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Adiponectin in obese children and its association with blood pressure and anthropometric markers

Hassan, Nayera E.a; EL-Ashry, Hala H.b; Awad, Amina H.b; El-Masry, Sahar A.a; Youssef, Mai M.b; Sallam, Mona M.b; Anwar, Monac

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Medical Research Journal: June 2011 - Volume 10 - Issue 1 - p 1-4
doi: 10.1097/01.MJX.0000397204.63056.f3
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Obesity is currently regarded as a public health problem that affects both young people and adults [1]. The World Health Organization (WHO) has declared that obesity is a disease of pandemic significance, which threatens the developing world and developed countries as well [2].

The prevalence and magnitude of obesity are increasing dramatically [3]. Now there is a global increase in the prevalence of obesity and its accompanying health risks such as type 2 diabetes mellitus, insulin resistance, and cardiovascular diseases [4]. This alarming increase of obesity in children occurring globally is raising the concern about the implications for development of atherosclerosis, cardiovascular diseases, and type 2 diabetes at earlier ages, and is driving efforts to evaluate and predict risks in young adults [5].

Childhood obesity epidemic has become a threat to the health of the pediatric population by promoting premature development of atherosclerosis and the metabolic syndrome, both of which may significantly increase the risk of cardiovascular disease early in life [6]. Obesity among Egyptian children and adolescents has shown a dramatic increase. It was found to be 2.4% among boys and 4.5% among girls of primary school children in 2004 [7]. It was increased to 5.5% among boys and 5.6% among girls in 2007 [8]. This rise will lead to further rising in the prevalence of hypertension, type 2 diabetes, metabolic syndrome, and cardiovascular diseases.

The adipose tissue serves not only as an energy storage organ, but also as an endocrine organ by releasing factors into the circulation that have sites of action [9]. The secretory products of adipose tissue, collectively referred to as adipocytokines, adiponectin is the most abundant adipose-specific protein and is exclusively expressed and secreted from the adipose tissue. It has been shown to have an important role in glucose metabolism [10]. Adiponectin is secreted by adipocytes; it circulates abundantly in the blood in the form of multimeres [11]. It has an anti-inflammatory effect that suppresses tumor necrosis factor (α) production from cultured macrophages [12] and an insulin-sensitizing effect that is antidiabetic and antiatherogenic [13].

Prevention of obesity during childhood is a key to the largest possible impact on adult health at the population level [14,15]. This study aimed at examining the association of adiponectin, blood pressure, and anthropometric markers of adiposity in obese Egyptian children.


A cross-sectional survey that comprised 2083 children, 874 (42%) boys and 1209 (58%) girls, aged from 7 to 11 years, was conducted by the National Research Centre, Egypt. The pupils were recruited from two primary public schools situated in Giza governorate, during the period October 2007 to April 2009. Permission to carry out the study was granted by the Ministry of Education, and the directors of the school included in the research. Parents were informed about the purpose of the study and their permission in the form of written consents was obtained. Another assent was taken from the students who were involved in this research. The protocol was approved by the Ethics Committee of the National Research Centre.

Of the total sample, only 124 obese children were included. The prevalence of obesity (6.0%) comprised 32 (3.7%) boys and 92 (7.6%) girls; their mean age was 9.83±1.43 years. These children were required to meet the following inclusion criteria: age 7–11 years and body mass index (BMI) greater than the 95th percentile for age and sex based on the Egyptian Growth Reference Charts [16]. Children were excluded if they were used to have an earlier major illness, including type 1 or 2 diabetes, if they have taken medications or used to have a condition that is known to influence their growth, insulin action, or insulin secretion (e.g. glucocorticoid therapy, hypothyroidism, and Cushing's disease). Informed consent and assent were obtained from parents of 68 children only for the laboratory data.

Each child was subjected to a complete physical examination, as well as anthropometric measures. The height and weight were measured. The height was measured to the nearest 0.1 cm using a Holtain portable anthropometer, and the weight was determined to the nearest 0.01 kg using a Seca scale Balance with the patient dressed in minimal clothes and without shoes. The BMI was calculated as weight (in kilograms) divided by height (in meters) squared. Waist circumference was measured at the level of the umbilicus with the child standing and breathing normally, hip circumference at the level of the iliac crest, using a nonstretchable plastic tape to the nearest 0.1 cm. The waist/hip ratio was calculated (centimeter/centimeter). Each measurement was taken as the mean of three consecutive measurements, using standardized equipment and following the recommendations of the International Biological Program [17].

