ArticlePloS one
Lack of Postprandial Peak in Brain-Derived Neurotrophic Factor in Adults with Prader-Willi Syndrome.
Article in PloS one. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
14 citing papers in PubMed, 1 synthesis or guideline pooled it, 45 citations in OpenAlex.
- Multidimensional Characterisation of Eating Behaviour in Genetic Obesity: A Systematic Review.Obesity facts · 2026Pooled it
- The Role of the Arcuate Nucleus in Regulating Hunger and Satiety in Prader-Willi Syndrome.Current issues in molecular biology · 2025Review
- The Pivotal Role of Oxytocin's Mechanism of Thermoregulation in Prader-Willi Syndrome, Schaaf-Yang Syndrome, and Autism Spectrum Disorder.International journal of molecular sciences · 2024Review
- Updates on Obesity in Prader-Willi Syndrome: From Genetics to Management.Ewha medical journal · 2023Review
- Hormonal Imbalances in Prader-Willi and Schaaf-Yang Syndromes Imply the Evolution of Specific Regulation of Hypothalamic Neuroendocrine Function in Mammals.International journal of molecular sciences · 2023Review
- Hyperphagia in Prader-Willi syndrome with obesity: From development to pharmacological treatment.Intractable & rare diseases research · 2023Review
- Serum alpha-melanocyte-stimulating hormone (a-MSH), brain-derived neurotrophic factor (BDNF), and agouti-related protein (AGRP) levels in children with Prader-Willi or Bardet-Biedl syndromes.Journal of endocrinological investigation · 2022Article
- Hunger and Satiety Peptides: Is There a Pattern to Classify Patients with Prader-Willi Syndrome?Journal of clinical medicine · 2021Article
- Hypothalamic neuropeptides and neurocircuitries in Prader Willi syndrome.Journal of neuroendocrinology · 2021Review
- Behavioral features in Prader-Willi syndrome (PWS): consensus paper from the International PWS Clinical Trial Consortium.Journal of neurodevelopmental disorders · 2021Review
- Appetite- and weight-inducing and -inhibiting neuroendocrine factors in Prader-Willi syndrome, Bardet-Biedl syndrome and craniopharyngioma versus anorexia nervosa.Endocrine connections · 2021Review
- What can we learn from PWS and SNORD116 genes about the pathophysiology of addictive disorders?Molecular psychiatry · 2021Review
- Postprandial leptin and adiponectin in response to sugar and fat in obese and normal weight individuals.Endocrine · 2019Article
- Obesity management in Prader-Willi syndrome: current perspectives.Diabetes, metabolic syndrome and obesity : targets and therapy · 2018Review
Corrections and comments
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Authors and funding
15 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
contextPrader-Willi syndrome (PWS) is characterized by severe hyperphagia. Brain-derived neurotrophic factor (BDNF) and leptin are reciprocally involved in energy homeostasis.
objectivesTo analyze the role of BDNF and leptin in satiety in genetic subtypes of PWS.
designExperimental study.
settingUniversity hospital. SUBJECTS: 90 adults: 30 PWS patients; 30 age-sex-BMI-matched obese controls; and 30 age-sex-matched lean controls.
interventionsSubjects ingested a liquid meal after fasting ≥10 hours.
main outcome measuresLeptin 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.
resultsFasting 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.
conclusionsLow 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.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.