HbA1c is commonly used to evaluate the level of blood glucose control. However, HbA1c has limitations. The DCCT study found that HbA1c explained only 11% of diabetes complications, and 89% of diabetes problems no longer needed explanation, once speculated to be related to variability in blood sugar. Clinical studies have shown that the repeated fluctuation of the hyperglycemic environment causes more serious damage to the morphology and function of endothelial cells than continuous safe hyperglycemia [14], which is more likely to lead to microangioplasia and cardiovascular disease in T2DM patients. With the development of blood glucose monitoring technology, CGM can be applied to evaluate the blood glucose of patients. A new index, TIR, can directly reflect whether the blood glucose level reached the optimal level under various interventions. Lu [15] studied TIR assessed by CGM in 2215 patients with T2DM and carotid intima-media thickness (CIMT), a legitimate marker of subclinical atherosclerosis. The results showed that TIR in patients with abnormal thickening (≥ 1.0 mm) was significantly lower than that in patients with normal CIMT. For each 10% increase in TIR, the risk of abnormal CIMT was reduced by 6.4 percentage points, suggesting that TIR may play an additional predictive role in atherosclerosis progression. TIR is associated not only with macrovascular complications but also with microvascular complications of diabetes. A survey of 3262 patients with T2DM confirmed that the incidence and severity of diabetic retinopathy (DR) were negatively correlated with TIR but not with HbA1c [16]. Studies on TIR in diabetic patients have shown that TIR is significantly correlated with the incidence of retinopathy and microalbuminuria in T1DM patients. For each 10% TIR restriction, the risk of microalbuminuria increased by 40%, and the risk of DR increased by 64% [17]. Guo [18] analyzed the association between diabetic cardiovascular autonomic neuropathy (CAN) and TIR in a study including 349 T2DM patients and determined a reliable association between TIR and CAN independent of HbA1c. In conclusion, the clinical significance of TIR has been widely recognized. TIR was used as the main indicator to evaluate blood glucose levels in this study.

SUA is the product of purine metabolism and is an important component of cellular deoxyribonucleic acid (DNA). The uric acid concentration in humans is 3–10 times higher than that in other mammals [19]. According to evolutionary theory, the existence of reasonable uric acid in humans is conducive to evolutionary survival. However, due to changes in modern social lifestyle, uric acid can accumulate in the body as a result of excessive nutrition or nutritional imbalance, leading to metabolic disorders, which result in a series of medical issues. Hyperuricemia can lead to gout, chronic kidney disease, coronary heart disease, metabolic syndrome and other diseases. However, uric acid has clear and effective antioxidant and anti-inflammatory effects. Clinical hyperuricemia is occasionally a compensatory increase induced as a means of the body to combat against pathological stimuli or continual low-grade inflammation. To date, the results of uric acid in human diseases are controversial. Therefore, academic research on the physiological and pathological consequences of uric acid has been an important focus.

The results of the correlation analyses in this study revealed that weight, BMI, SCr and TG showed an overall increasing trend with the increase in SUA, and the variations were statistically significant (Table 1). According to the Third National Health and Nutrition Survey in the United States, the incidence of metabolic syndrome (MetS) increases drastically with the increase in serum uric acid [20], which is typically a group of conditions closely associated with lifestyle and characterized by obesity, hyperglycemia, fatty liver and dyslipidemia [21]. Intake of TG-rich meals will lead to hyperpurine synthesis and then increased SUA production. Moreover, the products of fat metabolism will inhibit the excretion of SUA. Conversely, the increase in SUA levels promotes lipid oxidation and peroxidation, leading to dyslipidemia [22].

