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© Borgis - Postępy Nauk Medycznych 10/2014, s. 672-677
*Małgorzata Rumińska1, Anna Majcher1, Beata Pyrżak1, Aneta Czerwonogrodzka-Senczyna2, Ewelina Witkowska-Sędek1, Danuta Janczarska1
Ocena zależności między stężeniem adiponektyny i składowymi zespołu metabolicznego u dzieci i młodzieży z otyłością prostą
Relationship between adiponectin levels and metabolic syndrome components in obese children and adolescents
1Department of Pediatrics and Endocrinology, Medical University of Warsaw
Head of Department: Beata Pyrżak, MD, PhD
2Department of Human Nutrition, Medical University of Warsaw
Head of Department: Dorota Szostak-Węgierek, MD, PhD
Streszczenie
Wstęp. Adiponektyna jest białkiem tkanki tłuszczowej pełniącym wiele funkcji i odgrywającym istotną rolę w patogenezie zespołu metabolicznego u dzieci.
Cel pracy. Ocena zależności między stężeniem adiponektyny i zespołem metabolicznym oraz jego składowymi u dzieci i młodzieży z otyłością prostą.
Materiał i metody. Badaniami objęto 122 otyłych pacjentów (52 dziewczynki, 70 chłopców) w wieku 5,3-17,9 roku i 58 pacjentów grupy kontrolnej. Otyłość oceniano według kryteriów IOTF. U każdego pacjenta wykonano pomiary antropometryczne oraz badania laboratoryjne. Stężenie adiponektyny oznaczano metodą radioimmunologiczną (RIA). Wyliczono wskaźnik HOMA do oceny insulinooporności. Zespół metaboliczny definiowano na postawie kryteriów IDF (2007).
Wyniki. Zespół metaboliczny (MetS) stwierdzono u 20,2% otyłych dzieci. Średnie stężenie adiponektyny było statystycznie znamiennie niższe w grupie dzieci otyłych w porównaniu do dzieci z grupy kontrolnej. Niższe stężenie adiponektyny miały dzieci otyłe z zespołem metabolicznym w porównaniu do otyłych niespełniających kryteriów MetS. U dzieci z grup badanej i kontrolnej rozpatrywanych łącznie adiponektyna korelowała z BMI, BMI SDS, HDL-C i CRP. Związek adiponektyny z HDL-C stwierdzono również w grupie dzieci otyłych. W analizie regresji logistycznej wykazano, że wzrost adiponektyny o jedną jednostkę zmniejsza o 0,9 raza ryzyko wystąpienia obniżonego < 40 mg/dl stężenia HDL-C.
Wnioski. Adiponektyna może być związana z zespołem metabolicznym poprzez jej wpływ na HDL-C i proces zapalny.
Summary
Introduction. Adiponectin is an adipocyte-derived multiple function protein involved in metabolic syndrome pathogenesis of children.
Aim. The aim of the study was to assess the correlation between adiponectin levels and the metabolic syndrome and its components in obese children and adolescents.
Material and methods. The study included 122 obese children (52 girls, 70 boys, aged 5.3-17.9 years) and a control group of 58 normal-weight children. Obesity was defined according to IOTF criteria. Anthropometric measurements and blood samples were taken from each participant. Adiponectin levels were assessed using the radioimmunoassay (RIA) method. HOMA was calculated to estimate the degree of insulin resistance. Metabolic syndrome components were applied using the 2007 IDF criteria.
Results. The metabolic syndrome (MetS) was diagnosed in 20.2% of the study group. The plasma adiponectin levels were significantly lower in obese children than in the control group. Lower mean adiponectin levels were found in obese children with MetS criteria as compared to those without. In study and control groups of children considered as a whole the adiponectin levels were correlated with BMI, BMI SDS, HDL-C and CRP. The correlation with HDL-C was observed in the obese group only. Logistic regression analysis demonstrated that a 1 unit increase in adiponectin level results in a 0.9 fold reduction of the risk of a low < 40 mg/dl HDL-C level.
Conclusions. Adiponectin may be associated with the metabolic syndrome through its impact on HDL-C and inflammation.
Introduction
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).
Aim
The aim of the study was to evaluate the correlation between adiponectin levels and metabolic syndrome and its components in obese children and adolescents.
Material and methods
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.
Results
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).
Table 1. Comparison of mean values and standard deviation of chosen anthropometric and biochemical parameters between the control group and the study group.
VariableControl groupStudy groupp-value
Height (cm)158.2 ± 14.0154.1 ± 16.20.148
Body weight (kg)46.7 ± 12.972.2 ± 24.10.000
Body Mass Index (kg/m2)18.7 ± 2.729.5 ± 4.90.000
SDS BMI0.0 ± 0.92.8 ± 0.50.000
Waist circumference (cm)64.3 ± 6.690.3 ± 12.30.000
Hip circumference (cm)82.4 ± 9.9101.4 ± 14.00.000
WHR 0.78 ± 0.040.89 ± 0.050.000
WHtR 0.4 ± 0.020.58 ± 0.470.000
% FAT (skinfold) 19.5 ± 6.334.2 ± 5.00.000
Fasting glucose (mg/dl)82.5 ± 10.483.6 ± 10.30.549
TC (mg/dl) 157.5 ± 22.4176.9 ± 300.000
HDL-C (mg/dl) 56 ± 11.944.4 ± 11.20.000
LDL-C (mg/dl) 85.1 ± 24.2105.8 ± 27.20.000
TG (mg/dl)76.9 ± 33.6133.2 ± 62.90.000
CRP (mg/dl) 0.49 ± 0.20.45 ± 0.30.446
Adiponectin (μg/ml)15.9 ± 6.613.1 ± 5.90.004
WHR – waist to hip ratio, WHtR – waist to height ratio, % FAT – % of body mass, TC – total cholesterol, TG – triglycerides, CRP – C-reactive protein

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otrzymano: 2014-07-02
zaakceptowano do druku: 2014-09-19

Adres do korespondencji:
*Małgorzata Rumińska
Department of Pediatrics and Endocrinology Medical University of Warsaw
ul. Marszałkowska 24, 00-576 Warszawa
tel. +48 (22) 522-73-60
malgorzata.ruminska@wum.edu.pl

Postępy Nauk Medycznych 10/2014
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