Beyond the Scale: Investigating Adiponectin, ICAM-1, and VCAM-1 as Metabolic Markers in Obese Adolescents with Metabolic Syndrome

Background Adiponectin acts to prevent vascular dysfunction due to obesity by inhibiting ICAM-1 and VCAM-1 expressions. Objective We investigate adiponectin ICAM-1, VCAM-1, and metabolic syndrome (MetS) in obese adolescents. Methods A cross-sectional study with healthy obese adolescents aged 13 to 18 years was conducted from October 2019 to January 2020. Statistical analysis conducted was a test of normality and homogeneity tests, ANOVA/Kruskal–Wallis, independent sample T-test/Mann–Whitney U test, and Spearman correlation and determined as significant if p value <0.05. Results 125 obese adolescents were recruited. 42 (33.6%) were obese with MetS (we grouped as MetS) and 83 (66.4%) subjects without MetS (non-MetS group). VCAM-1 was significantly higher on boys with MetS compared to girls with MetS, and even girls with MetS had lower levels of VCAM-1 than boys with non-MetS. ICAM-1 was significantly higher in boys with low-level HDL-c (p < 0.05) and correlated weakly with HDL-c, while adiponectin levels were significantly lower in girls with central obesity and hypertriglyceridemia. Path analysis showed that triglyceride had a direct effect on ICAM-1 but not VCAM-1 in both obese boys and girls. Adiponectin had a negative direct effect on ICAM-1 and VCAM-1 in girls. However, on boys, diastole blood pressure had a negative direct effect, which might be the role of sex hormones indirectly. Conclusion VCAM-1 was significantly higher in boys than girls, which showed that boys had a higher risk of atherosclerosis. ICAM-1 showed no significant difference in both gender and metabolic states. Adiponectin showed a protective effect by lowering ICAM-1 and VCAM-1 directly on girls.


Introduction
Adipose tissues secreting a number of adipokines regulate insulin sensitivity, energy metabolism, and vascular homeostasis, so the dysfunction of the adipose tissue is linked with the incidence of obesity accompanied with insulin resistance, hypertension, and cardiovascular disease [1].Obesity is known to alter the expression of adipokines due to the adipose tissue hypertrophy, including adiponectin, in which it is able to exert a potent anti-infammatory and vascular protective efect [2].Adiponectin is one of the most abundant adipokines known as the obesity hormone.and the levels of adiponectin in the circulation was 3 μg/mL to 30 μg/mL in humans [3].In a study, adiponectin is associated with body weight and abdominal obesity and MetS risk factor, especially low-level HDL-c and hypertriglyceridemia [4].
It has been proposed that adiponectin acts to prevent the vascular dysfunction due to obesity and diabetes by improving insulin sensitivity and metabolic profles to reduce the risk factors for cardiovascular disease and protects the vasculature through its pleiotropic actions on endothelial cells, endothelial progenitor cells, smooth muscle cells, and macrophages [1].Te concentrations of adiponectin of 5 to 25 mg/mL had a signifcant inhibitory efect on the expression of monocyte adhesion and adhesion molecule induced by TNF-α in vitro.
Atherosclerosis is an infammatory disease in which adhesion molecules on arterial endothelial cells are responsible for the accumulation of monocytes/macrophages and T lymphocytes.Obesity is a low-grade infammation which causes endothelial dysfunction process, by increasing free radicals derived from oxygen.Te free radicals was produced by adipocyte hypertrophy.Te imbalance of ROS and antioxidant system causes an oxidative stress which leads to endoplasmic reticulum (ER) stress and mitochondrial dysfunction [5].Adiponectin is accumulated in the vasculature, and it reduced on obesity due to suppression by TNF-α and lead to adiponectin-defciency, which stimulate the signifcant increases of vascular cell adhesion molecule 1 (VCAM-1) and intercellular adhesion molecule 1 (ICAM-1) or known as CD54 in aortic intima [6].
Here, we investigate the levels of adiponectin, ICAM-1, and VCAM-1 with the incidence of MetS in obese adolescents.

Ethical Approval.
Te study has been approved and declared as ethically appropriate by the Research and Ethics Scientifc Committee 23/EC/KEPK/FKUA/2021 released by Faculty of Medicine, Airlangga University, Surabaya, Indonesia.Screening of obesity was performed with the permission of the head school and parents of the subjects.

