Endocrine Abstracts

Introduction: Ghrelin, enhances appetite and increases food intake in healthy humans. The endogenous ligand ghrelin is the GH secretagogue receptor (GHSR), and effects of ghrelin are mediated via GHSR. The GHSR system plays a significant role in regulating the process of obesity and type 2 diabetes that are linked to metabolic syndrome (MS). Therefore, the GHSR gene 171C/T (rs495225) polymorphism is a good candidate for susceptibility to obesity and excellent MS.

Objective: To assess the frequencies of 171C/T (rs495225) GHSR polymorphism in obese children and adolescents (OCA) comparing to normal weight healthy controls and to investigate associations with MS and metabolic features in OCA.

Methods: A total of 428 Brazilian children: 91 normal healthy weight (43.9% boys; aged 10.6±1.5 years; BMI 17.0±2.4 kg/m²; ZBMI −0.3±0.9, 40.6% pubertal) and 337 obese (35.5% boys; aged 10.7±1.4 years; BMI 30.6±4.7 kg/m²; ZBMI 2.3±0.3; 46.3% pubertal; 43.0% with MS) participated into the study. The polymorphic region of GHSR gene was amplified by PCR and products were bidirectional sequenced. MS was diagnosed by adult treatment panel III (ATP III) adapted for children. SPSS v16 (SPSS, Inc.) was used for data preparation and initial analysis of the data.

Results: Genotype frequencies did not significantly differ between normal weight controls and obese children (X²=0.66; df=2; P=0.7). However, obese patients carrying the TT genotype in 171C/T polymorphism had significantly higher values of HOMA (4.21±0.19 vs 3.66±0.26; P=0.02), higher frequency of MS (44.1 vs 15.2%; P=0.04), hypertriglyceridemia (47.7 vs 14.1%; P<0.001) and trend toward a hyperglycemia (56.5 vs 17.4%; P=0.08) as compared to the CC genotype.

Conclusions: The results support the notion that the studied 171C/T (rs495225) polymorphism of GHSR might be a genetic risk factor for MS in OCA. Our findings also suggest a complex genotype-environmental interaction on obesity risk.

Declaration of interest: The authors declare that there is no conflict of interest that could be perceived as prejudicing the impartiality of the research project.

Funding: This work was supported, however funding details unavailable.