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Keywords:

  • exercise intervention;
  • adiponectin;
  • insulin resistance;
  • adolescents

Abstract

  1. Top of page
  2. Abstract
  3. Introduction
  4. Research Methods and Procedures
  5. Results
  6. Discussion
  7. Acknowledgments
  8. References

Objective: The objective of this study was to investigate the association among adiposity, insulin resistance, and inflammatory markers [high-sensitivity C-reactive protein (hs-CRP), interleukin (IL)-6, and tumor necrosis factor (TNF)-α] and adiponectin and to study the effects of exercise training on adiposity, insulin resistance, and inflammatory markers among obese male Korean adolescents.

Research Methods and Procedures: Twenty-six obese and 14 lean age-matched male adolescents were studied. We divided the obese subjects into two groups: obese exercise group (N = 14) and obese control group (N = 12). The obese exercise group underwent 6 weeks of jump rope exercise training (40 min/d, 5 d/wk). Adiposity, insulin resistance, lipid profile, hs-CRP, IL-6, TNF-α, and adiponectin were measured before and after the completion of exercise training.

Results: The current study demonstrated higher insulin resistance, total cholesterol, LDL-C levels, triglyceride, and inflammatory markers and lower adiponectin and HDL-C in obese Korean male adolescents. Six weeks of increased physical activity improved body composition, insulin sensitivity, and adiponectin levels in obese Korean male adolescents without changes in TNF-α, IL-6, and hs-CRP.

Discussion: Obese Korean male adolescents showed reduced adiponectin levels and increased inflammatory cytokines. Six weeks of jump rope exercise improved triglyceride and insulin sensitivity and increased adiponectin levels.


Introduction

  1. Top of page
  2. Abstract
  3. Introduction
  4. Research Methods and Procedures
  5. Results
  6. Discussion
  7. Acknowledgments
  8. References

The prevalence of obesity is increasing at an alarming rate (1, 2, 3). This phenomenon extends to children and adolescents in all countries of the industrialized world (3). Countries throughout the world have experienced a marked increase in the prevalence of overweight and obese children and adolescents (4, 5). The increase in the prevalence of overweight and obesity implies a substantial increase among children and adolescents (13) in lifestyle-associated diseases such as type 2 diabetes (6, 7), dyslipidemia (8, 9), hypertension (10, 11), coronary heart disease (12), and stroke, which are usually found in adults (14, 15).

The incidence of type 2 diabetes, although still uncommon in children and adolescent in most countries, has nevertheless increased dramatically in recent years (16), particularly in obese children who have family history of type 2 diabetes (17). The incidence of type 2 diabetes rose from 4% of all pediatric diabetic cases in 1990 to ∼20% a decade later in the United States (18). Another study suggests that type 2 diabetes accounts for up to 50% of all new cases of pediatric or adolescent diabetes (19). The most significant long-term consequence of childhood obesity is its persistence into adulthood.

The traditional view of adipose tissue as a passive reservoir for excess energy storage is no longer valid (20). The identification and characterization of leptin in 1994 firmly established adipose tissue as an endocrine organ (21). In addition to leptin, other cytokines, including tumor necrosis factor (TNF)1-α, interleukin (IL)-6, resistin, plasminogen activator inhibitor-1, monocyte chemoattractant protein-1, and adiponectin, have been identified as adipose-secreted proteins that are collectively referred to as adipocytokines (20). Adipocytokines have numerous functions, including regulation of satiety, carbohydrate and lipid metabolism, and insulin sensitivity (22). Interestingly, obesity increases the production of adipocytokines that cause insulin resistance (20) but decreases the production of adiponectin, which reduces insulin resistance (23). Adiponectin, also referred to as AdipoQ and Acrp 30, is a 30-kDa protein that is encoded by apM-1 and expressed and secreted mainly by adipose tissue (24, 25, 26). Adiponectin increases skeletal muscle fatty acid oxidation and reduces plasma glucose concentration through activation of adenosine monophosphate-activated protein kinase (27). Plasma adiponectin is positively associated with enhanced insulin signaling transduction in skeletal muscle and a reduced risk of developing diabetes (28, 29).

