| dc.contributor.author |
Bueno Díez, Marta |
| dc.contributor.author |
Esteba-Castillo, Susanna |
| dc.contributor.author |
Novell, Ramon |
| dc.contributor.author |
Giménez-Palop, Olga |
| dc.contributor.author |
Coronas, Ramon |
| dc.contributor.author |
Gabau, Elisabeth |
| dc.contributor.author |
Corripio, Raquel |
| dc.contributor.author |
Baena, Neus |
| dc.contributor.author |
Viñas-Jornet, Marina |
| dc.contributor.author |
Guitart, Míriam |
| dc.contributor.author |
Torrents-Rodas, David |
| dc.contributor.author |
Deus Yela, Juan |
| dc.contributor.author |
Pujol, Jesús |
| dc.contributor.author |
Rigla, Mercedes |
| dc.contributor.author |
Caixàs, Assumpta |
| dc.date |
2021-03-23T11:56:44Z |
| dc.date |
2021-03-23T11:56:44Z |
| dc.date |
2016 |
| dc.identifier |
1932-6203 |
| dc.identifier |
http://hdl.handle.net/10459.1/70854 |
| dc.identifier |
https://doi.org/10.1371/journal.pone.0163468 |
| dc.identifier.uri |
http://hdl.handle.net/10459.1/70854 |
| dc.description |
Context: 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. |
| dc.description |
This 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. |
| dc.language |
eng |
| dc.publisher |
Public Library of Science |
| dc.relation |
Reproducció del document publicat a https://doi.org/10.1371/journal.pone.0163468 |
| dc.relation |
Plos One, 2016, vol. 11, núm. 9, p. e0163468 |
| dc.rights |
cc-by (c) Bueno et al., 2016 |
| dc.rights |
http://creativecommons.org/licenses/by/4.0/ |
| dc.rights |
info:eu-repo/semantics/openAccess |
| dc.subject |
Prader-Willi, Síndrome de |
| dc.title |
Lack of Postprandial Peak in Brain-Derived Neurotrophic Factor in Adults with Prader-Willi Syndrome |
| dc.type |
info:eu-repo/semantics/article |
| dc.type |
info:eu-repo/semantics/publishedVersion |
