3.1 Prevalence of HUA
HUA and gout are continuous and chronic pathophysiological processes with significant heterogeneity in clinical phenotypes. The boundary between asymptomatic HUA and gout is becoming blurred with the wide use of new more sensitive and specific imaging methods [6, 7]. The prevalence of HUA which is associated with genetic factors and environmental factors varies in different regions . The prevalence of gout was 3.9% among US adults in 2015–2016 (5.2% and 2.7% among men and women, respectively) . While a cross-sectional study in Thailand showed the prevalence of HUA was 10.6% (18.4% in men and 7.8% in women) , which is higher than in the US, obviously. A community-based cross-sectional study showed the prevalence of HUA among adults aged 35-79 years was 13.5% (17.3% in men and 10.0%in women) in southwestern China . Meta-analysis indicated that the pooled prevalence of HUA was 17.4% (ranged from 15.5 to 24.6% by regions) among the general population in mainland China, which had become another common metabolic disease after diabetes . In our study, the prevalence of HUA was 10.54% in the population, and in males (21.68%) was significantly higher than that in females (1.34%), which is consistent with the above scholars' studies.
The prevalence of HUA in different regions was mainly associated with regional financial conditions and residents' daily exercise, diet and drinking habits. Increased SUA is due to abnormalities in purine metabolism, excessive uric acid production and/or reduced excretion; higher levels of estrogen in women favor the excretion of SUA, whereas androgens promote reabsorption of UA and inhibit the excretion of SUA  and affect the liver's purine metabolism . Besides, the high prevalence of HUA in men may also be related to lifestyle habits such as unhealthy diet, alcohol consumption, smoking habits, and little exercise.
Our study also showed that increased BMI was a risk factor for HUA, which was consistent with the conclusions of Wang YY et al  and Ali N et al . The reasons may be related as follow. On the one hand, the accumulation of visceral fat leads to a large amount of plasma free fatty acids flowing into the live and hepatic portal vein, which stimulates the synthesis of triglyceride, and then leads to the surge of uric acid generation by activating the uric acid synthesis pathway . On the other hand, in participants with visceral fat and obesity, urate excretion, clearance, and creatinine clearance were significantly reduced, leading to high uric acid accumulation in the body . However, the correlation between age and HUA was not shown in this study, which may be due to the fact that the population included in this study was employed population, and its distribution trend in different ages was not obvious.
3.2 The association between SUA levels and hypertension, diabetes and hyperlipidemia
The number of patients suffering from hypertension is 245 million in China in 2015 . Data from CHS  showed that the prevalence in people ≥ 18 years was higher among men than women (crude rate: 28.6% vs 27.2%, weighted rate: 24.5% vs 21.9%), and increased with age and BMI. In 2002, 2010, 2011 and 2012, the prevalence rates of dyslipidemia in Chinese people aged ≥ 18 years were 18.60%, 33.97%, 39.91% and 40.40%, respectively, demonstrating an increasing trend . The age-standardized prevalence of dyslipidemia aged ≥35 years during 2015-2017 in Inner Mongolia was 31.2%, and male sex and obesity were positively correlated with dyslipidemia . Furthermore, a cohort study from Japan also showed that the prevalence of dyslipidemia was higher in men than in women and tended to increase with age . In 2013, a large sample of 170287 urban and rural residents in 31 provinces showed that the standardized prevalence rate of diabetes mellitus in Chinese adults was 10.9%, with males (11.7%) higher than females (10.2%) . A Meta-analysis involving 80,775 persons showed that the pooled prevalence of diabetes in the general population in Bangladesh was 7.8% (95% CI: 6.4-9.3), and age was a risk factor. Conforming with the above studies, the prevalence rates of hypertension, hyperlipidemia and diabetes in this study were 27.76% (male 37.26% higher than female 19.91%), 48.10% (male 57.45% higher than female 40.38%) and 7.47% (male 10.98% higher than female 4.59%), respectively. The prevalence of hypertension, hyperlipidemia and diabetes increased with age and BMI.
