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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].

which would also contribute to no significant relationship between
SUA and CVD in men. Although additional studies are required, our
findings suggest the increased need to focus on hyperuricemia in women
with obesity, as compared to men, to reduce the risk of incident CVD
events.
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. Although a similar U-shaped association of SUA
with a CVD risk has been reported in various populations [36–38], the
mechanistic details have not been fully understood. Regarding hyper
uricemia, detrimental effects of elevated SUA levels would be implicated
in the increased risk of CVD in obesity, as discussed above. 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]. Another possibility is
that lower SUA levels reflect aggravation of hyperglycemia, a risk factor
for CVD. Reportedly, exacerbation of glucose metabolism resulted in the
decrease in SUA levels [39]. Our study also revealed a negative associ
ation of SUA levels with FPG and antidiabetic usage rate. 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.
As assumed by the U-shaped relationships, the pathological impacts
of SUA levels would change according to its concentrations, thereby
suggesting the need to control SUA levels within an appropriate range to
prevent CVD events. In this respect, we found that the optimal target
window of SUA levels to reduce the risk of CVD events differs between
male and female 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]. Similarly, the appropriate SUA values for women would
not be applicable to men with obesity. These findings highlight the need
to revisit the guideline recommendations for reference values of SUA