Medical and Dental Consultantsí Association of Nigeria
Home - About us - Editorial board - Search - Ahead of print - Current issue - Archives - Submit article - Instructions - Subscribe - Advertise - Contacts - Login 
  Users Online: 259   Home Print this page Email this page Small font sizeDefault font sizeIncrease font size
 

  Table of Contents 
ORIGINAL ARTICLE
Year : 2020  |  Volume : 23  |  Issue : 4  |  Page : 481-488

Determination of the relationship between total antioxidant capacity and dietary antioxidant intake in obese patients


1 Yaşam Pınarım Nutrition and Dietary Counseling Center, Specialist Dietetician, Kayseri, Turkey
2 Nutrition and Dietetic Department, Erciyes University Health Science Faculty, Kayseri, Turkey

Date of Submission16-Apr-2019
Date of Acceptance07-Dec-2019
Date of Web Publication4-Apr-2020

Correspondence Address:
Dr. S Çalapkorur
Erciyes University Health Science Faculty, Kayseri
Turkey
Login to access the Email id

Source of Support: None, Conflict of Interest: None


DOI: 10.4103/njcp.njcp_212_19

Rights and Permissions
   Abstract 


Background: Adipokines secreted from adipose tissue in obese individuals increase oxidative stress in the body and sufficient antioxidant consumption is recommended to reduce the effects of this stress. Consumption of foods rich in antioxidants is thought to be related to serum total antioxidant capacity (TAC) but the effect of dietary antioxidant amount on serum antioxidant capacity is not yet clear. Objective: The aim of this study was to investigate the relationship between dietary antioxidant intake and serum TAC in obese and normal-weight individuals. Methods: Around 36 obese and 24 normal weighted volunteers participated in this study. Demographic characteristics, anthropometric measurements, and antioxidant food consumption from frequency questionnaires (questionnaire TAC) of individuals were recorded. The amount of antioxidant intake from diet (dietary TAC) was calculated from food consumption records. Serum TAC values were measured calorimetrically according to the Trolox equivalent antioxidant capacity (TEAC). Results: The dietary TAC levels of the experimental group were higher than the control group (5.45 ± 6.15 mmol/day vs. 3.20 ± 7.27 mmol/day, P = 0.006); whereas, the ratio of serum TAC per body weight was significantly lower in obese participants (0.013 ± 0.0134 mmol/L vs. 0.017 ± 0.003 mmol/L, P< 0.001). However, a positive relation (r = 0.339, P = 0.008) was observed between dietary TAC and serum TAC. Moreover, a positive correlation between the serum TAC levels of the individuals and the weight in both groups (r = 0.335, P = 0.046 in obese participants, and r = 0.523, P = 0.009 in control group), and the BMI in the experimental group (r = 0.384, P = 0.021). Likewise, there is an association between the diet TAC level and the diet protein ratio (r = 0.478, P = 0.018) in obese participants.Conclusıon: Dietary TAC intake was significantly higher and the TAC/weight lower in the experimental group. Moreover, the relationship between diet TAC and serum TAC was significant.

Keywords: Antioxidant, nutrition, obesity, total antioxidant capacity


How to cite this article:
Besagil P S, Çalapkorur S, Şahin H. Determination of the relationship between total antioxidant capacity and dietary antioxidant intake in obese patients. Niger J Clin Pract 2020;23:481-8

How to cite this URL:
Besagil P S, Çalapkorur S, Şahin H. Determination of the relationship between total antioxidant capacity and dietary antioxidant intake in obese patients. Niger J Clin Pract [serial online] 2020 [cited 2020 Sep 28];23:481-8. Available from: http://www.njcponline.com/text.asp?2020/23/4/481/281915




   Introduction Top


A major release of adipokines depending upon the increased adipose tissue mass occurs in obesity. These adipokines releasing from adipose tissue have been shown to induce chronic inflammation and signals that lead to increased oxidative stress in the body.[1],[2] In addition to increased adipokine release; hyperglycemia, hyperleptinemia, insufficient antioxidant defense, and increased reactive oxygen species (ROS) are among the factors that increase oxidative stress in obesity.[1],[3] Obesity is also defined as ” increased chronic oxidative stress state” and the increased oxidative stress in the body damages large biomolecules such as proteins, DNA, and lipids.[4],[5]