Study Design.
A cross-sectional study with healthy obese adolescents aged 13-18 years was conducted from October 2019 to January 2020.Obesity was determined based on the body mass index (BMI) for age based on gender ≥percentile 95th of CDC growth chart 2000.

Samples.
Te subjects must be healthy (did not take corticosteroids 6 months before the study or dyslipidemia medication 3 months before the study, did not take antibiotic or hormonal therapy, did not smoke or consume alcohol, and did not have autoimmune disease or endocrinology disorders).
Sample size was measured with where n is the sample number, P is the subject proportion in the study � 0.5, d 2 is the absolute value � 0.1, Z 1−α/5 is the expected signifcant � 1.96, CI is the confdence interval � 95%, and n � 97 subjects.

Blood Sample
Examination.Blood samples were withdrawn via cubital vein as much as 5 ml by the trained analyst and placed on vacutainer with EDTA.After that, the vacutainer was replaced in an icebox to transport to the laboratory.Blood analysis includes lipid profle, fasting blood glucose, and fasting insulin by a designated medical laboratory.For adiponectin, ICAM-1, and VCAM-1 analyses, the blood that has been taken was not immediately analysed.Te blood was centrifuged to remove the serum and then stored at −70 °C until the analysis was performed in the laboratory.Adiponectin was analysed using the Human Adiponectin ELISA kit (Bioassay Technology Laboratory).ICAM-1 was analysed using the Human Intercellular Adhesion Molecule 1 ELISA kit (Bioassay Technology Laboratory) while sVCAM-1 was analysed using the Human Vascular Cell Adhesion Molecule-1 ELISA kit (Bioassay Technology Laboratory).

Anthropometry Measurements.
Body weight was measured using Seca Robusta 813 digital scale in standing position, by stepping on the scale w,hile the body height was measured using Seca 206 Body Meter.Height was measured from the vertex of the head to the heel in standing position.Waist circumference and hip circumference were measured using Seca 201 measuring tape.Waist circumference was measured by wrapping the measuring tape around the subject's stomach, at the midpoint between the lowest rib and the endpoint of the iliac crest upon expiration, in line with the navel.Hip circumference was measured by asking the subjects to keep the feet together, then wrapping the measuring tape around the widest part of hips, at the point of the greatest gluteal protuberance.Te subjects were measured using light cloth without footwear and other accessories such as belt, hat, or hair accessories.BMIs were calculated by dividing body weight (in kg) with body height square (in m) (body weight (kg)/body height 2 (m 2 )), in kg/m 2 unit.Blood pressure was measured using Omron Automatic Blood Pressure Monitor HEM-8712 (Omron Health Care Co., Ltd, Japan) by placing the cuf on the right arm and then pulling and tightening it according to the size of the arm.After it was installed correctly (fastened and did not move), the power button on the digital tension tool was pressed, and then the microprocessor started to drive air pressure into the cuf, and then the value of blood pressures will appear in the manometer tube column.Blood pressure measurement was performed in a sitting position after the subject had rested for 10 minutes.
Table 2 summarizes the levels of adiponectin, ICAM-1, and VCAM-1 on the subjects based on MetS risk factors on boys.Tere was no signifcant diference on adiponectin, ICAM-1, and VCAM-1 between the subjects with central obesity and hyperglycemic compared to noncentral obesity and nonhyperglycemic (p > 0.05).Tere was a signifcant diference of ICAM-1 levels on low-level HDL-c subjects compared to normal HLD-c (3,138.68 ± 15,018.66 vs. 995.04± 1,567.86 pg/ml; p < 0.05).Tere was a signifcant diference of VCAM-1 levels on the boys with hypertension, lower on the hypertension boys compared to nonhypertension boys (9.01 ± 4.98 vs. 18.17 ± 21.78 pg/ml; p ≤ 0.001).
Path analysis to analyse the efect of MetS components (waist circumference, fasting blood glucose, triglycerides, HDL-c, and systole and diastole blood pressure) on ICAM-1 showed that diastole-BP and triglyceride levels had a direct efect on ICAM-1 in boys, as summarized in Figure 1, while insulin and adiponectin levels did not show their efect on ICAM-1 or VCAM-1 directly or indirectly.
Diastole-BP and triglyceride levels had a signifcant direct efect on ICAM-1 (p < 0.05).Diastole-BP also had a signifcant direct efect on VCAM levels, but triglycerides did not exert the same efect (p > 0.05).Both MetS components, diastole-BP and triglycerides, did not have a indirect efect on VCAM-1 via ICAM-1 (the value of indirect efect < direct efect).
On girls, the path analysis of MetS variables is summarized in Figure 2, which showed that triglyceride and adiponectin levels exert its efect on ICAM-1 directly (p < 0.05).Adiponectin had a negative direct efect on

