which would also contribute to no significant relationship between 
SUA and CVD in men.Reportedly, exacerbation of glucose metabolism resulted in the 
decrease in SUA levels [39].Conversely, 
the pathological roles of hypouricemia would be caused by the attenu
ation of beneficial effects of UA. Since UA is one of the major endoge
nous antioxidants in humans [4], hypouricemia would result in 
exacerbation of oxidative stress and subsequent vascular dysfunction, 
thereby leading to the increased risk for CVD [37].In this study, a U-shaped relationship was observed between the SUA 
levels and incident CVD events in both sexes, suggesting the patholog
ical roles of hypouricemia and hyperuricemia in CVD events develop
ment in obese patients.Thus, reduc
tion of UA-related beneficial activities and/or aggravation of glucose 
metabolism in hypouricemia would be implicated in a high CVD risk in 
obese patients.The SUA values corresponding to the 
lowest risk of incident CVD events were lower in women (5.2 mg/dL) 
than in men (6.6 mg/dL) with obesity in this study, suggesting that the 
optimal SUA values for male obese patients rather increased the CVD 
risk for female obese patients, as previously reported in a general pop
ulation [19].