J Korean Soc Study Obes 2003; 12(1): 44-53
Published online March 1, 2003
Copyright © Korean Society for the Study of Obesity.
Mi-Jung Kim,Young-Sung Suh1
Department of Internal medicine, Department of Family medicine1, Keimyung University School of Medicine, Daegu, Korea
Background: Uncoupling protein 3 (UCP3) is a mitochondria1 tansmembrane carrier that uncouples oxidative ATP phosphorylation. With the capacity to participate in thermogenesis and energy balance, UCP3 is an important obesity candidate gene. A variant in the putative promoter region of UCP3 (-55 C/T) has recently been identified, and an association with obesity reported. We studied the association of this polymorphism with obesity and lipid profile.
Methods: The -55 C/T polymorphism of the UCP3 gene has been genotyped in 226 subjects (obese 141, normal 85). Anthropometric data was obtained from physical examination and medical records. Fasting plasma glucose, lipid profiles were measured. And body fat distributions were measured by computerized tomography (CT). The 55C/T polymoprhism of UCP3 gene were determined by polymerase chain reaction (PCR) and restriction fragment length polymorphism (RFLP) method.
Results: The frequency of heterozygotes (-55C/T) was 46.5%. The frequency of heterozygotes was similar (49.4 vs 44.7 %) in the control and obese group. For male obese group, the heterozygotes male had higher body mass index (BMI) (P<0.05) and higher total abdominal fat mass (P<0.05) and visceral fat mass (P=0.54). For obese and control group, the heterozyotes male had lower Low-density lipoprotein cholesterol than homozygotes male (P<0.05).
Conclusion: These results suggest that mutations in the UCP3 gene are likely to be a cause of human obesity.
Keywords: Uncoupling protein 3, Polymorphism, obesity, Body mass index