Discussion
Obesity and metabolic syndrome in children and adolescents are associated with adverse consequences in adulthood, especially coronary heart disease due to overproduction of infammatory mediators and insulin resistance [9].Te prevalence of MetS was 4.8% in boys and 3.4% in girls according to the study conducted in South Korea, higher in girls aged more than 12 years; however, on boys, higher in those aged 13 years or above [10], which was lower than this study, especially in boys.Te prevalence of MetS was increased 17% in boys during nine years (2010-2019) in Arab adolescents, higher than in girls, which count only 2.9%, and the prevalence was higher in boys [11], which is similar with this study.Other study conducted in Tehranian children and adolescents showed the same results; the prevalence on boys was increased by 3.2% during phase I (1999-2001) to phase III (2006-2008), while on girls, the prevalence was decreased by 5.2% [9].However, the changes on dietary practices and sedentary lifestyle were suspected to increase the obesity prevalence in developing countries [12].Factors infuenced the high prevalence in boys was the increasing of age, meal habits (having one meal per day), and body awareness (weight maintenance) [11].Excess body weight leads to overweight and obesity [13], which contributes to the risk factor of MetS in early onset, on adolescents [14,15].Te prevalence of MetS in obese adolescents was 12.4% to 44.2%, and in some populations, it reaches 50% [16], which was in line with this study.Te incidence of MetS was developed due to the interaction between obesity, insulin resistance, and infammation [17].Te BMI could estimate the body fat indirectly and an excellent screening method to predict obesity on paediatric population, but it cannot be used as single diagnostic tools [18].
Fasting insulin levels are higher in MetS.Gender, puberty stage, BMI, and waist circumference have a correlation with fasting insulin levels [19].In healthy conditions, glucose is transported into myosin by GLUT-4 under the infuence of insulin through the process of Glut4 translocation [20] which is then phosphorylated into glucose-6-phosphate.Tis intermediate product is then stored as glycogen or becomes a substrate in the glycolytic pathway [21].In obesity, fat tissues, especially in the abdominal area, are prone to lipolysis which causes an increase in free fatty acids (FFA) in the body.High concentrations of FFA mediated IR by reducing the strength of insulin signals through insulin receptor substrate (IRS)-1/phosphatidylinositol (PI) 3kinase pathway [22].In addition, adipokines produced by adipocytes such as resistin and retinol-binding protein 4 which reduced the insulin sensitivity [23].
Te pathogenesis of endothelium infammation was triggered by cytokines in which the endothelium is stimulated, so that the endothelium is more adhesive for leucocytes and leads to the development of infammatory lesions.Te leucocyte adhesion to the vascular endothelium is the most important process of the leucocyte extravasation during the infammation process in which it is mediated by E-selectin.Te unity and transendothelial migration depend on the interaction between adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), and the ligands [24].ICAM-1 and VCAM-1 have functions as the adhesion of leucocyte to the vascular endothelium [25], by facilitating the leukocyte transmigration across the endothelium [26].So, both ICAM-1 and VCAM-1 have been used as infammation marker and endothelial dysfunction [27] because the expression of both CAMs is enhanced by a variety of proatherogenic stimuli such as proinfammatory cytokines and reactive oxygen species [28].Obesity induces early endothelial activation [29] due to its low-grade chronic infammation [29] and increases the expression of adhesion molecules mRNA and protein levels in the visceral adipose tissue, which is linked to central obesity (visceral adiposity) and the risk of cardiovascular diseases [30].6

