Contribution of NTRK2 to the genetic susceptibility to anorexia nervosa, harm avoidance and minimum body mass index

Mol Psychiatry. 2005 Sep;10(9):851-60. doi: 10.1038/sj.mp.4001670.

Abstract

Anorexia nervosa (AN) and bulimia nervosa (BN) are eating disorders (ED) with complex genetic and environmental components. Genetic studies and animal models support the participation of brain-derived neurotrophic factor (BDNF) in the vulnerability to AN and BN. We investigated the genetic contribution of the BDNF-specific receptor neurotrophic tyrosine kinase receptor type 2 (NTRK2) to the susceptibility to ED. We have screened the entire NTRK2 gene in 91 patients with ED and have identified 14 single-nucleotide polymorphisms (SNPs). A population-based association study with six SNPs from the NTRK2 locus was performed in 164 ED patients and 121 controls. Significant evidence of association for markers -69C>G and IVS13+40G>A was detected. We also observed a strong association between the C-A-insC haplotype (-69/IVS13+40/2784-2785) and binge-eating/purging AN (ANP, P=0.006; OR=2.27), and a reduced frequency of haplotype G-A-delCl in BN patients (P=0.034; OR=0.6). The analysis of ED-related phenotypes revealed a clear association between NTRK2, high scores of Harm avoidance measured by the temperament and character inventory (TCI-R; P=0.003) and minimum body mass index (minBMI; P<0.001). Our data support a contribution of NTRK2 to the genetic susceptibility of ED, mainly ANP, and ED-related phenotypic traits, such as Harm avoidance and minBMI.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Anorexia Nervosa / genetics*
  • Avoidance Learning*
  • Body Mass Index*
  • Bulimia / genetics
  • Chromosome Mapping
  • Exons
  • Female
  • Genetic Predisposition to Disease*
  • Humans
  • Introns
  • Male
  • Polymerase Chain Reaction
  • Polymorphism, Single Nucleotide*
  • Polymorphism, Single-Stranded Conformational
  • Receptor, trkB / genetics*
  • Reference Values
  • Risk-Taking*

Substances

  • Receptor, trkB