Blood pressure was measured with a standard mercury sphygmomanometer after the patients had rested for at least 10 min. Systolic blood pressure was recorded at the appearance of sounds, and the diastolic blood pressure was recorded at the disappearance of sounds.

Fasting venous blood samples were collected in plain tubes using a standard venipuncture aseptic technique. The samples were allowed to clot and sera were separated by centrifugation and stored in aliquots at −80°C until assays. Fasting glucose was measured using a quantitative enzymatic colorimetric commercial kit provided by Stanbio according to the glucose oxidase method [18]. Serum insulin and adiponectin levels were measured using commercially available enzyme linked immunosorbent assay kits, provided by DRG Instruments GmbH, Germany and AviBion Orgenium Laboratories, Finland, respectively. The homeostatic model assessment for insulin resistance (HOMA-IR) was calculated according to the following equation:

Statistical analysis

Data were expressed as mean±standard deviation. Student's paired t-test was used to examine the sex differences. Pearson's correlation coefficients were used to assess the relationships between independent variables. The level of significance was set at a probability of less than 5% (P<0.05). All statistical analyses were carried out using the Statistical Package for Social Sciences (SPSS/Windows Version 9.05, SPSS Inc., Chicago, Illinois, USA).


In this study, the prevalence of obesity was 6.0% (3.7% in boys and 7.6% in girls); their mean age was 9.83+1.43 years. However, the prevalence of overweight (BMI lies between 85th and 95th percentile for age and sex based on the Egyptian Growth Reference Charts [16]) was 10.5%; 7.7% in boys and 12.6% in girls (Table 1).

Table 1:
Distribution of the study sample

The clinical characteristics of obese children are provided in Table 2. A significant sex difference was observed in weight, in which girls were heavier than boys. However, there were insignificant sex differences in the age, anthropometric measurements such as height, waist circumference, hip circumference, and waist/hip ratio, systolic and diastolic blood pressures and the laboratory data such as fasting glucose, insulin, adiponectin levels, and HOMA-IR. Thus, the analysis was completed as one sample.

Table 2:
Descriptive data of the obese children by sex

Correlations between laboratory data, blood pressure, and anthropometric data for the total sample are presented in Table 3. Serum adiponectin level had significant negative correlation with both systolic and diastolic blood pressures, which in turn had highly significant positive correlations with each other. However, insignificant correlation was detected between adiponectin level and any one of the used anthropometric parameters. Blood pressure, both systolic and diastolic, has shown significant positive correlations with age, weight, and height. Moreover, systolic blood pressure had highly significant positive correlation with the hip circumference, whereas diastolic blood pressure had highly significant positive correlation with waist circumference and waist/hip ratio (markers for central obesity). HOMA-IR had highly significant positive correlation with fasting blood insulin.

Table 3:
Correlations between laboratory data, blood pressure, and anthropometric data for the total sample


This study was carried out to examine the association between adiponectin, blood pressure, fasting glucose, and anthropometric markers in obese children. It was found that the prevalence of obesity among primary school children was 6% and of overweight was 10.5%, with higher percentage in girls. Diet, lack of physical activity, and sedentary behavior are the universal risk factors of obesity in any obesogenic environment. The trends toward more energy-dense diet and sedentary lifestyles were apparent here in this study as elsewhere in different parts of the world. This was previously shown in Greece in the study by Codrington et al. [19] in which the rates of obesity among adults and children have been raised increasingly in short time, that is, in less than a generation due to the same behaviors.

This study revealed reduction in serum adiponectin levels in obese children, compared with the used Kits norm. It also showed a significant negative correlation with both systolic and diastolic blood pressures, with a P value of less than 0.003 and less than 0.0027, respectively. This was previously reported by Degawa-Yamauchi et al. [11] on African boys and Weiss et al. [20] on French adolescents. They proposed that relative reduction of serum adiponectin level in some childhood populations and in adults was considered as a marker of obesity and a risk factor for developing cardiovascular disease as well as type 2 diabetes. It was found to be lower in patients with diabetes and coronary artery disease and with high blood pressure [11]. Moreover, it was also a biomarker of insulin sensitivity in obese children, and independent risk factors for atherosclerosis in insulin-resistant adults [11,20]. Palomer et al. [21] also stated that obesity is a state of adiponectin deficiency, which makes this hormone to be added on the list as a very exciting player in the field of obesity-related insulin resistance and atherosclerosis. The decreased level of adiponectin has been attributed to the accumulation of visceral fat [22].

Blood pressure of our children, both systolic and diastolic, was found to show significant positive correlations with age, height, and the anthropometric markers of adiposity in the form of body weight, waist circumference, hip circumference, and waist/hip ratio. The same results were found in the study by Degawa-Yamauchi et al. [11] and Arnaiz et al. [23] who found same correlations between blood pressure and obesity markers.

