ArticleThe Journal of rare disorders2015
EVALUATION OF PLASMA SUBSTANCE P AND BETA-ENDORPHIN LEVELS IN CHILDREN WITH PRADER-WILLI SYNDROME.
Article in The Journal of rare disorders, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
What it found
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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
12 citing papers in PubMed, 12 citations in OpenAlex.
- Neuropeptides and the Autonomic Nervous System in Prader-Willi Syndrome.International journal of molecular sciences · 2025Review
- The Role of the Arcuate Nucleus in Regulating Hunger and Satiety in Prader-Willi Syndrome.Current issues in molecular biology · 2025Review
- Give me five! A modern perspective on addiction from the up-dated Freudian drive theory.Frontiers in psychiatry · 2025Article
- 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
- Article
- Appetite- and weight-inducing and -inhibiting neuroendocrine factors in Prader-Willi syndrome, Bardet-Biedl syndrome and craniopharyngioma versus anorexia nervosa.Endocrine connections · 2021Review
- Association of Acute Postoperative Pain and Cigarette Smoking With Cerebrospinal Fluid Levels of Beta-Endorphin and Substance P.Frontiers in molecular neuroscience · 2021Article
- Prader-Willi Syndrome - Clinical Genetics, Diagnosis and Treatment Approaches: An Update.Current pediatric reviews · 2019Review
- Prader-Willi syndrome and early-onset morbid obesity NIH rare disease consortium: A review of natural history study.American journal of medical genetics. Part A · 2018Review
- Causes of death in Prader-Willi syndrome: Prader-Willi Syndrome Association (USA) 40-year mortality survey.Genetics in medicine : official journal of the American College of Medical Genetics · 2017Article
- Targeting the endocannabinoid/CB1 receptor system for treating obesity in Prader-Willi syndrome.Molecular metabolism · 2016Article
- Prader-Willi Syndrome: Clinical Genetics and Diagnostic Aspects with Treatment Approaches.Current pediatric reviews · 2016Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
backgroundPrader-Willi syndrome (PWS) is a rare obesity-related genetic disorder often caused by a deletion of the chromosome 15q11-q13 region inherited from the father or by maternal disomy 15. Growth hormone deficiency with short stature, hypogonadism, cognitive and behavioral problems, analgesia, decreased gastric motility and decreased ability to vomit with hyperphagia are common in PWS leading to severe obesity in early childhood, if not controlled. Substance P (SP) and beta-endorphin (BE) are neuropeptides involved with centrally and peripherally mediated pain perception, emotional regulation, and gastric motility impacting nausea, emesis and feeding patterns.
objectiveThe goal of this study was to investigate potential mechanisms for PWS symptom development for pain, emotion and gastric motility and plasma levels of substance P and beta-endorphin between PWS and unrelated unaffected children. METHODOLOGY: Plasma samples were collected from 23 Caucasian children with PWS and 18 unrelated, unaffected siblings with an average age of 8.2 ±2.0 years and age range of 5 to 11 years following an overnight fast and neuropeptide substance p and beta-endorphin levels were assessed using Multiplex sandwich immunoassays using the Luminex magnetic-bead based platform. Linear regression analysis was carried out on log-transformed values adjusted for age, sex, and body mass index (BMI).
resultsThe mean plasma SP (57 ± 23 pg/ml) and BE (592 ± 200 pg/ml) levels in PWS were significantly higher than SP (35 ± 20 pg/ml, F=10.5,
conclusionsThe increased BE and SP plasma levels relative to unrelated, unaffected siblings may contribute to hyperphagia, abnormal pain sensation and adrenal insufficiency seen in PWS. Increases in SP levels may be modulated by central and/or peripheral actions of BE on opioid, GABA or POMC precursors and may reflect loss of feedback inhibitory control. Further studies are needed to confirm and elucidate the biochemical basis for observed disturbances in neuropeptide levels seen in our study and may impact on the development and persistence of symptoms commonly seen in PWS.
Identifiers
27570781PMC4997806W2513803239What OpenQuestion holds
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.