Antioxidant molecules play an important role in preventing the oxidative stress created by the free radicals thereby minimizing its effects. These molecules eliminate the damage caused by oxidants by intracellular and extracellular defenses.[6],[7],[8]

Many antioxidant enzyme level measurements are used to measure oxidative stress-related tissue damage and antioxidant defense. At present, total antioxidant capacity (TAC) measurement developed in 1993 by Miller et al.,[9] is widely applied using different techniques. The main advantage of this method is that total antioxidants in a biological sample can be measured by methods as Trolox equivalent antioxidant capacity (TEAC), oxygen radical absorbance capacity (ORAC), and ferric reducing antioxidant power capacity (FRAP).[10]

Plasma and serum TAC concentration has been shown to be associated with antioxidant-rich vegetable and fruit consumption, thus the importance of consuming sufficient amount of antioxidants in the diet has been emphasized. Vegetable foods such as whole grains, fruits, and vegetables containing vitamins, minerals, and polyphenols such as A, C, E vitamins, β carotene, lycopene, and Se reduce the risk of chronic illness by protecting the cells from oxidative stresses. However, there is limited information on the relationship between individual endogenous and exogenous components and the amount of dietary TAC and the serum/ plasma TAC level.[7],[8]

This study was planned and conducted to investigate the relationship between dietary antioxidant intake and serum TAC levels in obese regarding normal-weight individuals.


   Materials and Method Top


Study design

A descriptive and observational study was conducted in a private hospital in Kayseri province between March-August 2013. The sample of the study consisted of 36 obese (experimental group) and 24 normal weight (control group) individuals who applied to the Nutrition and Dietary or Internal Medicine Outpatient Clinic of Kayseri Private Sevgi Hospital. Individuals with BMI >30 kg/m2, over 18 years of age, nonsmokers, not using vitamin-mineral or nutritional supplements, and without diabetes or kidney disease were selected in the experimental group. In the control group; healthy individuals who did not use cigarettes, alcohol, vitamin supplements, and who were within the normal BMI limits (20–27 kg/m2) according to their age were included. The study and control groups were similar in terms of age, gender, and sociodemographic characteristics. Both groups did not follow any diet plan prepared specifically during the study and maintained their current eating habits.

At the beginning of the study, participants were informed about the study in accordance with the Helsinki Declaration and volunteers were asked to sign the informed consent form. Furthermore, approval was obtained from the Medical Faculty Ethics Committee of Erciyes University (Decision No: 2012/569).

Dietary data

The food consumption records were recorded retrospectively by four telephone calls in 1 month to the participants including two calls on the weekdays and two on weekends. Data on daily energy, nutrients and antioxidant intake, 24-hour nutrient intake, and antioxidant nutrient consumption frequency of the individuals were analyzed in the BeBiS (Nutrition Information Systems, İstanbul, Turkey) program. Dietary TAC values were calculated through these data.

In addition, the antioxidant food consumption questionnaire was applied to patients. This questionnaire was conducted by Satia et al.[8] and was developed from a 92-item questionnaire. The questionnaire TAK value was calculated using these data.

For the calculation of total antioxidant contents of foods, TAC values of 3100 foods were entered into the BeBiS program as a new database using the results of the study by Carlsen et al.[11] since there were no database in Turkey and in the BeBiS program and dietary and questionnaire, TAC values were calculated through these data.

Anthropometric measurements

Demographic information and anthropometric measurements of the individuals participating in the study were obtained by conducting face-to-face interviews with the individuals; whereas, the food consumption records were questioned and obtained by telephone and they were recorded in the questionnaire.

The body weight and height measurements were carried out using an automatic height scale (SECA 769, Germany); and without shoes, with light clothes, while standing straight, looking across, in such a way that the highest point of the ears and the lower margin of orbit of the eye were in a line parallel to the plane (Frankfort plane). Body mass index (BMI) was calculated by dividing weight (in kg) into the height squared (in m). The body analysis was performed using the Tanita BC 418 device. While performing the body analysis measurement, attention was paid on factors such as the patients were fasting for at least 4 h, they were rested, they did not use any medication, which speeds up the metabolism, before the measurement, and there were no metal objects on them during the measurement.

