In this cross-sectional study, the overall prevalence rate of hyperuricemia was 29.7%, which was significantly more common in males than in females (47.6% vs. 17%). This rate was higher than those in most Asian epidemiological studies: Bangladesh, 9.3% 21; Japan, 25.8% 22; and Thailand, 10.6% 23. These disparities may be attributable to racial or ethnic differences. A more recent Thai study reported that the prevalence of hyperuricemia in men has reached 59% 24. Age differences may also partly explain this phenomenon. In the present study, the participants were young adults In a Spanish study, the prevalence rate of hyperuricemia in children was 53% 25. In China, students had high-intensity learning and accompanying high nutrition, including plenty of purine-rich foods in senior high school, which may lead to increased uric acid level and weight gain.
The results of the present study showed that the prevalence of MetS increased linearly in the quaternion of SUA, which confirmed the strong association between SUA level and MetS in Chinese young adults. These results were consistent with several epidemiological studies which reported in Asian population9,10, European population14,26, North American population27. After adjustment for confounding factors, SUA remained a risk factor for MetS in males. Low prevalence of MetS in the young participants may explain the possible reason. In a longitudinal study on Taiwanese adults, SUA seems an important predictor for the risk of incident MetS in 30–40 years but not in 20–30 years age groups 28. The mechanism for the positive association between SUA levels and MetS has not been fully elucidated, but some studies have suggested several possible explanations. Xanthine oxidoreductase (XOR) is a key enzyme in the formation of UA. It may participate in the pathogenesis of metabolic syndrome through oxidative stress and inflammation induced by XOR derived reactive oxygen species and UA29. Animal experiments showed that XOR knockout mice could not produce UA, which led to the defect of fat accretion, suggesting that UA is involved in the adipogenesis30. Hyperuricemia has been demonstrated to impair nitric oxide generation and subsequent endothelial dysfunction31. Another important mechanism may be that hyperuricemia involved in insulin resistance through the production of reactive oxygen species and Deficiency of endothelial-formed nitric oxide 32.
In addition, a positive association of SUA levels with low HDL-C and high TG was observed independent sex. However, the association with low HDL-C was no longer significant, whereas associated with high TG in males in multivariable regressions. This finding was partly similar to that of previous study which conducted among US children and adolescents 33. In a survey of 234 male seafarers, SUA levels was associated with MetS and high TG 34. Studies on the association between SUA levels and dyslipidemia were primarily conducted in elderly or middle-aged adults even though the results were controversial 35–37. However, these results were likely to be disturbed by other confounding factors, such as chronic cardiovascular diseases and long-term medication. This observation indicated that SUA level might be a biomarker in the development of high TG in males.
Our results further found an association between SUA levels and abdominal obesity in females. The finding, which was more relevant to women, was similar to a Japanese study 38. As we know, abdominal obesity is characterized by accumulation of visceral fat. Hikita et al. 39 reported that SUA level was positively correlated with visceral fat area and subcutaneous fat area. According to a recent study, saliva UA has been proved to be an important marker of fat accumulation in adolescents40. Hyperuricemia reduces serum leptin levels, thereby inhibiting the decomposition of visceral fat and increasing the accumulation of TG in non-adipocytes, promoting the development of obesity 41. Rats model experiments indicated that inhibition of UA production could block the conversion of fructose to TG in hepatocytes and reduce the accumulation of TG 42. It is suggested that the increase of SUA level is involved in the occurrence and development of abdominal obesity.
Of the MetS components, high blood pressure showed an increased prevalence across the SUA levels in males, but the difference failed to reach statistical significance adjustment for other MetS components. This result is different from that shown by a 5-year cohort study, which indicated that hyperuricemia was associated with increased incidence rates of hypertension 43. The difference might be attributed to the different subjects that subjects in our study were younger (18 to 26 years) than the reported study (30 to 85 years). Additionally, we adjusted abdominal obesity, hyperglycemia, high TG and low HDL-C that maybe interferes or modify this relationship. A Japanese cross-sectional study revealed that serum TG level may interfere with the relationship between SUA and prehypertension 44. These results suggest that, if there are other metabolic factors or interactions interfere with or alter this relationship.
Our results should be interpreted in the context of potential limitations. Firstly, as it is a cross-sectional study, this study cannot prove the causal relationship between SUA and MetS and its components. Therefore, more prospective studies need to be conducted. Secondly, as the subjects of this study were young adults, the prevalence of hyperglycemia in females was 1.12% and 0.87% in males, and the prevalence of MetS in the total subjects was 2%. This low prevalence may affect the confidence of the results. Finally, this study was conducted in a medical university and may not be applicable to other ethnic populations.