Leptin receptor gene K656N polymorphism is associated with low body fat levels and elevated high-density cholesterol levels in Mexican children and adolescents.

INTRODUCTION

This study evaluated the association between obesity and the K109R, Q223R, and K656N polymorphisms of the leptin receptor (LEPR) locus. Such polymorphisms cause changes in the extracellular extreme of the LEPR gene product and appear to be related to signal transduction toward the cell.

SUBJECTS AND METHODS

A total of 128 participants between 6 and 17 years of age from a Mexican Mestizo population were included in the study. Individuals were classified as overweight-obese (n = 76) and normal (n = 52), based on anthropomorphic measurements. The K109R, Q223R, and K656N polymorphisms of the LEPR were determined by the size of restriction fragments obtained from polymorphic fragment amplification (polymerase chain reaction-restriction fragment length polymorphism) obtained from genomic DNA. Allele frequency was compared using the chi-square test. Odds ratio was calculated to determine allele obesity risk factor.

RESULTS

Variant allele frequency was 109R = 0.35, 223R = 0.49, and 656N = 0.11 for the K109R, Q223R, and K656N polymorphisms, respectively. No statistically significant association with obesity was found in any of the alleles. The N allele of the K656N polymorphism was associated with nonobesity markers, such as high concentrations of high-density lipoproteins, normal body mass index, less thickness of skinfolds, and body perimeters. None of the alleles studied were shown to be obesity risk factors.

CONCLUSIONS

Our results suggest that there is no association between the K109R, Q223R, and K656N polymorphisms of the LEPR gene with obesity, and none of the alleles of the LEPR gene K109R, Q223R, and K656N polymorphisms are an obesity risk factor.