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dc.contributor.authorBueno Díez, Marta
dc.contributor.authorEsteba-Castillo, Susanna
dc.contributor.authorNovell, Ramon
dc.contributor.authorGiménez-Palop, Olga
dc.contributor.authorCoronas, Ramon
dc.contributor.authorGabau, Elisabeth
dc.contributor.authorCorripio, Raquel
dc.contributor.authorBaena, Neus
dc.contributor.authorViñas-Jornet, Marina
dc.contributor.authorGuitart, Míriam
dc.contributor.authorTorrents-Rodas, David
dc.contributor.authorDeus Yela, Juan
dc.contributor.authorPujol, Jesús
dc.contributor.authorRigla, Mercedes
dc.contributor.authorCaixàs, Assumpta
dc.date.accessioned2021-03-23T11:56:44Z
dc.date.available2021-03-23T11:56:44Z
dc.date.issued2016
dc.identifier.issn1932-6203
dc.identifier.urihttp://hdl.handle.net/10459.1/70854
dc.description.abstractContext: Prader-Willi syndrome (PWS) is characterized by severe hyperphagia. Brain-derived neurotrophic factor (BDNF) and leptin are reciprocally involved in energy homeostasis. Objectives: To analyze the role of BDNF and leptin in satiety in genetic subtypes of PWS. Design: Experimental study. Setting: University hospital. Subjects: 90 adults: 30 PWS patients; 30 age-sex-BMI-matched obese controls; and 30 age-sex-matched lean controls. Interventions: Subjects ingested a liquid meal after fasting ≥10 hours. Main Outcome Measures: Leptin and BDNF levels in plasma extracted before ingestion and 30’, 60’, and 120’ after ingestion. Hunger, measured on a 100-point visual analogue scale before ingestion and 60’ and 120’ after ingestion. Results: Fasting BDNF levels were lower in PWS than in controls (p = 0.05). Postprandially, PWS patients showed only a truncated early peak in BDNF, and their BDNF levels at 60' and 120' were lower compared with lean controls (p<0.05). Leptin was higher in PWS patients than in controls at all time points (p<0.001). PWS patients were hungrier than controls before and after eating. The probability of being hungry was associated with baseline BDNF levels: every 50-unit increment in BDNF decreased the odds of being hungry by 22% (OR: 0.78, 95%CI: 0.65–0.94). In uniparental disomy, the odds of being hungry decreased by 66% (OR: 0.34, 90%CI: 0.13–0.9). Postprandial leptin patterns did no differ among genetic subtypes. Conclusions: Low baseline BDNF levels and lack of postprandial peak may contribute to persistent hunger after meals. Uniparental disomy is the genetic subtype of PWS least affected by these factors.ca_ES
dc.description.sponsorshipThis project was supported by a grant from Fondo de Investigacio´n Sanitaria del Instituto Carlos III (PI-14/02057), and by two grants from Fundacio´ Parc Taulı´(CIR 2010/006 and CIR 2011/ 004), all to AC. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.ca_ES
dc.language.isoengca_ES
dc.publisherPublic Library of Scienceca_ES
dc.relation.isformatofReproducció del document publicat a https://doi.org/10.1371/journal.pone.0163468ca_ES
dc.relation.ispartofPlos One, 2016, vol. 11, núm. 9, p. e0163468ca_ES
dc.rightscc-by (c) Bueno et al., 2016ca_ES
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/*
dc.subject.otherPrader-Willi, Síndrome deca_ES
dc.titleLack of Postprandial Peak in Brain-Derived Neurotrophic Factor in Adults with Prader-Willi Syndromeca_ES
dc.typeinfo:eu-repo/semantics/articleca_ES
dc.type.versioninfo:eu-repo/semantics/publishedVersionca_ES
dc.rights.accessRightsinfo:eu-repo/semantics/openAccessca_ES
dc.identifier.doihttps://doi.org/10.1371/journal.pone.0163468


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