Journal of Obesity
However, the study of CAMs on paediatric population is still in controversial results.A study in Vienna, Austria, showed that both ICAM-1 and VCAM-1 showed no signifcant diference in lean or obese children [31].On healthy obese adult, it has been proved that sICAM-1, E-selectin, and P-selectin were signifcantly higher than those in healthy lean adults, but there is no signifcant diference on sVCAM-1 serum concentrations on both groups [32].While in this study, there is no signifcant diference between MetS and non-MetS groups due to the subject being healthy obese adolescents.Other study investigating sVCAM-1 concentration on healthy subjects with myocardial infarction supported this fnding; it showed there is no signifcant diference between control and case subjects, which are similar with this study [33].
Intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) are transmembrane immunoglobulins in which they are upregulated during the endothelial activation.Both ICAM-1 and VCAM-1 have adhesion molecules on leucocytes (monocytes, lymphocytes, and neutrophils) as ligand that are CD11⁄ CD18 for ICAM-1 and very late antigen-4 (VLA-4) for VCAM-1 [34], in which they play a critical role in monocyte adherence to endothelial cells.ICAM-1 and VCAM-1 are overexpressed on endothelial lumen in many pathological states, and the level is increased in atherosclerotic lesion [25].Te average of soluble ICAM-1 was signifcantly higher in individuals with low-level of HLD-c than them with normal levels of HDL-c in adults, which indicated that HDL-c efectively modulate sICAM-1 in vivo [28], which was in line with the result on boys.It is well known that HDL-c had a protective efect to prevent the development of atherosclerosis by inhibiting the expression of adhesion molecules (ICAM-1, VCAM-1 and E-selectin) induced by cytokines on the cell surface and also acts as antioxidant and mitogen and also binds the lipopolysaccharide [35].Tere is evidence that the incidence of cardiovascular disease (CVD) is greater in men, and it was suspected that sex hormones, particularly estrogen, have modulatory efects on the endothelium and circulating cells which have been implicated in vascular infammation.Estrogens upregulate the synthesis, release and activity of protective agent on endothelial, and suppress the expression of pathogenic agents by endothelium via estrogen receptor (ER), Erα and Erβ, on vasculature [36], while androgens are suspected to be proatherogenic [37].Moreover, estrogen is able to reduce the fat accumulation in women [38] and showed that its level is higher than men/boys at any age [37].Te in vitro study exhibited that estrogen inhibits smooth muscles by activating potassium efux and inhibiting calcium infux.Furthermore, estrogen inhibits vascular smooth muscle cell proliferation [39].
VCAM-1 levels in obesity with hypertension showed no signifcant diference with normotensive subjects on adults [40], or on healthy obese adults and unhealthy obese adults [32].However, it showed lower levels on hypertensive boys with obesity, which contradicted with those results.Te expression of VCAM-1 was inducted by proinfammatory cytokines such as IL-1 and TNF-α [35].A study on adolescents showed that the increase of the BMI was associated with the elevation of hs-CRP and reduced HDL-c and indirectly elevated ICAM-1 but not VCAM-1 [27], which showed that infammation is more profound infuencing VCAM-1 expression.Tis fnding is supported by the study on adults with left ventricular (LV) hypertrophy and sVCAM-1 was elevated [41,42].Te increment of VCAM-1 levels depends on age, but there was no signifcant diference with gender on healthy adults [43].It was reported that testosterone attenuated atherogenesis in vitro by converting testosterone into estradiol, which inhibits the expression of VCAM-1 (protein and mRNA) in dose-dependent manner by aromatase enzyme in human umbilical vein endothelial cells (HUVEC) [44], so we suspected the pubertal stage was infuencing VCAM-1 levels in this study.However, we did not evaluate the pubertal stage of the subjects.
In adult population, ICAM-1, VCAM-1, and E-selectin were signifcantly correlated with fasting blood glucose (r � 0.59; p < 0.001); the increased ICAM-1 was suspected related to hyperglycaemia in type-2 diabetes mellitus subjects [45] which was in line with this study in both genders, but genetic study showed ICAM-1 was correlated positively with fasting insulin, HOMA IR, BMI, and waist circumference, and negative correlation with HDL-c [46].Hyperglycemia decreases the expression of ICAM-1 and afects low proliferation of endothelial cells [47].Endothelial cells exposed to high concentration of glucose leads to upregulation of the expression of adhesion molecules (ICAM-1, VCAM-1, and E-selectin) and proinfammatory cytokines due to the activation of poly ADP-ribose polymerase (PARP) enzyme.Moreover, glucose exposure also triggers the production of nitrotyrosine and induces the expression of adhesion molecules [48].