Blood collection and assessment of total antioxidant capacity

A blood sample of 10 mL was drawn *using red cap gel tubes **(BD vacutainer serum tubes, 10 ml) from venous vessels of each participant after at least 12-hours fasting to obtain the serum. Each gel tube was centrifuged for 15 min in 2500 × g within a maximum of 20 min and separated into Eppendorf tubes. Eppendorf tubes were put in a deep freezer of -24°C within a maximum of 30 min after the samples were taken and they were kept there for up to 6 months -80°C until they were analyzed. The samples were transported by the cold chain method to a laboratory to be analyzed.

Serum TAC was measured by Biotek Synergy™ HT Multi-Detection Microplate Reader Model (Winooski, Vermont, USA) and TAC assay kit (Rel Assay Diagnostics®, Gaziantep, Turkey) through a colorimetric method. In this method, 2.2×- azino-bis (3-ethylbenzothiazoline -6- sulfonic acid) radical (ABTS radical) was used. It is based on the principle that the blue-green color formed by ABTS + radical is reduced by antioxidants in the sample added in the medium. ABTS is incubated with methemoglobin (HX-Fe+) and H2O2 which is a peroxidase to form ABTS + radical. The resultant ferrylmyoglobin reacts with ABTS to form ABTS + radical. The ABTS + radical is partially stable and has a blue-green color. The color formation is inhibited by the ratio of antioxidants in the added sample. This color change is measured at a wavelength of 660 nm. Trolox, a vitamin E analog, was used as a standard in the calculation of TAC, which was expressed as mmol Trolox equivalent/L.[12]

TAC/kg was calculated by dividing the serum TAC level by body weight.

Statistical analysis

The data obtained from the study were evaluated in the SPSS 21 statistical package program. Categorical variables were given as a number (n) and percentage (%); whereas, mean, standard deviation (X ± S), median were given as 25th and 75th percentile (Q1-Q3) for numerical variables. Shapiro Wilk test was used to determine whether or not the numerical variables were normally distributed. While the t-test was used in the evaluation of normally distributed data, the Mann Whitney U test was used in data showing not a normal distribution. Chi-square test was used to determine the differences between the groups by giving the number-percentage tables and distribution of the counted data; on the other hand, Fisher's Exact Chi-Square test was used in the 2 × 2 patterns for those that Chi-square test cannot be applied. Spearman correlation analysis was applied to compare numerical variables with another one. The value of P < 0.05 was accepted as statistically significant. Analysis of variance was performed to compare the means between the groups.


   Results Top


It was found that 76.7% of the individuals in the experimental group were female and 23.3% were male. While the age range varied between 20–69 years, 46.7% of the participants were in the age group of 40–59 years. While the average age of the experimental group was 44.9 ± 13.6 years, the average age of the control group was 41.9 ± 12.7 years (P = 0.346). [Table 1] shows the mean anthropometric measurements of the individuals according to gender.
Table 1: Anthropometric characteristics of the volunteers

Click here to view


[Table 2] shows the energy and nutrient intake levels of the individuals. Mean cholesterol and niacin intake of the experimental group (197.5 ± 510.04 and 12.30 ± 22.20 mg/day, respectively) were found to be significantly lower than the control group (307.6 ± 92.5 and 17.40 ± 17.50 mg/day, respectively) (P < 0.05).
Table 2: Energy and nutrient intake levels of individuals

Click here to view


[Table 3] shows the means of serum TAC, dietary TAC, and questionnaire TAC. The mean of questionnaire TAC values was higher in the control group (13.68 ± 4.91 mmol/day) than the experimental group (12.41 ± 5.14 mmol/day). Median dietary TAC values were higher in the experimental group than the control group (P = 0.006); whereas, the ratio of serum TAC per weight was significantly lower (P < 0.001).
Table 3: Total antioxidant capacity average of individuals from serum, dietary, and consumption survey questionnaires

Click here to view


Serum TAC had a positive correlation with dietary TAC (r = 0.339, P = 0.008) in both groups. No significant correlation was found between the questionnaire TAC and the other parameters (P > 0.05) [Table 4].
Table 4: Correlation of total antioxidant capacity values with each other

