title: The role of catechol-O-methyl transferase Val(108/158)Met polymorphism (rs4680) in the effect of green tea on resting energy expenditure and fat oxidation: a pilot study.
abstract: BACKGROUND
  Green tea(GT) is able to increase energy expenditure(EE) and fat oxidation(FATox) via inhibition of catechol-O-methyl transferase(COMT) by catechins. However, this does not always appear unanimously because of large inter-individual variability. This may be explained by different alleles of the functional COMT Val108/158Met polymorphism that are associated with COMT enzyme activity; high-activity enzyme, COMT(H)(Val/Val genotype), and low-activity COMT(L)(Met/Met genotype).
  
  
  METHODS
  Fourteen Caucasian subjects (BMI: 22.2±2.3 kg/m2, age: 21.4±2.2 years) of whom 7 with the COMT(H)-genotype and 7 with the COMT(L)-genotype were included in a randomized, cross-over study in which EE and substrate oxidation were measured with a ventilated-hood system after decaffeinated GT and placebo(PL) consumption.
  
  
  RESULTS
  At baseline, EE, RQ, FATox and carbohydrate oxidation(CHOox) did not differ between groups. Significant interactions were observed between COMT genotypes and treatment for RQ, FATox and CHOox (p<0.05). After GT vs. PL, EE(GT: 62.2 vs. PL: 35.4 kJ.3.5 hrs; p<0.01), RQ(GT: 0.80 vs. PL: 0.83; p<0.01), FATox(GT: 18.3 vs. PL: 15.3 g/d; p<0.001) and CHOox(GT: 18.5 vs. PL: 24.3 g/d; p<0.001) were significantly different for subjects carrying the COMT(H) genotype, but not for subjects carrying the COMT(L) genotype (EE, GT: 60.3 vs. PL: 51.7 kJ.3.5 hrs; NS), (RQ, GT: 0.81 vs. PL: 0.81; NS), (FATox, GT: 17.3 vs. PL: 17.0 g/d; NS), (CHOox, GT: 22.1 vs. PL: 21.4 g/d; NS).
  
  
  CONCLUSIONS
  Subjects carrying the COMT(H) genotype increased energy expenditure and fat-oxidation upon ingestion of green tea catechins vs, placebo, whereas COMT(L) genotype carriers reacted similarly to GT and PL ingestion. The differences in responses were due to the different responses on PL ingestion, but similar responses to GT ingestion, pointing to different mechanisms. The different alleles of the functional COMT Val108/158Met polymorphism appear to play a role in the inter-individual variability for EE and FATox after GT treatment.
  
  
  BACKGROUND
  Nederlands Trial register NTR1918.
authors.affiliation: Department of Human Biology, Nutrition and Toxicology Research Institute Maastricht (NUTRIM), Maastricht University, Maastricht, The Netherlands.
authors.forename: Rick
authors.initials: R
authors.lastname: Hursel
authors.affiliation: Department of Human Biology, Nutrition and Toxicology Research Institute Maastricht (NUTRIM), Maastricht University, Maastricht, The Netherlands.
authors.forename: Pilou L H R
authors.initials: PL
authors.lastname: Janssens
authors.affiliation: Department of Human Biology, Nutrition and Toxicology Research Institute Maastricht (NUTRIM), Maastricht University, Maastricht, The Netherlands.
authors.forename: Freek G
authors.initials: FG
authors.lastname: Bouwman
authors.affiliation: Department of Human Biology, Nutrition and Toxicology Research Institute Maastricht (NUTRIM), Maastricht University, Maastricht, The Netherlands.
authors.forename: Edwin C
authors.initials: EC
authors.lastname: Mariman
authors.affiliation: Department of Human Biology, Nutrition and Toxicology Research Institute Maastricht (NUTRIM), Maastricht University, Maastricht, The Netherlands.
authors.forename: Margriet S
authors.initials: MS
authors.lastname: Westerterp-Plantenga
mesh_terms: D000328:Adult; D028241:Camellia sinensis / Q000737:chemistry*; D002392:Catechin / Q000494:pharmacology*; D002394:Catechol O-Methyltransferase / Q000737:chemistry / Q000235:genetics*; D018592:Cross-Over Studies; D004734:Energy Metabolism / Q000235:genetics*; D005260:Female; D005838:Genotype; D006801:Humans; D050356:Lipid Metabolism / Q000235:genetics*; D008297:Male; D010084:Oxidation-Reduction; D010865:Pilot Projects; D011110:Polymorphism, Genetic; D044465:White People / Q000235:genetics
chemical_list: D002392:Catechin; D002394:Catechol O-Methyltransferase