Because exercise training improves insulin sensitivity and prevents the development of type 2 diabetes, it is logical, therefore, to speculate that exercise-induced improvement in insulin sensitivity is mediated through regulation of plasma adiponectin levels. However, the effects of exercise training on circulating plasma adiponectin levels are controversial. Although there have been many studies examining the effects of exercise training on adiponectin and other inflammatory markers, few studies have been conducted among Asian adolescents. Therefore, the purpose of the present study was to investigate the association of body adiposity, insulin resistance, inflammatory markers, and adiponectin among lean and obese male Korean youth and to examine the effects of 6 weeks of jump roping exercise on obesity, insulin sensitivity, TNF-α, IL-6, and adiponectin levels among obese male Korean youth.

Research Methods and Procedures

  1. Top of page
  2. Abstract
  3. Introduction
  4. Research Methods and Procedures
  5. Results
  6. Discussion
  7. Acknowledgments
  8. References

Subjects

Twenty-six obese (BMI, 29.5 ± 2.2 kg/m2) and 14 lean (BMI, 21.5 ± 0.7 kg/m2) male adolescents were recruited from a high school in Su-won City (Kyounggi-Do, Korea). This study was approved by an institutional ethics review board at the Department of Sport and Leisure Studies, Yonsei University. All subjects gave their written informed consent to participate in the study. Subjects had no personal history of diabetes or any major medical condition that would preclude them from participating in the exercise intervention. Subjects were not participating in regular physical activity except school physical education class. Body weight was measured to the nearest 0.1 kg, and height was measured to the nearest millimeter using JENIX (DS-102, Seoul, Korea). BMI was calculated as weight in kilograms divided by the square of height in meters. Waist circumferences (WCs) and hip circumferences were obtained in duplicate with a Gullick II tape. Percent body fat and total body fat mass were measured by the Tanita foot-to-foot scale impedance meter (Tanita Co., Tokyo, Japan).

Study Design

Once subjects were recruited and baseline measurements were completed, obese subjects were randomly assigned to either the obese exercise group (OEG; n = 14) or the obese control group (OCG; n = 12). Subjects in the OEG participated in jump roping exercise in addition to regular physical education class, while the OCG participated in only a regular physical education class. Lean control group (LCG) participated in only regular physical education class. Anthropometric variables, fasting glucose, fasting insulin, triglyceride (TG), total cholesterol (TC), low-density lipoprotein-cholesterol (LDL-C), high-density lipoprotein-cholesterol (HDL-C), adiponectin, TNF-α, IL-6, and high-sensitivity C-reactive protein (hs-CRP) were measured before and after 6 weeks of jump rope exercise. For lean controls, variables were measured only once at baseline.

Exercise Training

Subjects in the OEG participated in supervised jump roping exercise five times per week, 40 min/d for 6 weeks. The detailed exercise training program is summarized in Table 1.

Table 1. . Jump rope exercise program
  Exercise duration
WeekIntensity (jumps/min)Warm-up (5 mins)Exercise (30 mins)Cool down (5 mins)
160 1 min of exercise, 30 secs of rest 
260 1.5 mins of exercise, 30 secs of rest 
360Stretching2 mins of exercise, 30 secs of restStretching
490 2.5 mins of exercise, 30 secs of rest 
590 3 mins of exercise, 30 secs of rest 
690 4 mins of exercise, 30 secs of rest 

Biochemical Analyses

Biochemical tests were performed on blood samples collected after overnight fast (<12 hours). Venous blood was drawn, and after centrifugation of the specimen, serum and plasma were frozen immediately at −80°C. Serum levels of fasting glucose, TC, HDL-C, and TG were assayed using an ADVIA 1650 Chemistry system (Bayer, Tarrytown, NY). LDL-C was calculated using Friedenwald's formula (30). Fasting insulin was assayed by electrochemiluminescence immunoassay using Elecsys 2010 (Roche, Indianapolis, IN). hs-CRP was measured by a latex-enhanced immunoturbidimetric assay using an ADVIA 1650 Chemistry system (Bayer). Insulin resistance was estimated by the homeostasis model assessment of insulin resistance (HOMA-IR): [insulin (microunits per milliliter) × fasting blood glucose (millimolar)/18]/22.5. Plasma adiponectin, TNF-α, and IL-6 levels were measured by an EIA kit (Adipogen, Seoul, Korea).

