title: Elevated serum leptin in patients with coronary artery disease: no association with the Trp64Arg polymorphism of the beta3-adrenergic receptor.
abstract: BACKGROUND
  Serum leptin is associated with the occurrence of cardiovascular risk factors but it is unknown whether leptin is also associated with cardiovascular disease. Another open question is whether the Trp64Arg polymorphism of the beta3-adrenergic receptor (beta3-AR) is a determinant of circulating leptin.
  
  
  OBJECTIVE
  We measured serum leptin concentrations in a large group of patients with angiographically assessed coronary artery disease (CAD) and investigated the relationship between the Trp64Arg polymorphism of the beta3-adrenergic receptor (AR) and serum leptin.
  
  
  METHODS
  Leptin was measured in the fasting state in 1000 consecutive patients with angiographically confirmed CAD by radioimmunoassay. The codon 64 T/C polymorphism of the beta3-AR gene was analysed by the polymerase chain reaction/restriction fragment length polymorphism (PCR/RFLP) technique. Controls were 1000 age-, gender- and weight-matched subjects without clinical signs of CAD.
  
  
  RESULTS
  Serum leptin concentrations were significantly higher in patients with CAD than in those without CAD (median: 6.8 vs 6.1 ng/ml, P < 0.001). In a multiple regression analysis leptin was found to be a determinant of CAD (P = 0.005) along with established risk factors. No differences in serum leptin were observed between wild-type and heterozygous carriers of the Trp64Arg mutation of the beta3-AR gene, whereas the small group of homozygous carriers had higher leptin due to their higher BMI. In a multiple linear regression analysis, body mass index, gender and fasting insulin were the main significant determinants of serum leptin, whereas the beta3-AR polymorphism had no effect.
  
  
  CONCLUSIONS
  Patients with coronary artery disease exhibit higher serum leptin concentrations than age- and gender-matched controls of comparable BMI, indicating that leptin could contribute to the development of cardiovascular disease, possibly via activation of the sympathetic nervous system. The Trp64Arg variant of the beta3-adrenoceptor did not influence serum leptin.
authors.affiliation: Medizinische Klinik und Poliklinik 1, Kardiologie, Charité, Berlin, Germany.
authors.forename: K
authors.initials: K
authors.lastname: Stangl
authors.forename: I
authors.initials: I
authors.lastname: Cascorbi
authors.forename: M
authors.initials: M
authors.lastname: Laule
authors.forename: V
authors.initials: V
authors.lastname: Stangl
authors.forename: M
authors.initials: M
authors.lastname: Vogt
authors.forename: S
authors.initials: S
authors.lastname: Ziemer
authors.forename: I
authors.initials: I
authors.lastname: Roots
authors.forename: K
authors.initials: K
authors.lastname: Wernecke
authors.forename: G
authors.initials: G
authors.lastname: Baumann
authors.forename: H
authors.initials: H
authors.lastname: Hauner
mesh_terms: D000368:Aged; D001120:Arginine; D015992:Body Mass Index; D003327:Coronary Disease / Q000097:blood*; D005260:Female; D005838:Genotype; D006801:Humans; D007328:Insulin / Q000097:blood; D020738:Leptin / Q000378:metabolism*; D008297:Male; D008875:Middle Aged; D016133:Polymerase Chain Reaction; D012150:Polymorphism, Restriction Fragment Length; D011943:Receptors, Adrenergic, beta / Q000235:genetics*; D022702:Receptors, Adrenergic, beta-3; D054411:Receptors, Leptin; D012044:Regression Analysis; D014364:Tryptophan
chemical_list: D007328:Insulin; C515448:LEPR protein, human; D020738:Leptin; D011943:Receptors, Adrenergic, beta; D022702:Receptors, Adrenergic, beta-3; D054411:Receptors, Leptin; D014364:Tryptophan; D001120:Arginine