Title: Adipocytokines concentration and metabolic parameters in obese children
- Joanna Chrzanowska, Agnieszka Zubkiewicz-Kucharska, Anna Noczyńska
- Original articles
- Pediatric Endocrinology, Diabetes and Metabolism
- Start page:
- Final page:
- Obesity, insulin resistance, metabolic syndrome, adipocytokines
Introduction: Adipose tissue secretes metabolically active proteins.
Aim of the study: 1. To evaluate the prevalence of insulin resistance (IR) and metabolic syndrome
(MS) in obese children as well as to measure plasma hormones concentrations: leptin, adiponectin,
resistin in obese adolescents. 2. To assess the relationship between the studied adipocytokines and
markers of metabolic syndrome.
Material and methods: The study was carried out in 79 obese children, 10-18 years old, (mean
14.3±1.9 years) and 35 normostenic healthy children (mean age 14.6±2.37 years) as a control group.
In all children adiponectin, leptin, resistin, lipid profile (triglycerides and HDL cholesterol) were
estimated and plasma glucose and insulin levels were measured during the oral glucose tolerance
test (OGTT). HOMA-IR was calculated.
Results: MS was diagnosed in 28/78 of children (36% of subjects), IR in 54/79 patients (68% of
subjects). There were higher concentrations of leptin and resistin (p <0.0001) and lower of adiponectin
(p <0.05) in obese children in comparison to normostenic children. In obese girls with IR
a higher concentration of leptin was observed comparing to obese girls without IR (p <0.05).
A lower concentration of adiponectin was present in patients with IR and MS (p <0.05). There were
no correlations between resistin concentration and IR level nor insulin concentration observed.
Conclusions: 1. A sex-related relationship between plasma leptin and IR was observed. 2 Hypoadiponectinemia
was connected with IR and other metabolic disorders typical for the metabolic
syndrome, independently of BMI. 3. There were no statistically significant correlations between the
resistin concentration and IR nor metabolic disorders, which might contradict the hypothesis of the
role of resistin in the pathogenesis of insulin resistance in humans.