Statistical Analysis

The normality of distribution was checked for all variables with the Kolmogorov-Smirnov test. Pre-training and post-training differences were assessed with the Student's t test for dependent samples. The relationships between variables were tested with Pearson's correlation coefficient. A p value < 0.05 was used as the criterion of statistical significance. Statistical analysis was completed with the SPSS software, version 10.0 (SPSS, Inc., Chicago, IL). Values are presented as mean ± standard error.

Results

  1. Top of page
  2. Abstract
  3. Introduction
  4. Research Methods and Procedures
  5. Results
  6. Discussion
  7. Acknowledgments
  8. References

Cross-sectional Observational Study

The age, body weight, BMI, percent body fat, serum levels of fasting glucose, fasting insulin, HOMA-IR, lipid profile, plasma level of adiponectin, and TNF-α and IL-6 levels are shown in Table 2.

Table 2. . Baseline values between obese and lean subjects
 Obese (N = 26)Lean (N = 14)
  • TC, total cholesterol; TG, triglyceride; HDL-C, high-density lipoprotein-cholesterol; LDL-C, low-density lipoprotein-cholesterol; hs-CRP, high-sensitivity C-reactive protein; HOMA-IR, homeostasis model assessment of insulin resistance; TNF, tumor necrosis factor; IL, interleukin; SBP, systolic blood pressure; DBP, diastolic blood pressure. Data are shown as means ± standard error.

  • *

    p < 0.05 compared with lean controls.

  • p < 0.01 compared with lean controls.

Age (yrs)17 ± 0.1116.8 ± 0.13
Height (cm)174.37 ± 1.3173.54 ± 2.8
Weight (kg)90.04 ± 2.164.70 ± 0.8
BMI (kg/m2)29.50 ± 0.421.47 ± 0.7
Fat (%)31.19 ± 0.819.5 ± 0.6
Fat mass (kg)28.1 ± 1.212.5 ± 0.4
Fasting glucose (mg/dL)84.38 ± 1.3890.9 ± 2.0
TC (mg/dL)172.6 ± 6.6*152.9 ± 5.1
TG (mg/dL)109.7 ± 12.564.1 ± 5.5
HDL-C (mg/dL)44.4 ± 1.2*49.9 ± 2.5
LDL-C (mg/dL)106.2 ± 6.090.2 ± 4.5
hs-CRP (mg/mL)0.13 ± 0.03*0.04 ± 0.02
Insulin (µU/mL)13.1 ± 1.15.8 ± 0.4
HOMA-IR2.4 ± 0.31.35 ± 0.12
Adiponectin (µg/mL)7.6 ± 0.5*9.42 ± 0.6
TNF-α (pg/mL)1.7 ± 0.11.2 ± 0.1
IL-6 (pg/mL)0.53 ± 0.03*0.37 ± 0.1
SBP (mm Hg)126.2 ± 1.8114.3 ± 2.0
DBP (mm Hg)81.9 ± 1.774.3 ± 2.0

Compared with lean adolescents, obese adolescents showed lower HDL-C and increased TC, TG, LDL-C, hs-CRP, fasting insulin, HOMA-IR, TNF-α, IL-6, systolic blood pressure (SBP), and diastolic blood pressure (DBP). Adiponectin, however, was reduced among obese adolescents (Table 2). Plasma concentrations of adiponectin were significantly inversely correlated with TC, LDL-C, BMI, and WC and positively correlated with HDL-C. TNF-α was positively correlated with BMI, body fat, WC, hs-CRP, and IL-6 (Table 3). On the other hand, IL-6 was positively correlated only with hs-CRP and TNF-α.

Table 3. . Correlation between adiposity and fasting insulin, HOMA-IR, hs-CRP, adiponectin, IL-6, and TNF-a
 BMI (kg/m2)Fat mass (%)WC (cm)
  • HOMA-IR, homeostasis model assessment of insulin resistance; IL, interleukin; TNF, tumor necrosis factor; WC, waist circumference; hs-CRP, high-sensitivity C-reactive protein.

  • *

    p < 0.5.

  • p < 0.01.

Fasting insulin0.6620.6440.699
HOMA-IR0.4160.5300.443*
hs-CRP0.381*0.4480.370*
Adiponectin−0.299−0.226−0.318*
IL-60.5280.4270.472
TNF-α0.4800.402*0.388*

Intervention Study

OEG participated in supervised group jump rope exercise for 6 weeks (40 min/d, 5 d/wk). Six-week exercise training decreased WC, hip circumference, body weight, BMI, fat mass, and percent body fat significantly (Table 4). Consistent with decreased adiposity after training, TG, HOMA-IR, and fasting insulin levels decreased with 6 weeks of training. However, fasting glucose, TC, HDL-C, LDL-C, and hs-CRP were not changed after training. Plasma adiponectin levels were also increased significantly after exercise training; however, TNF-α and IL-6 did not change with exercise training (Table 5).

