A next generation sequencing gene panel for use in the diagnosis of anorexia nervosa.
Anorexia nervosa
Eating disorders
NGS analysis
Rare variants
Journal
Eating and weight disorders : EWD
ISSN: 1590-1262
Titre abrégé: Eat Weight Disord
Pays: Germany
ID NLM: 9707113
Informations de publication
Date de publication:
Jun 2022
Jun 2022
Historique:
received:
07
09
2021
accepted:
07
11
2021
pubmed:
26
11
2021
medline:
25
5
2022
entrez:
25
11
2021
Statut:
ppublish
Résumé
The aim of this study was to increase knowledge of genes associated with anorexia nervosa (AN) and their diagnostic offer, using a next generation sequencing (NGS) panel for the identification of genetic variants. The rationale underlying this test is that we first analyze the genes associated with syndromic forms of AN, then genes that were found to carry rare variants in AN patients who had undergone segregation analysis, and finally candidate genes intervening in the same molecular pathways or identified by GWAS or in mouse models. We developed an NGS gene panel and used it to screen 68 Italian AN patients (63 females, 5 males). The panel included 162 genes. Family segregation study was conducted on available relatives of probands who reported significant genetic variants. In our analysis, we found potentially deleterious variants in 2 genes (PDE11A and SLC25A13) associated with syndromic forms of anorexia and predicted deleterious variants in the following 12 genes: CD36, CACNA1C, DRD4, EPHX2, ESR1, GRIN2A, GRIN3B, LRP2, NPY4R, PTGS2, PTPN22 and SGPP2. Furthermore, by Sanger sequencing of the promoter region of NNAT, we confirmed the involvement of this gene in the pathogenesis of AN. Family segregation studies further strengthened the possible causative role of CACNA1C, DRD4, GRIN2A, PTGS2, SGPP2, SLC25A13 and NNAT genes in AN etiology. The major finding of our study is the confirmation of the involvement of the NNAT gene in the pathogenesis of AN; furthermore, this study suggests that NGS-based testing can play an important role in the diagnostic evaluation of AN, excluding syndromic forms and increasing knowledge of the genetic etiology of AN. Level I, experimental study.
Identifiants
pubmed: 34822136
doi: 10.1007/s40519-021-01331-0
pii: 10.1007/s40519-021-01331-0
doi:
Substances chimiques
Mitochondrial Membrane Transport Proteins
0
SLC25A13 protein, human
0
Slc25a13 protein, mouse
0
Cyclooxygenase 2
EC 1.14.99.1
PTPN22 protein, human
EC 3.1.3.48
Protein Tyrosine Phosphatase, Non-Receptor Type 22
EC 3.1.3.48
3',5'-Cyclic-GMP Phosphodiesterases
EC 3.1.4.35
Pde11a protein, mouse
EC 3.1.4.35
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
1869-1880Subventions
Organisme : PROVINCIA AUTONOMA DI BOLZANO
ID : 222474/2021
Informations de copyright
© 2021. The Author(s), under exclusive licence to Springer Nature Switzerland AG.
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