Eating disorders: the current status of molecular genetic research

被引:51
|
作者
Scherag, Susann [1 ]
Hebebrand, Johannes [1 ]
Hinney, Anke [1 ]
机构
[1] Univ Duisburg Essen, Dept Child & Adolescent Psychiat & Psychotherapy, LVR Klinikum Essen, D-45147 Essen, Germany
关键词
5-HT2A receptor gene; Melanocortin 4 receptor gene; GWAS; MELANOCORTIN-4 RECEPTOR GENE; BODY-MASS-INDEX; GENOME-WIDE ASSOCIATION; 5-HT2A PROMOTER POLYMORPHISM; SEROTONIN TRANSPORTER GENE; ONSET EXTREME OBESITY; SERUM LEPTIN LEVELS; ANOREXIA-NERVOSA; BULIMIA-NERVOSA; NEUROTROPHIC FACTOR;
D O I
10.1007/s00787-009-0085-9
中图分类号
B844 [发展心理学(人类心理学)];
学科分类号
040202 ;
摘要
Anorexia nervosa (AN) and bulimia nervosa (BN) are complex disorders characterized by disordered eating behavior where the patient's attitude towards weight and shape, as well as their perception of body shape, are disturbed. Formal genetic studies on twins and families suggested a substantial genetic influence for AN and BN. Candidate gene studies have initially focused on the serotonergic and other central neurotransmitter systems and on genes involved in body weight regulation. Hardly any of the positive findings achieved in these studies were unequivocally confirmed or substantiated in meta-analyses. This might be due to too small sample sizes and thus low power and/or the genes underlying eating disorders have not yet been analyzed. However, some studies that also used subphenotypes (e.g., restricting type of AN) led to more specific results; however, confirmation is as yet mostly lacking. Systematic genome-wide linkage scans based on families with at least two individuals with an eating disorder (AN or BN) revealed initial linkage regions on chromosomes 1, 3 and 4 (AN) and 10p (BN). Analyses on candidate genes in the chromosome 1 linkage region led to the (as yet unconfirmed) identification of certain variants associated with AN. Genome-wide association studies are under way and will presumably help to identify genes and pathways involved in these eating disorders. The elucidation of the molecular mechanisms underlying eating disorders might improve therapeutic approaches.
引用
收藏
页码:211 / 226
页数:16
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