title: Additive effect of the mutations in the beta3-adrenoceptor gene and UCP3 gene promoter on body fat distribution and glycemic control after weight reduction in overweight subjects with CAD or metabolic syndrome.
abstract: OBJECTIVE
  To analyze the effects of the mutations in the beta3-adrenoceptor (beta3-AR) gene and/or uncoupling protein3 (UCP3) gene promoter on body fat distribution and glycemic control after mild weight reduction in overweight-obese subjects with coronary artery disease (CAD) or metabolic syndrome.
  
  
  METHODS
  Clinical intervention study of the -300 kcal/day mild weight reduction program for 12 weeks.
  
  
  METHODS
  A total of 224 overweight-obese subjects with CAD or metabolic disorder, subdivided into the following four categories: (1) wild type (TT-CC, n=73); (2) only UCP3 promoter variant (TT-CT/TT, n=90); (3) only beta3-AR variant (TA/AA-CC, n=29); (4) both variants (TA/AA-CT/TT, n=32).
  
  
  METHODS
  Body mass index (BMI), blood pressure, calorie intakes, body fat distribution, serum glucose, insulin, free fatty acids, C-peptide and lipids before and after weight reduction.
  
  
  RESULTS
  After 12 weeks, all subjects lost approximately 5% of their initial body weight. Despite similar weight reduction, the highest decreases in abdominal adipose tissue at both L1 and L4 levels were observed in the 'wild-type' group (P<0.001) and the second highest in 'only UPC3 promoter variant' group (P<0.001). On the other hand, both variant-carriers had the smallest reduction only in visceral fat area at the L4 level. All subjects except both variant-carriers showed significant reductions in the fasting levels of glucose and FFA. The response areas of glucose (P<0.01) and insulin (P<0.05) were reduced largest in the 'wild-type' group and second largest in the 'UCP3 promoter variant' group.
  
  
  CONCLUSIONS
  All the four groups showed similar weight reduction after -300 kcal/d for 12 weeks. However, the beneficial effects on body fat distribution and glycemic control were greatest in the 'wild-type' group and smallest in 'both variants' group. In addition, these effects were less beneficial in carriers with beta3-AR gene variant than with UCP3 gene promoter variant.
authors.affiliation: Yonsei University Research Institute of Science for Aging, Yonsei University, Seoul, Korea.
authors.forename: O Y
authors.initials: OY
authors.lastname: Kim
authors.forename: E Y
authors.initials: EY
authors.lastname: Cho
authors.forename: H Y
authors.initials: HY
authors.lastname: Park
authors.forename: Y
authors.initials: Y
authors.lastname: Jang
authors.forename: J H
authors.initials: JH
authors.lastname: Lee
mesh_terms: D000273:Adipose Tissue / Q000473:pathology*; D001786:Blood Glucose / Q000378:metabolism; D002352:Carrier Proteins / Q000235:genetics*; D003327:Coronary Disease / Q000097:blood / Q000235:genetics; D004038:Diet, Reducing; D005260:Female; D005951:Glucose Tolerance Test; D006801:Humans; D007473:Ion Channels; D008055:Lipids / Q000097:blood; D008297:Male; D024821:Metabolic Syndrome / Q000097:blood / Q000235:genetics; D008875:Middle Aged; D024101:Mitochondrial Proteins; D009154:Mutation; D009765:Obesity / Q000178:diet therapy / Q000235:genetics* / Q000473:pathology; D011401:Promoter Regions, Genetic; D022702:Receptors, Adrenergic, beta-3 / Q000235:genetics*; D000071247:Uncoupling Protein 3; D015431:Weight Loss
chemical_list: D001786:Blood Glucose; D002352:Carrier Proteins; D007473:Ion Channels; D008055:Lipids; D024101:Mitochondrial Proteins; D022702:Receptors, Adrenergic, beta-3; C000604392:UCP3 protein, human; D000071247:Uncoupling Protein 3