Lack of association of genetic variants in genes of the endocannabinoid system with anorexia nervosaReport as inadecuate




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Child and Adolescent Psychiatry and Mental Health

, 2:33

First Online: 17 November 2008Received: 06 August 2008Accepted: 17 November 2008

Abstract

BackgroundSeveral lines of evidence indicate that the central cannabinoid receptor 1 CNR1 as well as the major endocannabinoid degrading enzymes fatty acid amide hydrolase FAAH, N-acylethanolamine-hydrolyzing acid amidase NAAA and monoglyceride lipase MGLL are implicated in mediating the orexigenic effects of cannabinoids. The aim of this study was to analyse whether nucleotide sequence variations in the CNR1, FAAH, NAAA and MGLL genes are associated with anorexia nervosa AN.

MethodsWe analysed the association of a previously described AATn repeat in the 3- flanking region of CNR1 as well as a total of 15 single nucleotide polymorphisms SNPs representative of regions with restricted haplotype diversity in CNR1, FAAH, NAAA or MGLL in up to 91 German AN trios patient with AN and both biological parents using the transmission-disequilibrium-test TDT. One SNP was additionally analysed in an independent case-control study comprising 113 patients with AN and 178 normal weight controls. Genotyping was performed using matrix-assisted laser desorption-ionization time-of-flight mass spectrometry, ARMS-PCR or using 3730xl capillary sequencers.

ResultsThe TDT revealed no evidence for association for any of the SNPs or the AATn repeat with AN all two-sided uncorrected p-values > 0.05. The lowest p-value of 0.11 was detected for the A-allele of the CNR1 SNP rs1049353 for which the transmission rate was 59% 95% confidence interval 47%

.70%. Further genotyping of rs1049353 in 113 additional independent patients with AN and 178 normal weight controls could not substantiate the initial trend for association p = 1.00.

ConclusionAs we found no evidence for an association of genetic variation in CNR1, FAAH, NAAA and MGLL with AN, we conclude that genetic variations in these genes do not play a major role in the etiology of AN in our study groups.

Timo Dirk Müller, Kathrin Reichwald contributed equally to this work.

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Author: Timo Dirk Müller - Kathrin Reichwald - Günter Brönner - Jeanette Kirschner - Thuy Trang Nguyen - André Scherag - Wolfg

Source: https://link.springer.com/



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