BibTex format
@article{Hinney:2017:10.1038/mp.2016.71,
author = {Hinney, A and Kesselmeier, M and Jall, S and Volckmar, AL and Föcker, M and Antel, J and GCAN and WTCCC3 and Heid, IM and Winkler, TW and GIANT and Grant, SF EGG and Guo, Y and Bergen, AW and Kaye, W and Berrettini, W and Hakonarson, H and Price, Foundation Collaborative Group and Childrens, Hospital of PhiladelphiaPrice Foundation and Herpertz-Dahlmann, B and de, Zwaan M and Herzog, W and Ehrlich, S and Zipfel, S and Egberts, KM and Adan, R and Brandys, M and van, Elburg A and Boraska, Perica V and Franklin, CS and Tschöp, MH and Zeggini, E and Bulik, CM and Collier, D and Scherag, A and Müller, TD and Hebebrand, J},
doi = {10.1038/mp.2016.71},
journal = {Mol Psychiatry},
pages = {192--201},
title = {Evidence for three genetic loci involved in both anorexia nervosa risk and variation of body mass index.},
url = {http://dx.doi.org/10.1038/mp.2016.71},
volume = {22},
year = {2017}
}
RIS format (EndNote, RefMan)
TY - JOUR
AB - 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 pr
AU - Hinney,A
AU - Kesselmeier,M
AU - Jall,S
AU - Volckmar,AL
AU - Föcker,M
AU - Antel,J
AU - GCAN
AU - WTCCC3
AU - Heid,IM
AU - Winkler,TW
AU - GIANT
AU - Grant,SF EGG
AU - Guo,Y
AU - Bergen,AW
AU - Kaye,W
AU - Berrettini,W
AU - Hakonarson,H
AU - Price,Foundation Collaborative Group
AU - Childrens,Hospital of PhiladelphiaPrice Foundation
AU - Herpertz-Dahlmann,B
AU - de,Zwaan M
AU - Herzog,W
AU - Ehrlich,S
AU - Zipfel,S
AU - Egberts,KM
AU - Adan,R
AU - Brandys,M
AU - van,Elburg A
AU - Boraska,Perica V
AU - Franklin,CS
AU - Tschöp,MH
AU - Zeggini,E
AU - Bulik,CM
AU - Collier,D
AU - Scherag,A
AU - Müller,TD
AU - Hebebrand,J
DO - 10.1038/mp.2016.71
EP - 201
PY - 2017///
SP - 192
TI - Evidence for three genetic loci involved in both anorexia nervosa risk and variation of body mass index.
T2 - Mol Psychiatry
UR - http://dx.doi.org/10.1038/mp.2016.71
UR - http://www.ncbi.nlm.nih.gov/pubmed/27184124
VL - 22
ER -