Table 4. . Body composition before and after training
 OEG (n = 14)OCG (n = 12)LCG (n = 14)
 BeforeAfterBeforeAfterAfter
  • SBP, systolic blood pressure; DBP, diastolic blood pressure; OEG, obese exercise group; OCG, obese control group; LCG, lean control group.

  • *

    p < 0.05 compared with pre-training levels among OEG.

  • p < 0.01 compared with pre-training levels among OEG.

  • p < 0.01 compared with pre-training levels among OCG.

Height (cm)173.9 ± 1.8174.5 ± 1.8174.9 ± 2.0175.6 ± 2.0173.5 ± 0.8
Weight (kg)89.7 ± 2.487.5 ± 2.590.4 ± 3.390.4 ± 3.664.7 ± 0.8
BMI (kg/m2)29.6 ± 0.628.6 ± 0.629.4 ± 0.729.1 ± 0.721.5 ± 0.2
Waist (cm)92.1 ± 2.289.6 ± 2.0*93.0 ± 2.491.2 ± 1.271.2 ± 0.9
Hip (cm)105.3 ± 1.3101.5 ± 1.6103.7 ± 1.9102.0 ± 2.8690.3 ± 2.9
Fat (%)31.5 ± 1.029.3 ± 1.030.8 ± 1.429.3 ± 1.919.5 ± 0.6
Fat mass (kg)28.1 ± 1.525.7 ± 1.428.1 ± 1.926.7 ± 2.412.5 ± 0.4
SBP (mm Hg)123.6 ± 2.0122.9 ± 1.9129.2 ± 2.9124.2 ± 3.1114.3 ± 2.0
DBP (mm Hg)79.3 ± 2.081.4 ± 2.985.0 ± 2.680.8 ± 3.174.3 ± 2.0
Heart rate (bpm)75.1 ± 2.070.4 ± 2.176.3 ± 1.976.2 ± 2.479.6 ± 1.8
Table 5. . Insulin resistance, lipid profile, and adipokine before and after training
 OEG (n = 14)OCG (n = 12)LCG (n = 14) After
 BeforeAfterBeforeAfter 
  • OEG, obese exercise group; OCG, obese control group; LCG, lean control group; TC, total cholesterol; TG, triglyceride; HDL-C, high-density lipoprotein-cholesterol; LDL-C, low-density lipoprotein-cholesterol; hs-CRP, high-sensitivity C-reactive protein; HOMA-IR, homeostasis model assessment of insulin resistance; TNF, tumor necrosis factor; IL, interleukin. Values are mean ± standard error.

  • *

    p < 0.05 compared with pre-training levels among OEG.

  • p < 0.01 compared with pre-training levels among OEG.

Fasting glucose (mg/dL)82.3 ± 1.985.0 ± 1.686.8 ± 1.285.1 ± 1.993.9 ± 2.0
TC (mg/dL)159.5 ± 6.8155.5 ± 7.1187.8 ± 10.1179.0 ± 10.1152.9 ± 5.1
TG (mg/dL)102.4 ± 17.168.8 ± 9.0*118.3 ± 18.0299.2 ± 14.664.1 ± 5.6
HDL-C (mg/dL)43.8 ± 1.643.5 ± 1.445.2 ± 2.044.6 ± 1.449.9 ± 2.5
LDL-C (mg/dL)95.2 ± 6.698.2 ± 7.6119.0 ± 9.2114.6 ± 9.590.2 ± 4.5
hs-CRP (mg/mL)0.17 ± 0.050.10 ± 0.060.09 ± 0.070.21 ± 0.070.04 ± 0.08
Fasting insulin (µU/mL)13.0 ± 1.68.9 ± 1.3313.6 ± 0.910.8 ± 1.35.8 ± 0.4
HOMA-IR2.47 ± 0.31.64 ± 0.232.85 ± 0.192.33 ± 0.291.35 ± 0.12
Adiponectin (µg/mL)8.1 ± 0.78.9 ± 0.8*6.6 ± 0.87.0 ± 1.09.0 ± 0.6
TNF-α (pg/mL)1.75 ± 0.151.93 ±.0.161.68 ± 0.11.76 ± 0.11.2 ± 0.1
IL-6 (pg/mL)0.67 ± 0.10.72 ± 0.230.53 ± 0.050.87 ± 0.330.37 ± 0.1

