Introduction: Obesity has been associated with leptin resistance and this might be caused by genetic factors. The aim of this study was to investigate the gene-lifestyle interaction between -866 G/A UCP2 (uncoupling protein 2) gene polymorphism, dietary intake and leptin in a population based study. Because leptin has an ability to regulate energy metabolism and dietary intake, leptin sensitivity was determined by analyzing the interaction between leptin, body mass index and dietary intake.
Methods: This is a cross sectional study conducted in adults living at urban area of Yogyakarta, Indonesia. Data of adiposity, lifestyle, triglyceride, high density lipoprotein (HDL) cholesterol, leptin and UCP2 gene polymorphism were obtained in 380 men and female adults.
Result and Discussion: UCP2 gene polymorphism was not significantly associated with adiposity, leptin, triglyceride, HDL cholesterol, dietary intake and physical activity (all p>0.05). Leptin was lower in overweight subjects with AA+GA genotypes than those with GG genotype counterparts (p=0.029). In subjects with AA+GA genotypes there was a negative correlation between leptin concentration and total energy intake (r=-0.324; p<0.0001) and this correlation was still significant after controlled for age, sex and body weight. The correlation between leptin and dietary intake was not seen in GG genotype (r=-0.111; p=0.188).
Conclusions: In summary, we showed how genetic variation in -866 G/A UCP2 affected individual response to leptin production. AA+GA genotype had a better leptin sensitivity shown by its response to dietary intake and BMI and this explained the protective effect of A allele to obesity.