The observed epidemic of childhood and adolescent obesity has serious health consequences. Numerous concomitant metabolic and hemodynamic disturbances as well as chronic inflammation process result in diabetes type 2, arterial hypertension, atherogenic dyslipidemia, which are components of the metabolic syndrome (MetS). These ailments may accompany obesity in middle age and lead to cardiovascular disease (1, 2). Adipocytokines, biologically active substances produced by the adipose tissue play the key role in the induction of the above-mentioned changes.

Adiponectin is one of the adipocytokines and the only one the concentration of which decreases with the increase of the adipose tissue. It is the most abundantly expressed adipokine in adipose tissue which exerts pleiotropic insulin-sensitizing effects. Through activation of the adenosine monophosphate-induced protein kinase (AMPK) pathway and peroxisome proliferator activated receptor α (PPARγ) adiponectin regulates carbohydrate and fat metabolism. Adiponectin inhibits hepatic gluconeogenesis, increases glucose uptake and fatty acid oxidation in skeletal muscle (3, 4). The insulin-sensitizing effects of adiponectin participate in activating insulin-receptor substrate 1 – associated phosphatidylinositol 3-kinase (PI-3K) which improves intracellular insulin action pathway, enhancing fatty acid transport protein 1 mRNA expression and decreases TNF α production (5). Adiponectin has an anti-inflammatory effect on the vascular wall and reduces arteriosclerosis. It inhibits endothelial nuclear factor kβ signaling, reduces adhesion molecule expression and smooth muscle cell proliferation, suppresses macrophage transformation in foam cells as well as stimulates nitric oxide production. Dysregulation of adiponectin expression and secretion may affect pathogenesis of metabolic disease in children and adolescents. Lower levels of adiponectin are observed in obese children with insulin resistance and metabolic syndrome. Hipoadiponectinemia is predictive of development of type 2 diabetes and coronary artery disease (CAD) (3-5).

The aim of the study was to evaluate the correlation between adiponectin levels and metabolic syndrome and its components in obese children and adolescents.

The study included 122 children with simple obesity (52 girls, 70 boys), aged 5.3-17.9 years (mean age 11.6 ± 3 years). The control group consisted of 58 children of the same age (mean age 11.7 ± 3 years) with normal somatic parameters.

Anthropometric measurements of all the children were taken, including body height (cm), body weight (kg), waist circumference and hip circumference (cm), thickness of 3 skinfolds (mm) and body composition using the bioelectrical impedance analysis (BIA) method. The results of these measurements were used to calculate BMI (Body Mass Index), waist to hip ratio (WHR), waist to height ratio (WHtR) and body fat percentage using the Slaughter equations based on skinfold measurements and the BIA method (7).

Obesity was assessed using the criteria developed by International Obesity Task Force (IOTF) (8). The threshold of obesity was set at BMI SDS ≥ +2, expressed in values normalized for each patient using LMS method (9). WHtR exceeding 0.5 was assumed to be a value indicating abdominal obesity. The norms for body fat percentage were set at 19% for girls and 15% for boys.

After a 12-hour fast the following parameters were measured: fasting adiponectin concentration using the radioimmunoassay (RIA) method, glucose and insulin concentrations (fasting and at 30, 60, 90 and 120 minutes of the oral glucose tolerance test – OGTT; glucose levels were measured using the enzymatic method, whereas insulin concentrations were measured using the chemiluminescence and immunoenzymatic methods), total cholesterol (TG), high-density lipoprotein cholesterol (HDL-C), triglyceride (TG) and the acute-phase protein CRP using the standard enzymatic method. Light-density lipoprotein cholesterol (LDL-C) was calculated using the Friedewald formula (10). The resulting data was used to calculate indicators of insulin resistance HOMA. The resulting values of lipid metabolism were interpreted according to the 2007 American Heart Association (AHA) recommendations, and glucose levels were interpreted in accordance with the 2013 Polish Diabetes Association guidelines (10, 11). Hyperinsulinism was defined as fasting insulin level ≥ 15 μIU/ml, and/or maximum OGTT level ≥ 150 μIU/ml, and/or insulin level at 120 minutes of OGTT ≥ 75 μIU/ml Homoeostasis Model Assessment (HOMA) ≥ 3 testify to severe insulin resistance (12).

Each child’s blood pressure was measured, and the results were evaluated using percentile charts for the population of children published by Nawarycz and Ostrowska-Nawarycz (13). Hypertension was diagnosed when the values of systolic or diastolic blood pressure were above the 95th percentile; mean blood pressure values between the 90th and 95th percentiles were defined as the border zone (13).

According to the 2007 International Diabetes Federation (IDF) consensus definition the metabolic syndrome criteria was applied (14).

The project received approval of the Ethical Committee at Medical University of Warsaw. The data were analyzed using the statistic package, SPSS. Statistical significance was considered to be p = value < 0.05.

The mean BMI of the obese children was 29.5 ± 4.9 kg/m², the mean BMI SDS was +2.8 ± 0.5. All the children were found to have high body fat percentage, averaging 38.1 ± 8.2%. The mean waist circumference was 90.3 ± 12.3 cm. In nearly all the children their WHtR met the criteria for diagnosing abdominal obesity. For most anthropometric parameters there were statistically significant differences between the control group and the study group (tab. 1).