Click here to view


A significant positive correlation was found between the serum TAC levels and weight and BMI and between dietary TAC level and protein ratio is taken with diet among the individuals in the experimental group. Serum TAC levels had a significant positive correlation with height, weight, and muscle tissue amount among the individuals in the control group. Those showing a positive correlation with dietary TAC levels were the amount of body water and protein, fiber, thiamin, riboflavin, iron, zinc, and magnesium from the diet (P < 0.05) [Table 5].
Table 5: Relationship between serum and dietary TAC levels with various parameters

Click here to view


In all individuals, a significant positive correlation was determined between the serum TAC value and weight, muscle tissue, TAC/weight, dietary TAC value (P < 0.05, data not shown in the table).


   Discussion Top


Although the relationship between increased oxidative stress and development of disease and complication in obesity has been revealed in numerous studies,[1],[13],[14],[15],[16],[17] there are limited studies investigating the relationship between the dietary antioxidant levels and serum TAC levels of the obese individuals.[8],[18],[19],[20],[21],[22],[23] In addition, it was observed in these studies that the results between BMI and oxidant and antioxidant levels were contradictories.[24],[25],[26],[27]

In a study investigating serum TAC in obese and normal-weight subjects, 87 healthy individuals were evaluated while the highest serum TAC level was found in the normal weight group, the lowest TAC level was observed in the obese group. On the other hand, total oxidant status (TOS) was found to be higher in overweight individuals than the normal weight or slightly overweight individuals.[24] In a study conducted with 106 (54 obese, 52 control) healthy children aged between 6–12 years, superoxide dismutase (SOD) enzyme activity was observed to be significantly higher in obese children compared to normal-weight children. This was associated with an increase in SOD activity as cell adaptation against an increase in radical production. Researchers also stated that these differences may be related to the developmental period of obesity, antioxidants will be stimulated among individuals in the developmental stage but antioxidant levels may decrease in the long term.[25] Unlike this study, in the study by Vehapoglu et al.,[26] it was observed that antioxidant capacity decreased in obese children and it was stated that this decrease may increase the vascular damage in the long term. In another study, it was reported that the antioxidant activity increased with the weight loss in obese individuals and this was associated with the dietary TAC level.[27]

In the present study, dietary TAC level in the experimental group was higher than the control group [P = 0.006, [Table 3]. This difference is thought to be due to the fact that the individuals in the experimental group were generally selected from those who applied to the dietary outpatient clinic for weight loss [Table 2]. Individuals did not follow any diet program during the study but the fact that the obese individuals in the experimental group often participated in a weight loss program previously and received nutrition training may have led them to consume healthier foods. In fact, it has been seen that these patients who previously received a weight loss diet consumed more vegetables, fruits, oilseeds, whole grains, or wholemeal bread in their 4-day food consumption compared to the control group (data which were not in the results). In addition, there was no difference between the groups in mean serum TAC levels. It may also be considered that the antioxidant levels may increase for defense purposes as a response to the increased oxidative stress in obesity.[1],[2] What is important is that TAC/kg values were found to be lower in obese subjects compared to normal-weight subjects. In the literature, no other study calculating serum TAC/kg was found.

The previous studies revealed a parallel relationship between the consumption of foods containing strong dietary antioxidant compounds, receiving support, and TAC intake and plasma TAC.[22],[28],[29] A significant correlation was found in a study between dietary TAC and serum C vitamin equivalent TAC, FRAP, plasma-erythrocyte GPx, alpha-tocopherol, and lutein. As a result, it was concluded that plasma antioxidant status can be estimated by knowing the amount of dietary TAC.[22] It was observed in another study that as the consumption of foods containing flavonoids increased, serum TAC increased.[30] One of the results of another study was that dyslipidemia reduced and TAC increased with anthocyanin-rich diet in diabetic patients.[31] Because TAC measurements in the diet were examined in vitro, the bioavailability of these antioxidants in the oral and gastrointestinal system, their absorption level, or the interactions of nutrients with each other are unknown. Therefore, calculations were performed considering the amounts remaining without being metabolized.[32]

