Introduction
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.
Materials and methods
Study design and participants
The present cross-sectional study was performed from
October to December 2025. A total of 86 adult subjects with
abdominal obesity were recruited [Asian population cut-off, waist
circumference (WC) >90 cm in men and >80 cm in women]
(13). The subjects of the study
were residents enrolled in specialist medical programs and students
in the master's program of Biomedical Sciences at the University of
Hasanuddin (Makassar, Indonesia). Sampling was performed at
Hasanuddin University Hospital (Makassar, Indonesia) and laboratory
tests were performed at Hasanuddin University Medical Research
Center (Makassar, Indonesia). Subjects with a history of diabetes
mellitus, current infection, inflammation, or who were taking
cholesterol-lowering, uric acid-lowering or anti-hypertensive drugs
were excluded from the study. The present study was ethically
approved by the Health Ethics Committee, Medical Faculty,
University of Hasanuddin (recommendation no. 812/2025; protocol no.
UH25080659; approved on October 17, 2025).
Anthropometry and laboratory
tests
Patients fasted overnight for 8-10 h, then the
following morning at 8 a.m., body mass index, WC, systolic blood
pressure (SBP), diastolic blood pressure (DBP) and blood samples
were assessed. Blood pressure was measured using a mercury
sphygmomanometer (Rudolf Riester GmbH), after the subjects had been
seated for 15 min. Fasting serum glucose (FSG) and 2-h oral glucose
tolerance test examinations were performed using ABX Pentra 400
(Horriba, Ltd.), while serum MPO (cat. no. E-EL-H6244; Elabscience
Bionovation Inc.), Ox-LDL (cat. no. E-EL-H6021; Elabscience
Bionovation Inc.) and XO (cat. no. EH1036; FineTest®;
Wuhan Fine Biotech Co., Ltd.) levels were assessed using ELISA.
Statistical analysis
The role of MPO, XO, Ox-LDL, WC and other parameters
as determinant factors of SBP and DBP was assessed using
multivariate linear regression analysis. Statistical power
estimation performed via G*Power indicated that a sample size of at
least 85 participants was required based on four input predictors.
SBP and DBP were logarithmically transformed to normalize the data.
Age, WC, FSG, Ox-LDL, XO and MPO were assessed as independent
variables, while log SBP and log DBP were evaluated as dependent
variables. A collinearity analysis was performed to assess and
eliminate interfering variables. P<0.05 was considered to
indicate a statistically significant difference. SPSS version 21
software (IBM Corp.) was used for analyses.
Results
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.
 | Table IBasic characteristics of the subjects
in the present study. |
Table I
Basic characteristics of the subjects
in the present study.
| Variables | Mean ± SD | Median (min-max) |
|---|
| Age (years) | 34.81±3.05 | 35 (28-42) |
| Height (cm) | 157.19±7.10 | 156 (143-172) |
| Weight (kg) | 69.17±11.02 | 68.70
(48.80-100.00) |
| BMI
(kg/m2) | 27.88±3.29 | 27.60
(20.60-37.20) |
| WC (cm) | 93.07±6.82 | 93 (81-106) |
| SBP (mmHg) | 120.60±13.65 | 119 (94-158) |
| DBP (mmHg) | 78.40±10.83 | 78 (52-100) |
| FSG (mg/dl) | 95.31±10.98 | 94.20
(74.80-120.80) |
| OGTT (mg/dl) | 111.45±25.27 | 108.20
(68.60-156.30) |
| XO (ng/ml) | 1.25±0.80 | 1.02 (0.30-4.30) |
| MPO (pg/ml) | 33.32±38.65 | 19.94
(7.01-205.02) |
| Ox-LDL (pg/ml) | 1,660.73±880.75 | 1,455.52
(458.11-4740.39) |
| Table IIUnivariate linear regression analysis
of the determinant factors of log systolic blood pressure. |
Table II
Univariate linear regression analysis
of the determinant factors of log systolic blood pressure.
