Abstract
Aim:
In this study, we aimed to investigate the possible role of the Cannabinoid Receptor-1 (CNR1) gene polymorphisms in the development of morbid obesity in obese children.
Method:
The study was carried out with 48 morbidly obese (27 female/21 male) and 52 obese (28 female/24 male) children. The relative weight ratio >140 was considered as morbid obesity. The 1359G/A polymorphism of the CNR1 gene was determined using polymerase chain reaction restriction method. The SPSS version 13.0 and Graphpad Instat version 3 were used for the statistical analysis. The Hardy-Weinberg equilibrium was calculated using the De-Finetti program. Statistical significance was considered at p<0.05.
Results:
The distributions of G/G, G/A, and A/A genotypes for the 1359G/A polymorphism of the CNR1 gene were 64.6%, 31.3%, and 4.2% in morbidly obese patients, compared with 59.6%, 36.5%, and 3.8% in obese patients (p>0.05). The allele frequencies of G and A were 80.2% and 19.8% in morbidly obese children and 77.9% and 22.1% in obese children (p>0.05). In morbidly obese children, family history of obesity was determined in 25.0% (12) of mothers and in 16.7% (8) of fathers. In patients with obese mothers, A/A genotype was more common (with obese mother: 2/12, 16.7%; without obese mother: 0/36, 0.0%; p=0.020). In patients with A/A genotype, triglyceride ≥150 mg/dL was more frequent (A/A: 2/2, 100.0%; G/A: 2/13, 15.4%; G/G: 11/31, 35.5%; p=0.050).
Conclusion:
In this study, no association was found between the CNR1 gene 1359G/A polymorphism and development of morbid obesity in obese children. However, our study suggests that A/A genotype of human CNR1 gene may play a possible role as a risk factor in the familial inheritance of obesity. Since this is a preliminary study, further investigations are needed to confirm the exact role(s) of this gene in morbid obesity in childhood.
Keywords: Children, obesity, morbid obesity, gene, polymorphism