Based on gender, ICAM-1 was correlated with HDL-c in boys, although the correlation was very weak, which is in contrast with the studies conducted in paediatric population, ICAM-1 was correlated negatively with HDL-c [27,49] and on adults [46].Other studies on adults with hypercholesterolemia and ischemic heart disease showed that there was no correlation between ICAM-1 and HDL-c [50], which contradicted with this study.Te in vitro study using human umbilical vein endothelial cells (HUVECs) treated with HDL-c from patients with T2DM showed that HDL-c stimulates the expression ICAM-1 and VCAM-1 on the cells' surface along with the protein kinase C (PKC) activity [51].A study on T2DM patients showed that HDL-c from diabetic patients with CAD enhanced monocyte adhesion on the endothelial cells, which was correlated with HDL carbamyl-lysine (HDL-CBL).Culture study showed that carbamylated HDL promoted the adhesion of monocyte to endothelial cells, which promote induced upregulation of cell adhesion molecules' expression and activating NF-κB/ p65 signalling pathways.So, carbamylated HDL-c potentiated proatherogenic [52].Moreover, dysfunctional HDL-c has proinfammatory efects on the endothelial cells [53], so we suspected that boys with obesity experience dysfunctional HDL-c, which induced the expression of ICAM-1.Te elevation of 100 ng/ml ICAM-1 will increase the risk of cardiovascular mortality by 1.10-folds (95% CI (1.05-1.15))Journal of Obesity and get worse due to the presence of hypertension and cardiovascular disease [54].
Te in vivo study on mice showed that the increment of LDL-c levels increased the expression of ICAM-1 and VCAM-1 in aortic endothelial cells which were regulated by AP-1 and TNF-α.Te expression pattern of ICAM-1 was pervasive, but VCAM-1 expression appears more focussed and less elevated [55].Tis fnding explained the weak correlation between LDL-c and ICAM-1.Te atherogenesis process is initiated when the accumulation of LDL-c particles in the arterial wall is trapped in subendothelial space.LDL-c will undergo oxidation processes by oxidants such as nitric oxide and its products, and myeloperoxidases.One of the key events of atherogenesis is the accumulation of LDL particles in the arterial wall.Once entrapped in the subendothelial space, LDL undergoes modifcation through oxidation (oxidized LDL) by cell-derived oxidants, such as nitric oxide and its products, and myeloperoxidases, in which it induces the expression of adhesive molecules on endothelial cells [56].
Hypertension contributed to the initiation of atherosclerosis due to its association with infammation [57] and sVCAM-1 [58].Several studies indicated positive association between blood pressures with VCAM-1 in adults [59][60][61], which was in contrast with this study.However, gender infuences the blood pressure regulation.Systole blood pressure 4 mmHg is higher in boys than girls aged 13 to 15 years , and 10 to 14 mmHg is higher in boys aged 16 to 18 years which showed that androgen, especially testosterone, plays a regulatory role on blood pressure, which made men at greater risk of cardiovascular and renal diseases than women at age-matched [62].Adolescence is the time of growth spurt and the onset of puberty, characterized by hormonal changes [63] in which there is elevation on androgens, in boys, testosterone, which leads to the elevation of blood pressure [62].Tis explains the negative relationship between blood pressure (systole and diastole) with VCAM-1; in other words, blood pressure in this study is likely linked with hormonal changes during pubertal period.Tis fact explains the signifcantly higher VCAM-1 in boys with MetS than girls with MetS, even girls with MetS had lower VCAM-1 levels than boys with non-MetS.An in vivo study showed that insulin concentration (10 −9 -10 −7 mol/L) induced VCAM-1 expression and markedly increased TNF-α via NF-kB activation and IkB-α accumulation [64], so we suspect that hyperinsulinemia stimulates the expression of VCAM-1, not the blood pressure.Moreover, VCAM-1 was correlated with age and becomes an independent predictor of VCAM-1 levels, but ICAM-1 was not infuenced by age and sex [50], which explained the levels of ICAM-1 which did not show a signifcant diference in this study.