Discussion

  1. Top of page
  2. Abstract
  3. Introduction
  4. Research Methods and Procedures
  5. Results
  6. Discussion
  7. Acknowledgments
  8. References

In the current study, we first measured body weight, fat mass, BMI, fasting glucose, fasting insulin, HOMA-IR, and adipocytokine levels in lean and obese male high school students in Korea. As expected, surrogate markers of insulin resistance, HOMA-IR, and fasting insulin levels were increased in obese adolescents. In addition, we observed elevated plasma TNF-α and CRP levels and reduced plasma adiponectin levels in obese adolescents. However, we did not observe increased IL-6 levels in obese adolescents compared with lean controls. Increased TNF-α and hs-CRP and reduced adiponectin levels among adolescents have been previously reported among white male and female adolescents but not yet among Asian male adolescents.

Plasma adiponectin levels are known to be associated with insulin sensitivity and the risk of developing type 2 diabetes (29, 31). The lower levels of plasma adiponectin are known to be a risk factor for insulin resistance, and the administration and overexpression of adiponectin reverse insulin resistance and reduce intramuscular TGs (32, 33). Therefore, we measured the relationship among adiponectin, HOMA-IR, fasting insulin levels, and other inflammatory markers known to affect insulin resistance. As expected, an inverse correlation between adiponectin and HOMA-IR and fasting insulin levels was observed; however, it did not reach statistical significance (p = 0.052 and 0.061, respectively). However, a previous report based on a large population showed a positive relationship between adiponectin levels and insulin resistance (34). Thus, the failure to obtain statistical significance in the relationship between adiponectin and insulin resistance may have been due to the rather small sample size in the current study.

In our study, plasma adiponectin levels were correlated with TC, HDL-C, and LDL-C. Balagopal et al. (35) also reported, in a study of U.S. adolescents, that adiponectin levels are correlated with the ratio of LDL to HDL, a measure of atherogenic potential. The strong relationship between plasma adiponectin levels and lipid metabolism has been previously reported (36, 37). Recent findings suggest that adiponectin levels predict HDL-C, partly independently of visceral adiposity, intra-abdominal fat, BMI, and insulin sensitivity in adults (37, 38). The current study also confirmed the previous findings in adults. Therefore, the lower concentration of adiponectin in the obese adolescents compared with that of lean controls may contribute to a worsening of the lipoprotein characteristics of obese adolescents.

Effects of Exercise Training on Adiposity, Insulin Resistance, and Adipocytokines

We found that 6 weeks of jump rope exercise training decreased WC, body weight, BMI, fat mass, and percent body fat significantly. Consistent with reduction in adiposity after training, TG, HOMA-IR, and fasting insulin levels were decreased with 6 weeks of exercise training. However, fasting glucose, TC, HDL-C, LDL-C, and hs-CRP were not changed after training.

Previous studies examining the effects of exercise training on adiponectin levels have reported conflicting results. Some have reported increased (35, 39, 40, 41) and others have reported no changes in adiponectin levels after exercise training (42, 43, 44, 45). Most studies that reported increased adiponectin levels after exercise training also observed significant weight loss (39, 40, 46, 47). Esposito et al. (47) observed a 48% increase in adiponectin levels after 2 years of a combined low-energy Mediterranean diet and increased physical activity. A recent study also reported increased adiponectin levels in subject groups with normal glucose tolerance, impaired glucose tolerance, and type 2 diabetes after only 4 weeks of aerobic exercise intervention, which induced 2.0%, 3.7%, and 1.7% weight reduction, respectively (40). In addition, one of the recent studies by Balagopal et al. (35) showed that 3 months of aerobic exercise increased plasma adiponectin levels from 4.44 ± 0.47 to 5.95 ± 0.49 µg/mL, with a significant reduction in body fat mass without changes in body weight. On the other hand, Yokoyama et al. (43) reported no changes in adiponectin levels after 3 weeks of combined intervention of diet and exercise, which induced slight weight loss among 40 patients with type 2 diabetes. In addition, Hulver et al. (44) also reported no changes in adiponectin levels despite significant increased insulin action and no changes in body weight or fat mass. From these previous studies, we can speculate that weight loss, more specifically body fat loss, is necessary for the exercise training effects on adiponectin to be revealed.