In this study, blood pressure, both systolic and diastolic, was inversely correlated with serum adiponectin. Despite the reduced serum adiponectin level in our obese children, insignificant correlations were found between adiponectin and anthropometric parameters. Schoppen et al. [24] found that adiponectin level was weakly related to anthropometric variables in children. Weyer et al. [25] had reported the same findings, but he found that waist/hip ratio was significantly independent determinants of adiponectin levels in Whites and Pima Indians. In contrast, Arnaiz et al. [23] stated that adiponectin levels were inversely correlated with anthropometric parameters of obesity. Ducluzeau et al. [26] concluded that adiponectin production and concentration actually decrease in obese patients and is more specifically associated with waist/ hip ratio and waist circumference. A negative correlation between serum adiponectin level and adiposity has been previously observed in Japanese adults, and a similar negative correlation has been reported recently in 5–10-year-old Pima Indian children [11] as well as in French adolescents [27]. These differences may be due to racial differences and sociocultural eating habits.

Insignificant relationship between adiponectin, fasting glucose, or insulin levels were found in this study. The same finding was previously shown in the study by Weyer et al. [25]. They stated that several studies in adults have demonstrated an association of serum adiponectin with hyperinsulinemia independent of adiposity, and that it was also found that fasting insulin and insulin sensitivity were significantly independent determinants of adiponectin levels in Whites and Pima Indians. Therefore, decreased level of adiponectin especially in obese children may be a risk factor of developing hyperinsulinemia later in adult life.

It is a point of interest to say that in a study by Asayama et al. [28], it was found that serum adiponectin level was decreased in obese children and was restored to normal by slimming. Thus, they concluded that weight reduction has significantly elevated serum adiponectin levels in diabetic and nondiabetic patients. This was also shown later in the study by Cambuli et al. [27]. In addition, Degawa-Yamauchi et al. [11] stated that higher level of serum adiponectin has protected against type 2 diabetes in Pima Indians. Therefore, determination of its level in overweight and obese children may help in prediction and prevention of obesity complications.


In conclusion, evaluation of blood pressure in obese children can reflect serum adiponectin level and be considered as an early marker for preventing obesity complications among this vulnerable group. Reduced serum adiponectin level is a risk factor for developing cardiovascular complications, and evaluation of its level may contribute to reverse the rising trend in the incidence of obesity in children. Further investigations on a wider scale are recommended. It is important to establish through researches the effectiveness of community (or school)-based approaches for obesity in our own settings. It is also important to improve the levels of knowledge and understanding of issues relating to food, diet, health, and fitness. Prevention of obesity during childhood is the key to the largest possible impact on adult health at the population level.