Abdominal obesity was associated with lower adiponectin levels on children aged 9-10 years [65], and its levels were infuenced by pubertal stage [66] and gender.Te similar results were also seen in other studies [4], which support this fnding.In healthy lean boy, adiponectin was reduced along with physical and pubertal development and was signifcantly lower than that in girls [67], which tend to be low at late obesity [68].Waist circumference, for detecting central obesity, was correlated negatively with adiponectin levels in girls [4,69], which was in line with this study; the levels of adiponectin was signifcantly lower in central obesity in girls.Based on gender, adiponectin is higher in girls than boys [67,70] until adulthood [68] and thought to be infuenced by sex hormones [71].It was found that adiponectin was correlated with androgens, not testosterone and estradiol [68,70,71] but the results were still controversial.In girls, adiponectin thought to act as female fertility regulation [72], which was also supported by others, and adiponectin promotes gonadal activities [73].Tat is why adiponectin afects ICAM-1 and VCAM-1 in girls in the path analysis.Adiponectin plays a role in steroidogenesis of ovarian.Together with insulin-like growth factor 1 (IGF-1), adiponectin improves the secretion of progesterone and estrogen in the animal model study [73].A study conducted on postmenopausal women concludes that more androgenic sex hormone profles (high testosterone) were associated with higher fow-mediated dilatation (FMD), which may impair the vasculature [74].Endogenous estrogen afects endothelial cells by upregulating the NO synthase, protects from lipid metabolism, and reduces oxidative stress [75].
A study conducted on adults showed that plasma Pselectin correlated positively with triglycerides only in the overweight/obese group [76].Te in vivo study on mice fed with high fat diet showed a signifcant correlation between sICAM-1 with body weight and visceral fat or central obesity due to the expression ICAM-1 mRNA on the adipose tissue, which is higher on male mice than female mice, followed by the increment of IL-6 and monocyte chemoattractant protein-1 (MCP-1) as the consequences of atherogenic lipid (LDL-c, cholesterol, and triglyceride) in the diet [77].But the study to assess the direct efect of triglycerides on ICAM-1 is limited.However, this study found out whether girls or boys with obesity experience the elevation of ICAM-1 due to the elevation of triglyceride, although it did not have a direct or indirect efect on VCAM-1, which was supported by ex vivo study using postprandial triglyceride-rich lipoproteins (PP-TGRLs) combined with TNF-α stimulation (at dose 0.3 ng/ mL), increasing the expression of VCAM-1, ICAM-1, and Eselectin by 10-15%.Te transcription and expression of VCAM-1 depends on postprandial serum triglycerides (PP-sTG) and waist circumference [78].
In girls, adiponectin had a negative infuence on ICAM-1, which was in line with other studies [79], in which adiponectin acts to suppress the expression of ICAM-1.In this function, adiponectin acted as protective agents against various obesity-linked diseases, including cardiovascular disorders, by attenuating infammatory response via signalling pathways in various cell types [80].Te fnding was in line with this study.Te activity was mediated via its receptors, adiponectin receptor 1 (AdipoR1), expressed abundantly in the skeletal muscle, and adiponectin receptor 2 (AdipoR2) found predominantly in the liver.Both receptors are transmembrane G-protein-coupled receptors and found on macrophages, endothelial cells, and smooth muscle cells within atherosclerotic plaques.Tese receptors were able to activate AMP-activated protein kinase (AMPK), p38 mitogen-activated protein kinase (p38 MAPK), and 8 Journal of Obesity peroxisome-proliferator-activated receptor-α (PPAR-α) and to stimulate fatty acid oxidation and glucose uptake [5].Tis functional role of adiponectin was exerted in dosedependent manner (5 to 25 µg/mL), in which TNFα-induced adhesion expression, including ICAM-1 and VCAM-1 on the in vivo study, was then inhibited [6].

Conclusion
VCAM-1 was signifcantly higher on boys which showed that boys had higher risk of atherosclerosis than girls, while ICAM-1 showed no signifcant diference on both gender and metabolic states.Adiponectin showed a protective efect by lowering ICAM-1 and VCAM-1 directly on girls.

Figure 1 :Figure 2 :
Figure 1: Path analysis of the efect of diastole-BP and triglycerides on ICAM-1 and VCAM-1 in boys.

Table 2 :
Te levels of adiponectin, ICAM-1, and VCAM-1 on MetS risk factor on boy adolescents with obesity.

Table 3 :
Te levels of adiponectin, ICAM-1, and VCAM-1 on MetS risk factors on girl obese adolescents.