| Variables | B | Standard error | β | P-value | Adjusted
R2 |
|---|
| Ox-LDL |
-1.560x10-6 | 0.000 | -0.029 | 0.793 | 0.011 |
| MPO | 0.000 | 0.000 | 0.230 | 0.033 | 0.042 |
| WC | 0.004 | 0.001 | 0.531 | <0.001 | 0.274 |
| XO | 0.016 | 0.006 | 0.264 | 0.014 | 0.059 |
| FSG | 0.001 | 0.000 | 0.279 | 0.009 | 0.067 |
| Age | -0.001 | 0.002 | -0.071 | 0.514 | 0.005 |
| Table IIIMultivariate linear regression
analysis of the determinant factors of log systolic blood
pressure. |
Table III
Multivariate linear regression
analysis of the determinant factors of log systolic blood
pressure.
| Variables | B | Standard error | β | P-value | Adjusted
R2 |
|---|
| Constant | 1.725 | 0.076 | N/A | <0.001 | 0.415 |
| Ox-LDL |
-5.261x10-6 | 0.000 | -0.097 | 0.274 | |
| MPO | 0.000 | 0.000 | 0.282 | 0.006 | |
| WC | 0.003 | 0.001 | 0.418 | <0.001 | |
| XO | 0.015 | 0.005 | 0.248 | 0.007 | |
| FSG | 0.001 | 0.000 | 0.328 | 0.001 | |
| Age | -0.002 | 0.001 | -0.142 | 0.113 | |
| Table IVUnivariate linear regression analysis
of the determinant factors of log diastolic blood pressure. |
Table IV
Univariate linear regression analysis
of the determinant factors of log diastolic blood pressure.
| Variables | B | Standard error | β | P-value | Adjusted
R2 |
|---|
| Ox-LDL |
-1.160x10-5 | 0.000 | -0.167 | 0.124 | 0.016 |
| MPO | 0.000 | 0.000 | 0.217 | 0.045 | 0.036 |
| WC | 0.003 | 0.001 | 0.356 | 0.001 | 0.116 |
| Age | -0.004 | 0.002 | -0.191 | 0.079 | 0.025 |
| FSG | 0.001 | 0.001 | 0.233 | 0.031 | 0.043 |
| XO | 0.000 | 0.008 | -0.004 | 0.97 | 0.012 |
| Table VMultivariate linear regression
analysis of the determinant factors of log diastolic blood
pressure. |
Table V
Multivariate linear regression
analysis of the determinant factors of log diastolic blood
pressure.
| Variables | B | Standard error | β | P-value | Adjusted
R2 |
|---|
| Constant | 1.632 | 0.111 | N/A | <0.001 | 0.248 |
| Ox-LDL |
-1.247x10-5 | 0.000 | -0.180 | 0.075 | |
| MPO | 0.000 | 0.000 | 0.274 | 0.017 | |
| WC | 0.003 | 0.001 | 0.284 | 0.006 | |
| Age | -0.004 | 0.002 | -0.201 | 0.059 | |
| FSG | 0.002 | 0.001 | 0.310 | 0.006 | |
| XO | 0.002 | 0.008 | 0.032 | 0.751 | |
Discussion
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.
Supplementary Material
Multivariate linear regression
analysis of the determinant factors of log systolic blood pressure
in males (18 subjects).
Multivariate linear regression
analysis of the determinant factors of log systolic blood pressure
in females (68 subjects).
Multivariate linear regression
analysis of the determinant factors of log diastolic blood pressure
in males (18 subjects).
Multivariate linear regression
analysis of the determinant factors of log diastolic blood pressure
in females (68 subjects).
Acknowledgements
Not applicable.
Funding
Funding: This work was funded by the Faculty of Medicine,
University of Hasanuddin (grant no. 2885/UN4.6/PT.01.05/2025).
Availability of data and materials
The data generated in the present study may be
requested from the corresponding author.
Authors' contributions
LBK, NN, AA, and HR conceived, designed the study,
wrote and edited the manuscript. LBK, WM, and SHY performed the
investigation and data analysis. HR supervised the project.
Ethics approval and consent to
participate
The study was conducted in accordance with the
Declaration of Helsinki and approved by Health Ethics Committee,
Medical Faculty, University of Hasanuddin, with recommendation
number: 812/2025, protocol: UH25080659 (approved on 17th of October
2025). Written informed consent was obtained from all subjects
involved in the study before participation.
Patient consent for publication
Not applicable.
Competing interest
The authors declare that they have no competing
interests.
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