Evidence map›Paper›PMID 28007570›Full record

ArticlePharmacological research2017

Dysfunctional oleoylethanolamide signaling in a mouse model of Prader-Willi syndrome.

Miki Igarashi, Vidya Narayanaswami, Virginia Kimonis, Pietro M Galassetti, Fariba Oveisi, Kwang-Mook Jung, Daniele Piomelli

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Pharmacological research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
2.1field-weighted citation impact, top 11% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

11 citing papers in PubMed, 17 citations in OpenAlex.

  1. MAGEL2 (patho-)physiology and Schaaf-Yang syndrome.Developmental medicine and child neurology · 2025
    Review
  2. Article
  3. Review
  4. Review
  5. Article
  6. Review
  7. Review
  8. Frontiers in pharmacology · 2019
    Article
  9. Article
  10. Obesity management in Prader-Willi syndrome: current perspectives.Diabetes, metabolic syndrome and obesity : targets and therapy · 2018
    Review
  11. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 1 institution in 1 country.

Miki IgarashiDepartment of Anatomy and Neurobiology, University of California, Irvine, CA, 92697, USA.
Vidya NarayanaswamiDepartment of Anatomy and Neurobiology, University of California, Irvine, CA, 92697, USA.
Virginia KimonisDepartment of Pediatrics, University of California, Irvine, CA, 92697, USA.
Pietro M GalassettiDepartment of Pediatrics, University of California, Irvine, CA, 92697, USA.
Fariba OveisiDepartment of Anatomy and Neurobiology, University of California, Irvine, CA, 92697, USA.
Kwang-Mook JungDepartment of Anatomy and Neurobiology, University of California, Irvine, CA, 92697, USA.
Daniele PiomelliDepartment of Anatomy and Neurobiology, University of California, Irvine, CA, 92697, USA; Department of Biological Chemistry, University of California, Irvine, CA, 92697, USA; Department of Pharmacology, University of California, Irvine, CA, 92697, USA. Electronic address: piomelli@uci.edu.
University of California, Irvine · US

Funding

University of California Health Participation in the National COVID Cohort Collaborative (N3C)UL1TR001414 · NCATS · UNIVERSITY OF CALIFORNIA-IRVINE · PI COOPER, DAN M, VILAIN, ERIC J. · 2015 to 2023
$35.1M
NCATS NIH HHS UL1 TR001414
6 · The paper itself

Abstract

Prader-Willi syndrome (PWS), the leading genetic cause of obesity, is characterized by a striking hyperphagic behavior that can lead to obesity, type-2 diabetes, cardiovascular disease and death. The molecular mechanism underlying impaired satiety in PWS is unknown. Oleoylethanolamide (OEA) is a lipid mediator involved in the control of feeding, body weight and energy metabolism. OEA produced by small-intestinal enterocytes during dietary fat digestion activates type-α peroxisome proliferator-activated receptors (PPAR-α) to trigger an afferent signal that causes satiety. Emerging evidence from genetic and human laboratory studies suggests that deficits in OEA-mediated signaling might be implicated in human obesity. In the present study, we investigated whether OEA contributes to feeding dysregulation in Magel2

Indexed as

AnimalsAntigens, NeoplasmBody WeightDisease Models, AnimalEatingEndocannabinoidsIntracellular Signaling Peptides and ProteinsIntrinsically Disordered ProteinsJejunumMaleMiceMice, Inbred C57BLMice, KnockoutOleic AcidsPrader-Willi SyndromeProteinsAntigens, NeoplasmEndocannabinoidsIntracellular Signaling Peptides and ProteinsIntrinsically Disordered ProteinsMagel2 protein, mouseOleic AcidsoleoylethanolamideProteinsFeeding behaviorHyperphagiaMagel2(m+/p−)MiceOleoylethanolamide (OEA)Peroxisome proliferator-activated receptor-α (PPAR-α)

Identifiers

PMID28007570
PMCPMC5922435
OpenAlexW2564782599

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

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.