Abstract
Eating disorders have a deep social, mental, and physical impact and multifactorial origins, but the strong genetic component is universally corroborated. Genetic factors account for approximately 56–84% of liability to anorexia nervosa, 28–83% of liability to bulimia nervosa, and 41–57% to binge eating disorder. Twins studies have provided an irrefutable proof on the heritability of these disorders. Other types of genetic studies in human and in animal models followed, including single nucleotide polymorphisms association studies, genome-wide association studies, whole genome sequencing, and linkage analysis, which allowed to delineate the etiology of eating disorders and to identify the genes and their variants associated with the pathologies. In this scenario, Next Generation Sequencing technologies can be considered as an ideal diagnostic approach. This chapter summarizes the present knowledge on the molecular etiology and genetic determinants of eating disorders including serotonergic genes, dopaminergic genes, opioid genes, endocannabinoid genes, appetite regulation genes, and others. Furthermore, the growing scientific interest to identifying causal genes behind EDs leads to identify some rare genetic variants. Eating disorders have been considered “sociocultural creations,” but probably the environments alone cannot explain the etiology. Genetic factors together with environmental triggers, mental status, and social pressure to thinness are interconnected and may influence epigenetic mechanisms and consequentially gene expressions.
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Abbreviations
- 5-HT:
-
5-Hydroxytryptamine
- 5-HTTLPR:
-
5HT-transporter-linked polymorphic region
- ACTH:
-
Adrenocorticotropic hormone
- AEA:
-
Arachidonoylethanolamine
- AGRP :
-
Agouti-related protein
- AN:
-
Anorexia nervosa
- ANGI:
-
Anorexia Nervosa Genetics Initiative
- ANKK1:
-
Ankyrin repeat and kinase domain containing 1
- BDNF:
-
Brain-derived neurotrophic factor
- BED:
-
Binge eating disorders
- BN:
-
Bulimia nervosa
- CART:
-
Cocaine and amphetamine regulated transcript
- CCK:
-
Cholecystokinin
- COMT:
-
Catecholamine-O-methyltransferase
- DA:
-
Dopamine
- DRD2:
-
Dopamine receptor 2
- DRD4:
-
Dopamine receptor 4
- DSM-V:
-
Diagnostic and Statistical Manual of Mental Disorders Fifth Edition
- EDs:
-
Eating disorders
- ESRRA:
-
Estrogen-related receptor alpha
- FAAH:
-
Fatty acid amide hydrolase
- GCAN:
-
Genetic Consortium for Anorexia Nervosa
- GLP-1:
-
Glucagon-like peptide 1
- GWAS:
-
Genome-wide association studies
- HDAC4:
-
Histone deacetylase 4
- OXM:
-
Oxyntomodulin
- PEA:
-
Palmitoylethanolamide
- POMC:
-
Proopiomelanocortin
- PP:
-
Pancreatic polypeptide
- PPARγ:
-
Peroxisome proliferator-activated receptor gamma
- PYY:
-
Peptide YY
- SNPs:
-
Single nucleotide polymorphisms
- WTCCC-3:
-
Wellcome Trust Case Control Consortium-3
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Ceccarini, M.R., Bertelli, M., Albi, E., Dalla Ragione, L., Beccari, T. (2023). Gene Variants Involved in the Etiopathogenesis of Eating Disorders: Neuropeptides, Neurotransmitters, Hormones, and Their Receptors. In: Patel, V.B., Preedy, V.R. (eds) Eating Disorders. Springer, Cham. https://doi.org/10.1007/978-3-031-16691-4_6
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DOI: https://doi.org/10.1007/978-3-031-16691-4_6
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Publisher Name: Springer, Cham
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Online ISBN: 978-3-031-16691-4
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