In recent years, a number of studies worldwide have shown that SUA levels are closely associated with the occurrence and development of hypertension. A survey by Kuwabara  in Japan showed that being in the highest quartile of SUA level increased the risk of hypertension by 3.7 times compared with being in the lowest. Baker  also reported that HUA was one of the causes of cardiovascular disease and might predict the development of hypertension. A systematic review and meta-analysis of 17 prospective cohort studies with 32,000 participants published in 2020 showed a dose-response relationship between SUA levels and the prevalence of hypertension, with each 1 mg/dL increase in uric acid concentration increasing the risk of hypertension by 10% . A possible reason is that a high level of SUA can stimulate renin secretion, causing renin-angiotensin activation and triggering the proliferation of arterial smooth muscle cells, resulting in increased blood pressure . Another possible cause is a mutation in the uricase gene in humans, it not only mediates microvascular changes in uric acid levels, but also induces reversible salt-sensitive hypertension [31, 32]. However, there was no correlation between hypertension and uric acid in our study, suggesting that such correlation was not obvious in the northeast China and regional differences may exist. This could not exclude the selective bias in the selection of research subjects as well. We will pay more attention to this content in the later study.
As early as 1975, Bansal  reported that SUA levels were associated with dyslipidemia. Our previous study also showed that total TC, TGs, and LDL-C were risk factors for HUA . The reason for this may be related to the inhibition of lipoprotein lipase activity by an increase in SUA levels . The decrease in lipoprotein lipase activity in vivo limits the catabolism of TGs and triggers increased triglyceride levels in the blood. On the other hand, HUA is often accompanied by low adiponectin , which can increase the oxidation of free fatty acids, reduce blood TGs and low-density lipoprotein levels and increase high-density lipoprotein. Adiponectin may be a key factor in abnormal HUA lipid metabolism . Dyslipidemia and increased SUA levels may aggravate atherosclerosis . The results of this study showed that the higher the SUA levels were in population, the higher the prevalence of hyperlipidemia. The prevalence of hyperlipidemia in the higher three quartiles of SUA was 3.519-, 2.049- and 1.570- times that of the lowest quartile in model 1. After adjusting for BMI, sex, and age, the prevalence of hyperlipidemia in the higher three quartiles of SUA was 3.719-, 2.091- and 1.632-times that of the lowest quartile, respectively.
At present, the association between SUA levels and diabetes is controversial and requires further investigation. In our study, there was no clear correlation between the different levels of SUA and the prevalence of diabetes in men and women. This is different from the finding of Xu Y  in the US, but consistent with the findings of Taniguchi Y in Japan . There are also studies that have shown a negative correlation between diabetes and SUA levels , which may be due to different geographical, temporal or age differences in surveys. A systematic review and meta-analysis  of the prevalence of SUA and type 2 diabetes mellitus (T2DM) showed that for each 1 mg/ dL increase in SUA, the risk of T2DM increased by 13.1% (pooled RR) and 48.4% (pooled OR). However, another meta-analysis  indicated that it is still debatable whether SUA is an independent risk factor for T2DM or it only emphasizes the association between other independent risk factors such as age, obesity, hypertension, gender, and dyslipidemia and T2DM. Therefore, the association between SUA and T2DM requires further evaluation.
The present study is characterized with several strengths. First, through a large sample of population epidemiological studies, we deeply studied the correlation between uric acid and metabolic indicators such as blood glucose and blood pressure, providing a useful reference for revealing the etiology and pathogenesis of HUA. Second, adjustments for some potential confounding factors, such as age, gender and BMI, increased reliability of the results. It should be noted that this work had several potential limitations. First, because this research was a cross-sectional study, it was not possible to find the causal relationship between SUA levels and hypertension, diabetes and hyperlipidemia. Second, a selection bias could be introduced, for the study participants volunteered for the health examination. Third, parameters of lifestyle factors such as diet and physical activity were not included in the questionnaire, which may affect the SUA levels. Fourth, the sample size of this study was relatively small; therefore, the findings may not represent for the whole population of China. However, this study findings are worthy as a reference for future investigations. Further, a longitudinal study is necessary for a deeper explanation and to clarify these issues.