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@ARTICLE{Hinney:828027,
      author       = {Hinney, A. and Kesselmeier, M. and Jall, S. and Volckmar,
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                      E and Davis, Oliver S P and Helder, Sietske and Bühren,
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                      André and Scherag, Susann and Zipfel, Stephan and Boni,
                      Claudette and Ramoz, Nicolas and Versini, Audrey and
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                      Hauser, Joanna and Karhunen, Leila and Meulenbelt, Ingrid
                      and Slagboom, P Eline and Tortorella, Alfonso and Maj, Mario
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      title        = {{E}vidence for three genetic loci involved in both anorexia
                      nervosa risk and variation of body mass indexcoh},
      journal      = {Molecular psychiatry},
      volume       = {22},
      number       = {2},
      issn         = {1476-5578},
      address      = {London},
      publisher    = {Macmillan},
      reportid     = {FZJ-2017-02041},
      pages        = {192 - 201},
      year         = {2017},
      abstract     = {The maintenance of normal body weight is disrupted in
                      patients with anorexia nervosa (AN) for prolonged periods of
                      time. Prior to the onset of AN, premorbid body mass index
                      (BMI) spans the entire range from underweight to obese.
                      After recovery, patients have reduced rates of overweight
                      and obesity. As such, loci involved in body weight
                      regulation may also be relevant for AN and vice versa. Our
                      primary analysis comprised a cross-trait analysis of the
                      1000 single-nucleotide polymorphisms (SNPs) with the lowest
                      P-values in a genome-wide association meta-analysis (GWAMA)
                      of AN (GCAN) for evidence of association in the largest
                      published GWAMA for BMI (GIANT). Subsequently we performed
                      sex-stratified analyses for these 1000 SNPs. Functional ex
                      vivo studies on four genes ensued. Lastly, a look-up of
                      GWAMA-derived BMI-related loci was performed in the AN
                      GWAMA. We detected significant associations (P-values <5 ×
                      10−5, Bonferroni-corrected P<0.05) for nine SNP alleles at
                      three independent loci. Interestingly, all AN susceptibility
                      alleles were consistently associated with increased BMI.
                      None of the genes (chr. 10: CTBP2, chr. 19: CCNE1, chr. 2:
                      CARF and NBEAL1; the latter is a region with high linkage
                      disequilibrium) nearest to these SNPs has previously been
                      associated with AN or obesity. Sex-stratified analyses
                      revealed that the strongest BMI signal originated
                      predominantly from females (chr. 10 rs1561589; Poverall:
                      2.47 × 10−06/Pfemales: 3.45 × 10−07/Pmales: 0.043).
                      Functional ex vivo studies in mice revealed reduced
                      hypothalamic expression of Ctbp2 and Nbeal1 after fasting.
                      Hypothalamic expression of Ctbp2 was increased in
                      diet-induced obese (DIO) mice as compared with age-matched
                      lean controls. We observed no evidence for associations for
                      the look-up of BMI-related loci in the AN GWAMA. A
                      cross-trait analysis of AN and BMI loci revealed variants at
                      three chromosomal loci with potential joint impact. The
                      chromosome 10 locus is particularly promising given that the
                      association with obesity was primarily driven by females. In
                      addition, the detected altered hypothalamic expression
                      patterns of Ctbp2 and Nbeal1 as a result of fasting and DIO
                      implicate these genes in weight regulation.},
      cin          = {INM-1},
      ddc          = {610},
      cid          = {I:(DE-Juel1)INM-1-20090406},
      pnm          = {571 - Connectivity and Activity (POF3-571) / HBP SGA1 -
                      Human Brain Project Specific Grant Agreement 1 (720270)},
      pid          = {G:(DE-HGF)POF3-571 / G:(EU-Grant)720270},
      typ          = {PUB:(DE-HGF)16},
      UT           = {WOS:000394102600007},
      pubmed       = {pmid:27184124},
      doi          = {10.1038/mp.2016.71},
      url          = {https://juser.fz-juelich.de/record/828027},
}