Please use this identifier to cite or link to this item: https://hdl.handle.net/10316/108113
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dc.contributor.authorGamero-Villarroel, Carmen-
dc.contributor.authorGonzález, Luz M.-
dc.contributor.authorRodríguez-López, Raquel-
dc.contributor.authorAlbuquerque, David-
dc.contributor.authorCarrillo, Juan A.-
dc.contributor.authorGarcía-Herráiz, Angustias-
dc.contributor.authorFlores, Isalud-
dc.contributor.authorGervasini, Guillermo-
dc.date.accessioned2023-08-11T15:55:30Z-
dc.date.available2023-08-11T15:55:30Z-
dc.date.issued2017-09-
dc.identifier.issn21623279pt
dc.identifier.urihttps://hdl.handle.net/10316/108113-
dc.description.abstractIntroduction: TFAP2B and KCTD15 are obesity-related genes that interact to regulate feeding behavior. We hypothesize that variability in these loci, isolated or in combination, could also be related to the risk of eating disorders (ED) and/or associated psychological traits. Methods: We screened 425 participants (169 ED patients, 75 obese subjects, and 181 controls) for 10 clinically relevant and tag single-nucleotide polymorphisms (SNPs) in KCTD15 and TFAP2B by the Sequenom MassARRAY platform and direct sequencing. Psychometric evaluation was performed with EDI-2 and SCL-90R inventories. Results: The KCTD15 rs287103 T variant allele was associated with increased risk of bulimia nervosa (BN) (OR = 4.34 [1.47–29.52]; p = .003) and with scores of psychopathological scales of these patients. Haplotype *6 in KCTD15 was more frequent in controls (OR = 0.40 [0.20–0.80], p = .009 for anorexia nervosa), while haplotype *4 in TFAP2B affected all three scales of the SCL-90R inventory in BN patients (p ≤ .01). Epistasis analyses revealed relevant interactions with body mass index of BN patients (p < .001). Genetic profiles in obese patients did not significantly differ from those found in ED patients. Conclusions: This is the first study that evaluates the combined role of TFAP2B and KCTD15 genes in ED. Our preliminary findings suggest that the interaction of genetic variability in these loci could influence the risk for ED and/or anthropometric and psychological parameters.pt
dc.language.isoengpt
dc.publisherWiley-Blackwellpt
dc.relationAlicia Koplowitz Foundation, Madrid, Spainpt
dc.relationgrant GR15012 from Junta de Extremadura, Consejería de Economía, Comercio e Innovación, Meridapt
dc.relationFCT - post-doctoral fellowship (SFRH/BPD/109043/2015)pt
dc.rightsopenAccesspt
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/pt
dc.subjectanorexia nervosapt
dc.subjectbody mass indexpt
dc.subjectbulimia nervosapt
dc.subjecteating disorderspt
dc.subjectepistasispt
dc.subjectfeedingpt
dc.subjectgenetic polymorphismspt
dc.subjectKCTD15pt
dc.subjectobesitypt
dc.subjectTFAP2Bpt
dc.subject.meshAdolescentpt
dc.subject.meshAdultpt
dc.subject.meshAllelespt
dc.subject.meshAnorexia Nervosapt
dc.subject.meshBody Mass Indexpt
dc.subject.meshBulimia Nervosapt
dc.subject.meshChildpt
dc.subject.meshFemalept
dc.subject.meshHaplotypespt
dc.subject.meshHumanspt
dc.subject.meshObesitypt
dc.subject.meshPersonalitypt
dc.subject.meshPersonality Inventorypt
dc.subject.meshPhenotypept
dc.subject.meshPotassium Channelspt
dc.subject.meshTranscription Factor AP-2pt
dc.subject.meshYoung Adultpt
dc.subject.meshPolymorphism, Single Nucleotidept
dc.titleInfluence of TFAP2B and KCTD15 genetic variability on personality dimensions in anorexia and bulimia nervosapt
dc.typearticle-
degois.publication.firstPagee00784pt
degois.publication.issue9pt
degois.publication.titleBrain and Behaviorpt
dc.peerreviewedyespt
dc.identifier.doi10.1002/brb3.784pt
degois.publication.volume7pt
dc.date.embargo2017-09-01*
uc.date.periodoEmbargo0pt
item.grantfulltextopen-
item.cerifentitytypePublications-
item.languageiso639-1en-
item.openairetypearticle-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.fulltextCom Texto completo-
crisitem.author.orcid0000-0001-8899-9020-
Appears in Collections:I&D CIAS - Artigos em Revistas Internacionais
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