ANALYSIS OF LEPTIN, ADIPONECTIN AND ADIPONECTIN GENE POLYMORPHISM AND LEPTIN RECEPTOR IN OBESE CHILDREN AND ADOLESCENTS

Abstract

Background: The aim of this study was to determine serum levels of leptin and adiponectin of obese children to identify the influence of leptin receptor gene polymorphisms on leptin resistance and leptin levels, as well as the association between the polymorphisms of adiponectin gene and adiponectin levels.

Materials and methods: A case-control study comparing a study group of 74 obese children (age 13.34±2.60 years) to a normal weight-age matched (age 13.39±2.64 years) control group of 69 children. In both groups, BMI and waist/hip circumference, systolic and diastolic blood pressure were measured. Also, the leptin and adiponectin levels, as well as glucose and lipid metabolism parameters, and high sensitive C-reactive protein (hs-CRP) were measured. Insulin sensitivity was evaluated using fasting insulinemia and HOMA-IR.

All subjects were tested for genetic polymorphisms in LEPRQ223R (rs1137101), ADIPOQ G276T (rs1501299) and ADIPOT45G (rs2241766).

Results: The phenotypes of the obese children study group were significantly higher than in the control group in weight, BMI, waist/hip circumferences and systolic blood pressure (SBP) (P< 0.001). We confirmed that in obese children levels of leptin in the blood are increased and levels of adiponectin are decreased (P<0.001). The differences of the genotype distributions of leptin receptor (LEPRQ223R) and adiponectin (ADIPOG276T and ADIPOT45G) gene polymorphisms in the study group of obese children and a control group was not observed.

Conclusion: In this study, we demonstrated increased leptin level and significantly decreased level of adiponectin in the obese children group compared with the control group. The results of the analysis of glucose metabolism and lipidogram between the two groups showed that insulin, HOMA-IR and triglycerides, as well as hsCRP were increased and significantly different in the group of obese children compared to the control group, as expected. However, by including additional subjects and controls of both sexes and age-specific groups, with larger and more homogeneous samples and a large number of SNPs tested, these genes of interest could provide additional explanations.