When the factors affecting serum TAC were examined, serum TAC had a significant positive correlation with TAC/weight, dietary TAC, body weight and muscle weight in all individuals in the study. In a study conducted with patients with coronary heart disease, body fat percentage, waist circumference, BMI, serum TG level, and plasma TAC concentrations of cardiac patients were found to be higher than healthy individuals.[33] It was found in another study that while there was a positive correlation between the serum TAC and waist/hip ratio and the muscle percentage, there was a negative correlation between the blood pressure, basal metabolic rate, BMI, waist circumference, hip circumference, body total fat percentage, and visceral and subcutaneous fat percentage.[34] In a study investigating the obesity-related factors and serum TAC levels, serum TAC level was determined to show a positive correlation with BMI. In addition, it was reported that as the serum TAC value decreased, the number of obesity-related factors increased. There was a positive correlation between the TAC and obesity-related factors and it was suggested that an increase in TAC levels can show a healthier state.[35]

Several mechanisms to increase oxidative stress associated with obesity have been suggested.[1],[3],[36] Progressive and cumulative cell injury caused by pressure associated with large body mass leads to the release of various cytokines, primarily TNF-α and this causes the formation of ROS in the tissues. The second suggested mechanism is that obesity increases the metabolic and mechanical workload of the myocardium. As a negative outcome of increased myocardial oxygen consumption; mitochondrial respiration increases which can result in the formation of ROS products.[3] One of the other possible mechanisms is directly related to the diet. Nutritional obesity is one of the most common causes of obesity and an excessive amount of free fatty acid intake in excess of the antioxidant capacity of the diet causes lipid peroxidation and induces oxidative stress.[1] In addition to these mechanisms, the molecular properties of fat tissue are considered one of the most important causes of obesity-related oxidative stress.[13]

Further studies to get a better understanding of the dietary antioxidant intake and its effect on serum TAC levels in obese and normal-weight individuals should be carried out.


   Conclusion Top


No significant difference was found between the serum TAC levels of obese and normal-weight individuals. This may be due to other factors such as obesity grade, duration of obesity, nutrition consumption style, and current diet.

Supporting obesity, which is known to increase oxidative stress, with healthy dietary habits and physical activity, and preferring the foods with high antioxidant content in obesity management is of great importance for the prevention of health problems caused by obesity.

A considered number of subjects included in this study (n = 60) and the limited number of works evaluating the relationship between dietary and serum TAC in Turkey are among the strengths of the study. Calculation of the serum TAC level/kg was also a powerful aspect of the study.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form, the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

This study was supported by Erciyes University Scientific Research Projects Unit with project code TYL-2013-4428.

Conflicts of interest

There are no conflicts of interest.



 
   References Top

1.
Furukawa S, Fujita T, Shimabukuro M, Iwaki M, Yamada Y, Nakajima Y, et al. Increased oxidative stress in obesity and its impact on metabolic syndrome. J Clin Invest 2004;114:1752-61.  Back to cited text no. 1
    
2.
Marseglia L, Manti S, D'Angelo G, Nicotera A, Parisi E, DiRosa G, et al. Oxidative stress in obesity: A critical component in human diseases. Int J Mol Sci 2015;16:378-400.  Back to cited text no. 2
    
3.
Khan NI, Naz L, Yasmeen G. Obesity: An independent risk factor for systemic oxidative stress. Pak J Pharm Sci 2006;19:62-9.  Back to cited text no. 3
    
4.
Rani V, Deepb G, Singh RK, Palle K, Yadav UCS. Oxidative stress and metabolic disorders: Pathogenesis and therapeutic strategies. Life Sci 2016;148:183-3.  Back to cited text no. 4
    
5.
Brighenti F, Valtuena S, Pelrgrini N, Ardigò D, Del Rio D, Salvatore S, et al. Total antioxidant capacity of the diet is inversely and independently related to plasma concentration of high-sensitivity C-reactive protein in adult Italian subjects. Br J Nutr 2005;93:619-25.  Back to cited text no. 5
    
6.
Espinosa-Diez C, Miguel V, Mennerich D, Kietzmann T, Sánchez-Pérez P, Cadenas S, et al. Antioxidant responses and cellular adjustments to oxidative stress. Redox Biology 2015;6:183-97.  Back to cited text no. 6
    
