At present, a large number of studies have found that HUA is closely related to cardiovascular disease. For example, it can affect vascular endothelium, increase the risk of hypertension , heart failure and increase the risk of cardiovascular disease, including coronary heart disease, myocardial infarction[5, 16]. Although many studies on the mechanism partly explain the relationship between UA and cardiovascular disease, it is not completely clear. Moreover, hyperuricemia is often accompanied by other diseases. At present, a large number of people who study uric acid and metabolic or cardiovascular diseases often have other metabolic or cardiovascular comorbidities or even metabolic syndrome. It is difficult to purely study the relationship between UA and specific risk factors or protective factors of cardiovascular disease. The characteristic of this study is to study in healthy people without diabetes, hypertension or metabolic syndrome, to clarify the relationship between UA and apo AI, one of the cardiovascular protective factors. The result plays a certain role in the occurrence and development mechanism of UA in cardiovascular disease.
The present study explored the association between UA and Apo AI in healthy people without diabetes, hypertension or metabolic syndrome. We found that in the HUA group, the Apo AI and HDL-c were higher than that in the NUA group. In the further analysis, HUA was found associated with decreased plasma Apolipoprotein AI and HDL-c independently. The results may suggest that hyperuricemia may promote the progress of the cardiovascular disease by reducing the levels of ApoA1 and HDL-C. Other previous studies are similar to our study. Kuwabara et al.  conducted a prospective study on Japanese patients with hyperuricemia but without typical symptoms and other complications. The study found that the incidence of cardiovascular related metabolic disorders such as abnormal lipid metabolism and hypertension in the asymptomatic hyperuricemia group was significantly higher than that in the normal UA group after five years of follow-up. A sub-analysis of the NHANES III study also found that HDL-c and apo-B to apo-AI were linearly positively associated with uric acid levels. However, different from our study, the participants included patients with diabetes, hypertension and other complications, and no significant correlation between apo AI and UA after adjusting for related factors.
At present, the mechanism of the interaction of uric acid with HDL-C and apo-AI is not completely clear. Animal studies have found that high uric acid can reduce the level of phospholipids of HDL subclasses, and induce the increase of fractional catabolic rate FCR significantly, resulting in decreased HDL-C and apo AI levels . Other studies have found that high UA is also closely related to small and dense HDL-C. At the same time, HDL-C volume is negatively correlated with fibrinogen concentration, and HUA was negatively correlated with large HDL-C level, which may present a mechanism that contribute to arteriosclerosis. There are different relationships between HUA and different subclasses of HDL-C ,HUA and HDL2, which are associated with alcohol consumption, waist circumference, smoking, and exercise had a negative correlation. However, HUA and HDL3 which only associated with alcohol consumption had a positive correlation. Moreover, most studies only studied the relationship between HDL and UA; the mechanism of the interaction between apo-AI and UA needs to be further explored.
In addition, instead of lipoprotein, the result of the current study showed that other metabolic index correlated to UA, including FBG and HOMA-IR. Similar to this study, many studies have found that HUA is closely related to insulin resistance and hyperglycemia[24–26]. Long term follow-up studies confirmed that hyperuricemia is an indicator for predicting abnormal glucose metabolism. Krishnan et al.  conducted a 15-year follow-up study on young people without diabetes. They found that the risk of developing diabetes, insulin resistance and prediabetes in the hyperuricemia group within 15 years was significantly higher than that in the non-hyperuricemia group. A 5.3-year follow-up study of the Chinese population also confirmed that HUA and is closely related to the development of hypertension . The mechanisms are complex; uric acid can reduce IR by promoting mitochondrial oxidative stress and NO bioavailability[29, 30]. However, hypouricemic drugs such as Allopurinol can reduce uric acid, improve insulin resistance and systemic inflammation in patients with hyperuricemia. On the contrary, IR can induce hyperuricemia by inhibiting uric acid excretion through increasing renal tubular sodium reabsorption.
The limitations of our study include that this is a cross-sectional study, and it is impossible to determine the causal relationship. A follow up study can be carried out next to further explore the relationship between UA, apoAI and cardiovascular disease. This study is calculated based on the data of a small number of subjects who receive health examination which had selection bias, and more large-scale studies will be carried out in the future.