Association of FTO rs9939609 and CD36 rs1761667 with Visceral Obesity

抄録

In 2016, more than 1.9 billion adults were overweight; of which, over 650 million of adults were obese. Genetics and lifestyle play important roles in the development of obesity. Studies have shown that genetic variants contribute in developing obesity; such as FTO and CD36, which regulate metabolism and food preferences. Many researches have also emphasized the importance of lifestyle in obesity prevention. However, the interactions of both factors were still underexplored. Therefore, this study was aimed to assess the interaction between FTO-CD36 variants and fat consumption on the metabolic status of healthy Indonesians. Twenty-one females and seventeen males were involved in this cross-sectional study. CD36 rs1761667 and FTO rs9939609 genotypes were identified from blood samples using PCR-RFLP. Data were compared with dietary patterns (24-h food recall), physical activities (IPAQ), medical records, and body compositions (InBody720). Results: CD36 rs1761667 AA and AG group showed higher —but not significant— fat consumption, WHR, and VFA compared to GG. The trend persisted after gender and physical activity adjustment. Meanwhile, FTO rs9939609 AT group showed significant higher WC, WHR and VFA in male subjects after gender and energy balance adjustment: WC (TT: 74.40±3.85, AT: 85.50±5.92, p=0.011), WHR (TT: 0.85±0.02, AT: 0.92±0.04, p=0.010), and VFA (TT: 48.65±10.61, AT: 78.48±15.18, p=0.010). CD36 rs1761667 might be correlated with higher fat consumption and visceral obesity; while FTO rs9939609 showed a significant association with male visceral obesity. These results indicates that both genetic variants were potential as visceral obesity markers.