1. Giugliano R, Carneiro EC. Factors associated with obesity in school children. J Pediatr (Rio J). 2004;80:17–22
2. Young LR, Nestle M. Expanding portion sizes in the US marketplace: implications for nutrition counseling. J Am Diet Assoc. 2003;103:231–234
3. Weiss R, Dziura J, Burgert TS, Tamborlane WV, Taksali SE, Yeckel CW, et al. Obesity and the metabolic syndrome in children and adolescents. N Engl J Med. 2004;350:2362–2374
4. Van Vliet M, Von Rosenstiel IA, Schindhelm RK, Brandjes DP, Beijnen JH, Diamant M. Ethnic differences in cardiometabolic risk profile in an overweight/obese paediatric cohort in the Netherlands: a cross-sectional study. Cardiovasc Diabetol. 2009;8:2
5. Jones KL. The dilemma of the metabolic syndrome in children and adolescents: disease or distraction? Pediatr Diabetes. 2006;7:311–321
6. Dhuper S, Cohen HW, Daniel J, Gumidyala P, Agarwalla V, St Victor R, et al. Utility of the modified ATP III defined metabolic syndrome and severe obesity as predictors of insulin resistance in overweight children and adolescents: a cross-sectional study. Cardiovasc Diabetol. 2007;6:4
7. Shaheen F, Hathout M, Tawfik A Prevalence of obesity in Egypt. National survey, final report. 2004 Cairo National Nutrition Institute
8. El-Masry SA. Nutritional assessment of Egyptian children. MJNRC. 2007;6:40–49
9. Kahn BB, Flier JS. Obesity and insulin resistance. J Clin Invest. 2000;106:473–481
10. Maeda K, Okubo K, Shimomura I, Funahashi T, Matsuzawa Y, Matsubara K. cDNA cloning and expression of a novel adipose specific collagen-like factor, apM1 (adiPose most abundant gene transcript 1). Biochem Biophys Res Commun. 1996;221:286–289
11. Degawa-Yamauchi M, Dilts JR, Bovenkerk JE, Saha C, Pratt JH, Considine RV. Lower serum adiponectin levels in African–American boys. Obes Res. 2003;11:1384–1390
12. Yokota T, Oritani K, Takahashi I, Ishikawa J, Matsuyama A, Ouchi N, et al. Adiponectin, a new member of the family of soluble defense collagens, negatively regulates the growth of myelomonocytic progenitors and the functions of macrophages. Blood. 2000;96:1723–1732
13. Hartman HB, Hu X, Tyler KX, Dalal CK, Lazar MA. Mechanisms regulating adipocyte expression of resistin. J Biol Chem. 2002;277:19754–19761
14. Brambilla P, Lissau I, Flodmark CE, Moreno LA, Widhalm K, Wabitsch M, et al. Metabolic risk-factor clustering estimation in children: to draw a line across pediatric metabolic syndrome. Int J Obes (Lond). 2007;31:591–600
15. Huang TT, Ball GD, Franks PW. Metabolic syndrome in youth: current issues and challenges. Appl Physiol Nutr Metab. 2007;32:13–22
16. Ghalli I, Salah N, Hussien F, Erfan M, El- Ruby M, Mazen I, et al.Satorio A, Buckler JMH, Marazzi N Egyptian growth curves for infants, children and adolescents. Crecere nel mondo. 2008 Italy Ferring Publisher
17. Tanner JM, Miernaux J, Jarman SWeiner JS, Lourie JA. Growth and physique studies. Human biology. A guide to field methods. 1969 Oxford Blackwell Scientific Publications:273
18. Keilin D, Hartree EF. The use of glucose oxidase for the determination of glucose in biological material and for the study of glucose-producing systems by manometric methods. Biochem J. 1948;42:230–238
19. Codrington C, Sarri K, Kafatos A. Stakeholder appraisal of policy options for tackling obesity in Greece. Obes Rev. 2007;8(Suppl 2):63–73
20. Weiss R, Dziura J, Burgert TS, Tamborlane WV, Taksali SE, Yeckel CW, et al. Obesity and the metabolic syndrome in children and adolescents. N Engl J Med. 2004;350:2362–2374
21. Palomer X, Pérez A, Blanco-Vaca F. Adiponectin: a new link between obesity, insulin resistance and cardiovascular disease. Med Clin (Barc). 2005;124:388–395
22. Wagner A, Simon C, Oujaa M, Platat C, Schweitzer B, Arveiler D. Adiponectin is associated with lipid profile and insulin sensitivity in French adolescents. Diabetes Metab. 2008;34:465–471
23. Arnaiz P, Acevedo M, Barja S, Aglony M, Guzmán B, Cassis B, et al. Adiponectin levels, cardiometabolic risk factors and markers of subclinical atherosclerosis in children. Int J Cardiol. 2010;138:138–144
24. Schoppen S, Riestra P, García-Anguita A, López-Simón L, Cano B, de Oya I, et al. Leptin and adiponectin levels in pubertal children: relationship with anthropometric variables and body composition. Clin Chem Lab Med. 2010;48:707–711
25. Weyer C, Funahashi T, Tanaka S, Hotta K, Matsuzawa Y, Pratley RE, et al. Hypoadiponectinemia in obesity and type 2 diabetes: close association with insulin resistance and hyperinsulinemia. J Clin Endocrinol Metab. 2001;86:1930–1935
26. Ducluzeau PH, Cousin P, Malvoisin E, Bornet H, Vidal H, Laville M, et al. Glucose-to-insulin ratio rather than sex hormone-binding globulin and adiponectin levels is the best predictor of insulin resistance in nonobese women with polycystic ovary syndrome. J Clin Endocrinol Metab. 2003;88:3626–3631
27. Cambuli VM, Musiu MC, Incani M, Paderi M, Serpe R, Marras V, et al. Assessment of adiponectin and leptin as biomarkers of positive metabolic outcomes after lifestyle intervention in overweight and obese children. J Clin Endocrinol Metab. 2008;93:3051–3057
28. Asayama K, Hayashibe H, Dobashi K, Uchida N, Nakane T, Kodera K, et al. Decrease in serum adiponectin level due to obesity and visceral fat accumulation in children. Obes Res. 2003;11:1072–1079

adiponectin; anthropometric obesity markers; blood pressure; children; obesity

© 2011 Medical Research Journal