significant reduction in the expression of eNOS in thoracic aorta sections.