The results of the current study showed a 10% increase in plasma adiponectin levels among subjects who underwent 6 weeks of exercise training, with concurrent reduction in body weight, WC, fat mass, TG, fasting insulin, and HOMA-IR. These results are consistent with two other recent studies that reported increased adiponectin levels after exercise training among adolescents (35, 39). In contrast to conflicting results on adiponectin levels after exercise training among adults and the elderly, studies that have examined the effects of exercise training on adiponectin levels among adolescents have consistently reported increased adiponectin levels after exercise training (35, 39). These results may suggest that adolescents have higher metabolic flexibility for adiponectin production and secretion in response to weight loss and exercise.

Interestingly, the current study did not observe any changes in TNF-α, IL-6, and hs-CRP levels after exercise training. Baseline measurements showed significantly increased TNF-α, IL-6, and hs-CRP levels and decreased adiponectin levels compared with lean controls. Exercise training for 6 weeks was able to increase adiponectin levels by 10%; however, it failed to reverse obesity-induced increases in TNF-α, IL-6, and hs-CRP. These results do not agree with a previous study that demonstrated reduction in TNF-α with increased adiponectin levels after 7 months of aerobic exercise (39). Also, Esposito et al. (47) demonstrated significantly increased adiponectin levels and significantly reduced hs-CRP and IL-6 levels after 2 years of low-energy Mediterranean diet and increased physical activity. Based on these results, we may speculate that the regulation of adiponectin levels precedes the regulation of other inflammatory markers such as IL-6, TNF-α, and hs-CRP.

The current study showed concurrent improvement in adiponectin levels and insulin resistance measured by HOMA-IR and fasting insulin levels. However, there are a few studies that did not observe an increase in adiponectin levels with significant improvement in insulin resistance (42, 43, 44). These results suggest that changes in adiponectin levels during/after exercise training are not necessary for improvement in exercise-associated improvement in insulin sensitivity. Excess fat accumulation causes insulin resistance by two different main pathways, including adipocyte-derived cytokine (20) and lipotoxicity-related altered insulin signaling (48, 49). Therefore, we can speculate that short-term exercise training-associated improvement in insulin sensitivity may be due to changes in peripheral insulin sensitivity by adenosine monophosphate-activated protein kinase and/or other insulin signaling pathways (50, 51). However, long-term exercise training that reduces the levels of fat accumulation may also cause further changes in adipokine levels and result in further improvement in insulin sensitivity.

In summary, the current study demonstrated that insulin resistance, TC, LDL-C levels, TG, and inflammatory markers were increased and adiponectin and HDL-C were reduced among Korean obese male adolescents. Six weeks of increased physical activity improved body composition, insulin sensitivity, and adiponectin levels in obese male Korean adolescents without changes in TNF-α, IL-6, and hs-CRP. Our results suggest that overweight and obese adolescents should be encouraged to increase their physical activity levels to prevent early development of chronic diseases related to obesity.

Acknowledgments

  1. Top of page
  2. Abstract
  3. Introduction
  4. Research Methods and Procedures
  5. Results
  6. Discussion
  7. Acknowledgments
  8. References

The authors gratefully acknowledge the assistance of Dongwon High School (Su-won, Korea). This work was supported, in part, by the Yonsei University Research Fund of 2005, the Korean Research Foundation (Grant KRF-2006-8-0900), and the Korea Science and Engineering Foundation (Grant R01-2006-000-11333-0).

Footnotes
  • 1

    Nonstandard abbreviations: TNF, tumor necrosis factor; IL, interleukin; WC, waist circumference; OEG, obese exercise group; OCG, obese control group; LCG, lean control group; TG, triglyceride; TC, total cholesterol; LDL-C, low-density lipoprotein-cholesterol; HDL-C, high-density lipoprotein-cholesterol; hs-CRP, high-sensitivity C-reactive protein; HOMA-IR, homeostasis model assessment of insulin resistance; SBP, systolic blood pressure; DBP, diastolic blood pressure.

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  4. Research Methods and Procedures
  5. Results
  6. Discussion
  7. Acknowledgments
  8. References
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