7.
Pitsavos C, Panagiotakos DB, Tzima N, Chrysohoou C, Economou M, Zampelas A, et al. Adherence to the Mediterranean diet is associated with total antioxidant capacity in healthy adults: The ATTICA study. Am J Clin Nutr 2005;82:694-9.  Back to cited text no. 7
    
8.
Satia JA, Watters JL, Galanko JA. Validation of an antioxidant nutrient questioniare in Whites and African Americans. J Am Diet Assoc 2009;109:502-8.  Back to cited text no. 8
    
9.
Miller NJ, Rice-Evans C, Davies MJ, Gopinathan V, Milner A. A novel method for measuring antioxidant capacity and its application to monitoring the antioxidant status in premature neonates. Clin Sci 1993;84:407-12.  Back to cited text no. 9
    
10.
Sies H. Total antioxidant capacity: Apprasial of a concept. J Nutr 2007;137:1493-5.  Back to cited text no. 10
    
11.
Carlsen HM, Halvorsen B, Holte K, Bøhn SK, Dragland S, Sampson L, et al. The total antioxidant content of more than 3100 foods, beverages, spices, herbs and supplements used worldwide. Nutr J 2010;9:1-11.  Back to cited text no. 11
    
12.
Erel O. A novel automated direct measurement method for total antioxidant capacity using a new generation, more stable ABTS radical cation. Clin Biochem 2004;37:277-85.  Back to cited text no. 12
    
13.
Rodrigo R, Part H, Passalacqua W, Araya J, Guichard C, Bächler JP. Relationship between oxidative stress and essential hypertension. Hypertens Res 2007;30:1159-66.  Back to cited text no. 13
    
14.
Brown LA, Kerr CJ, Whiting P, Finer N, McEneny J, Ashton T. Oxidant sress in healthy normal- weight, overweight and obese individuals. Obesity (Silver Spring) 2009;17:460-6.  Back to cited text no. 14
    
15.
Codoner-Franch P, Boix-Garcia L, Simo-Jorda R, Del Castillo-Villaescusa C, Maset-Maldonado J, Valls-Bellés V. Is obesity associated with oxidative stress in children?. Int J Pediatr Obes 2010;5:56.  Back to cited text no. 15
    
16.
Vincent HK, Powers SK, Stewart DJ, Shanely RA, Demirel H, Naito H. Obesity is associated with increased myocardial oxidative stress. Int J Obes 1999;23:67-74.  Back to cited text no. 16
    
17.
Vincent HK, Powers SK, Dirks AJ, Scarpace PJ. Mechanism for obesity-induced increase in myocardial lipid peroxidation. Int J Obes 2001;25:378-88.  Back to cited text no. 17
    
18.
Lopes FH, Martin LK, Nashar K, Morrow JD, Goodfriend TL, Egan BM. DASH diet lowers blood pressure and lipid induced oxidative stress in obesity. J Am Coll Cardiol 2003;41:422-30.  Back to cited text no. 18
    
19.
Özata M, Yılmaz MI, Mergen M, Öktenli Ç, Aydın A. Erkek obezitesinde bozulmuş antioksidan kapasite ve hipoçinkonemi. Turkish J Endocrin Metabolism 2003;2:47-51.  Back to cited text no. 19
    
20.
Codoner-Franch P, Alberola BA, Camarasa JVD, Escribano Moya MC, Valls Bellés V. İnfluence of dietary lipids on erythrocyte antioxidant status of hypercholesterolaemic children. Eur J Pediatr 2009;168:3217.  Back to cited text no. 20
    
21.
Lotito SB, Frei B. Consumption of flavonoid-rich foods and increased plasma antioxidant capacity in humans: Cause, consequence, or epiphenomenon? Free Radic Biol Med 2006;41:1727-46.  Back to cited text no. 21
    
22.
Wang Y, Yang M, Lee SG, Davis CG, Koo SI, Chun OK. Dietary total antioxidant capacity is associated with diet and plasma antioxidant status in healty young adults. J Acad Nutr Diet 2012;112:1625-35.  Back to cited text no. 22
    
