Obesity is a state marked by excessive body fat mass, which has become a global issue with increasing prevalence in recent decades (1). Fat deposition in intra-abdominal tissue causes a condition known as visceral/abdominal obesity, which is closely related to the incidence of metabolic and cardiovascular disorders (2,3). Obesity can trigger insulin resistance, oxidative stress and disrupt hemodynamics, which can ultimately lead to hypertension (4,5).

Myeloperoxidase (MPO) is a heme peroxidase enzyme found in monocytes and neutrophils that serves a role in oxidative and inflammatory processes through its role as a catalyst for the formation of hypochlorous acid. It has been reported to be associated with hypertension (6,7). Moreover, xanthine oxidase (XO) is an enzyme that has important role in purine metabolism, producing uric acid, which in turn serves a role in reactive oxygen species (ROS) formation that can trigger an increase in blood pressure (8-10). Furthermore, oxidized low-density lipoprotein (Ox-LDL) serves an important role in the process of atherosclerosis, reducing the amount of endothelial nitric oxide (NO) synthase, which leads to vasoconstriction (11,12).

The present research aimed to assess the combined contribution of MPO, XO and Ox-LDL as determinant factors of blood pressure in adults with abdominal obesity.

A total of 86 research subjects consisting of 68 women (79.1%) and 18 men (20.9%) participated in the present study. The basic characteristics of the research subjects are presented in Table I. Preliminary bivariate analysis using Spearman's rank correlation (data not shown) identified four candidate variables displaying significant or marginal associations with SBP: WC, FSG, XO, and MPO (r=0.528, P<0.001; r=0.306, P=0.004; r=0.277, P=0.010; r=0.189, P=0.081, respectively), whereas Ox-LDL and age demonstrated no clear correlation with SBP (r=0.098, P=0.369; r=-0.093, P=0.393). Regarding DBP, significant or trend-level correlations were noted only for WC, FSG, and MPO (r=0.391, P<0.001; r=0.229, P=0.034; r=0.193, P=0.076, respectively), while Ox-LDL, age, and XO displayed no statistically meaningful relationships (r=-0.200, P=0.854; r=-0.176, P=0.104; r=0.091, P=0.406, respectively). Univariate linear regression analysis regarding the determinant factors of log SBP is shown in Table II. Multivariate linear regression analysis revealed that WC, FSG, serum MPO and XO levels were determinant factors, accounting for ~41% of the log SBP variability, as presented in Table III. Univariate linear regression analysis regarding determinant factors of log DBP is shown in Table IV. Furthermore, multivariate linear regression analysis revealed that FSG, WC and serum MPO levels were determinant factors accounting for 24.8% of the log DBP variability, as shown in Table V. A post hoc statistical power evaluation conducted in G*Power for the SBP model (incorporating 6 predictors, R²=0.415, and an effect size f²=0.7094) yielded a robust statistical power of 99.99%. Similarly, the power analysis for the DBP model (6 predictors, R²=0.248, effect size f²=0.3298) confirmed a statistical power of 98.46%. Gender-stratified regression analyses are shown in Tables SI, SII, SIII and SIV. Sex-stratified subgroup analyses yielded disproportionately elevated standardized β coefficients among male participants; this outcome likely stems from reduced statistical power given the smaller male subgroup size, suggesting that these specific estimates should be interpreted with caution.

Obesity is one of the main causes of hypertension, where the relationship between them is mediated by several factors, including increased oxidative stress (4). The present study demonstrated that in subjects with abdominal obesity, 41.5% of SBP variability was determined by serum MPO, XO, WC and FSG, while 24.8% of DBP variability was determined by serum MPO, WC and FSG. MPO had a slightly higher contribution to SBP variability than XO (β, 0.282 vs. 0.248). Moreover, Ox-LDL was revealed to have no direct contribution to either SBP or DBP.

The involvement of MPO in hypertension, coronary heart disease and cardiovascular disease has been reported in previous studies (6,14). Buljubasic et al (15) reported higher serum MPO levels in hypertensive adults compared with that in normotensive individuals. Another study in obese children revealed a positive association between serum MPO levels and SBP and DBP (r=0.357 and r=0.354, respectively; P<0.05) (16). MPO produced by infiltrating neutrophils in perivascular tissues can lead to the formation of ROS, which may cause vascular dysfunction. ROS also reduce the bioavailability of NO, thereby reducing the vasodilatory capacity of blood vessels and causing hypertension (17).

The impact of XO on blood pressure has also been reported in several studies. Serum XO levels have been reported to be positively correlated with SBP and DBP in adult populations (r=0.309 and r=0.180, respectively; P<0.01) (8). Other research has reported findings similar to the present study, showing an increase in SBP with increasing serum XO quartiles but finding no relationship between DBP and serum XO quartiles (18). Another study reported higher serum XO and MPO levels in subjects with age-related cataracts accompanied by hypertension compared with that in those without hypertension; however, the contribution of XO and MPO to hypertension in that study was not investigated (10). XO, which serves a role in the metabolism of purine to uric acid, can produce ROS byproducts, which cause endothelial and vascular dysfunction, suppress NO levels, and cause vasoconstriction and increased blood pressure (8,18).

Ox-LDL is a compound that is pro-oxidant, pro-inflammatory and pro-thrombotic, which can cause endothelial dysfunction and atherosclerosis (11). A study in an elderly population reported that Ox-LDL was associated with arterial stiffness (19). However, in line with the results of the present study, Harmon et al (20) reported that no association was found between Ox-LDL with SBP and DBP in the adult population. This suggests that although Ox-LDL serves a role in the early formation of atherosclerotic plaques, it is not directly related to increased blood pressure, especially among young adults, as in the subjects of the present study.

Studies that evaluate combined contribution of MPO, XO and Ox-LDL to SBP and DBP in abdominally obese population are lacking. Whilst the present study demonstrated the contribution of MPO and XO to blood pressure elevation, there are several limitations of the study that should be addressed. The cross-sectional study design only provides an overview of the association between variables and cannot prove a causal relationship between them; therefore, further longitudinal research is needed to establish a temporal or causal relationship. Furthermore, the majority of the study subjects were women, thus the findings may reflect the biological conditions of women more prominently than that of men. Consequently, it is recommended that future studies perform separate analyses by sex with a more adequate sample size. Additionally, most of the variability in SBP (58.5%) and DBP (75.2%) is determined by other factors not analyzed in the present study, including genetic factors, diet, sodium intake, physical activity and alcohol consumption; therefore, in future studies, the effects of these factors should also be analyzed simultaneously. Multicenter studies involving different populations and a larger number of subjects are also needed to generalize the findings of the present study.

In conclusion, WC, FSG, MPO and XO were shown to be determinants of SBP, while FSG, WC and MPO were demonstrated to be determinants of DBP.