Oxidative stress is an important factor that leads to insufficient insulin secretion and accelerates the progression of T2DM. It is possible that oxidative stress induced by reactive oxygen and nitrogen species is closely associated with β-cell dysfunction in the development of diabetes [23, 24]. The oxidative stress environment can cause insulin resistance, β-cell dysfunction, impaired glucose tolerance, and mitochondrial dysfunction, which may ultimately lead to the occurrence and progression of diabetes [25]. Basic studies have shown that uric acid can inhibit nitrification mediated via nitrite peroxide with the aid of scavenging peroxide, hydroxyl and oxygen free radicals; enhance the antioxidant levels of erythrocyte membrane lipids; and decrease oxidative stress in the body [26]. Some studies suggest that higher levels of SUA are associated with better β-cell function. There are various methods for clinically assessing β-cell function, and the arginine stimulation test can effectively evaluate the first-phase secretion function of β-cells [27, 28]. A Chinese study [29] on the correlation between blood uric acid levels and β-cell function in patients with T2DM, a multi-angle analysis of the data from the arginine stimulation test was conducted, leading to the conclusion that high levels of uric acid have a protective effect on β-cell function in T2DM patients.

In this study, it was found that TIR showed an overall increasing trend with the increase in SUA, and the differences among Q4 vs Q1, Q4 vs Q2, and Q4 vs Q3 were all statistically significant. In addition, TAR, MAGE, SD, ADRR, MODD, and M value showed an overall decreasing trend with the increase in SUA. It was suggested that the increase in SUA was related to the better control and stability of blood glucose in T2DM. Multiple regression analysis showed that no matter whether other factors were adjusted, the relationship between SUA and TIR persisted in Q3 and Q4 groups, while the correlation was not significant in Q1 and Q2 groups. The results suggested that the higher the concentration of SUA, the more obvious the correlation with TIR and other blood glucose control indexes. As seen from the smooth curve fitting diagram of TIR and SUA (Fig. 1), TIR and SUA have a curve-like relationship, and the log-likelihood ratio test shows that there is a significant nonlinear relationship between them (P > 0.05). The inflection point of the fitted curve was SUA = 460 mmol/L. Before the inflection point, β was 0.1, indicating that when SUA increases by 10 mmol/L, the corresponding TIR increases by 1%. This could be attributed to the fact that SUA is a major antioxidant substance in the blood and exhibits significant antioxidant effects. The antioxidant properties of SUA can help eliminate various substances, including singlet oxygen, peroxyl radicals, and hydroxyl radicals, thereby reducing metabolic inflammation, improving insulin resistance, and promoting insulin secretion. Finally, the antioxidant effect of SUA may have a protective effect on β cell function and a positive effect on blood glucose control in T2DM patients.

Additionally, in the real world, the positive effects of uric acid are getting more and more attention, and this shows up in other areas. The antioxidant effect of uric acid can manifest through its shielding impact on nerves [30, 31]. Llull et al. [32] discovered in patients with acute ischemic stroke that the use of uric acid blended with alteplase may reduce the ischemic area of cerebral infarction; consequently, it was speculated that uric acid had a neuroprotective effect. Ye et al. [33] studied 271 healthy subjects, 596 patients with slight cognitive impairment and 97 patients with Alzheimer’s ailment (AD), to assess the effect of uric acid on cognitive characteristics. The results confirmed that an excessive serum uric acid level should slow cognitive decline in sufferers with moderate cognitive impairment and in the AD subgroup, especially in female patients. This finding suggests that higher levels of uric acid have a protective effect against cognitive decline in nondementia patients. Uric acid protects the human body and can also affect immune function. For example, Ma Xiaojun [34] used uric acid to treat in vitro cultured mature mouse bone marrow-derived dendritic cells (BMDCs) and assessed immune characteristics. The in vitro-precipitated augmentation of BMDCs and uric acid promoted differentiation and maturation, instantly stimulating molecules on the surface and increasing the potential to stimulate T-cell proliferation and IL-12 secretion levels. The effect of uric acid was associated with its concentration.

In our study, there was no significant correlation between TIR and SUA after the inflection point. This may be due to the small sample size of patients with SUA levels greater than 460 and the potential damage to the body caused by excessively high SUA levels. Since there are few basic and clinical studies on the effects of different levels of blood uric acid on glycemic control, we are willing to continue to monitor this relationship in future studies.