23.
Wang Y, Yang M, Lee SG, Davis CG, Kenny A, Koo SI, et al. Plasma total antioxidant capacity is associated with dietary intake and plasma level of antioxidants in postmenopausal women. J Nutr Biochem 2012;23:1725-31.  Back to cited text no. 23
    
24.
Söylemez N, Demirbaǧ R, Sezen Y, Yıldız A, Akpınar O. Vücut kütle indeksine göre leptin ve adiponektin seviyeleri ve bunların oksidatif parametrelerle ilişkisi. Anadolu Kardiyol Derg 2010;10:391-6.  Back to cited text no. 24
    
25.
Sfar S, Boussoffara R, Sfar TM, Kerkeni A. Antioxidant enzymes activities in obese Tunisian children. Nutr J 2013;12:1-7.  Back to cited text no. 25
    
26.
Vehapoglu A, Turkmen S, Goknar N, Özer ÖF. Reduced antioxidant capacity and increased subclinical inflammation markers in prepubescent obese children and their relationship with nutritional markers and metabolic parameters. Redox Report 2016;21:271-80.  Back to cited text no. 26
    
27.
Garcia-Lacarte M, Milagro FI, Zulet MA, Martinez JA, Mansego ML. LINE-1 methylation levels, a biomarker of weight loss in obese subjects, are influenced by dietary antioxidant capacity. Redox Rep 2016;21:67-74.  Back to cited text no. 27
    
28.
Puchau B, Zulet A, Echavarri GA, Hermsdorff HH, Martínez JA. Dietary total antioxidant capacity: A novel indicator of diet quality in healty young adult. J Am Coll Nutr 2010;28:648-56.  Back to cited text no. 28
    
29.
Chun KO, Floegel A, Chung SJ, Chung CE, Song WO, Koo SI. Estimation of antioxidant intakes from diet and supplements in U.S. adults. J Nutr 2009;140:317-24.  Back to cited text no. 29
    
30.
Alipour B, Rashidkhani B, Edalati S. Dietary flavonoid intake, total antioxidant capacity and lipid oxidative damage: A cross-sectional study of Iranian women. Nutrition 2016;32:566-72.  Back to cited text no. 30
    
31.
Li D, Zhang Y, Liu Y, Sun R, Xia M. Purified anthocyanin supplementation reduces dyslipidemia, enhances antioxidant capacity, and prevents ınsulin resistance in diabetic patients. J Nutr 2015;145:742-8.  Back to cited text no. 31
    
32.
Fraga GC, Oteiza IP, Galleano M. In vitro measurements and interpretation of total antioxidant capacity. Biochim Biophys Acta 2014;1840:931-4.  Back to cited text no. 32
    
33.
Skarbek GA, Chrzcvanowicz J, Kostka J, Nowak D, Drygas W, Jegier A, et al. Cardiovascular risk factors and total serum antioxidant capacity in healthy men and in men with coronary heart disease. Biomed Res Int 2014;2014:1-8.  Back to cited text no. 33
    
34.
Lim SH, Fan SH, Say YH. Plasma total antioxidant capacity (TAC) in obese Malaysian Subjects. Malays J Nutr 2012;18:345-54.  Back to cited text no. 34
    
35.
Amaya-Villalva MF, González-Aguilar G, Rouzaud-Sández O, Gorinstein S, Astiazarán-García H, Robles-Sánchez M. Obesity-related indicators and their relationship with serum antioxidant activity levels in Mexican adults. Nutr Hosp 2015;31:1989-95.  Back to cited text no. 35
    
36.
Vincent HK, Taylor AG. Biomarker and potential mechanisms of obesity-induced oxidant stres in humans. Int J Obes 2006;30:400-18.  Back to cited text no. 36
    



 
 
    Tables

  [Table 1], [Table 2], [Table 3], [Table 4], [Table 5]



 

Top
  
 
  Search
 
    Similar in PUBMED
   Search Pubmed for
   Search in Google Scholar for
 Related articles
    Access Statistics
    Email Alert *
    Add to My List *
* Registration required (free)  

 
  In this article
    Abstract
   Introduction
   Materials and Method
   Results
   Discussion
   Conclusion
    References
    Article Tables

 Article Access Statistics
    Viewed299    
    Printed7    
    Emailed0    
    PDF Downloaded85    
    Comments [Add]    

Recommend this journal