Evidence map›Paper›PMID 21239438›Full record

ArticleEndocrinology2011

Characterization of the hyperphagic response to dietary fat in the MC4R knockout mouse.

Dollada Srisai, Matthew P Gillum, Brandon L Panaro, Xian-Man Zhang, Naiphinich Kotchabhakdi, Gerald I Shulman, Kate L J Ellacott, Roger D Cone

Registry-linked trialOpen access · bronzeAbstract read
In one paragraph

Article in Endocrinology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT03766191 (The Relation of Genetic Factors, Food Cues, and Self-Regulation With Excess Consumption and Adiposity in Children), which is not on this map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
2.8field-weighted citation impact, top 9% 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.

NCT03766191 nacompletednot on this mapstarted 2019, after this paper: background citation

The Relation of Genetic Factors, Food Cues, and Self-Regulation With Excess Consumption and Adiposity in Children

TypeinterventionalSponsorTrustees of Dartmouth CollegeRan2019 to 2024Enrolled189ConditionsChildhood ObesityArmsFood Ads, Non-food Ads
3 · Its place in the literature

Who cites it

40 citing papers in PubMed, 71 citations in OpenAlex.

  1. Dietary Protein Modifies the Effect of theThe Journal of nutrition · 2017
    Trial
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. 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

8 authors at 3 institutions in 2 countries.

Dollada SrisaiResearch Center for Neuroscience, Institute of Molecular Biosciences, Mahidol University, Salaya, Nakornpathom 73170, Thailand.
Matthew P Gillum
Brandon L Panaro
Xian-Man Zhang
Naiphinich Kotchabhakdi
Gerald I Shulman
Kate L J Ellacott
Roger D Cone
Vanderbilt University Medical Center · USYale University · USMahidol University · TH

Funding

Yale Diabetes Research CenterP30DK045735 · NIDDK · YALE UNIVERSITY · PI Richard A Flavell · 1993 to 2026
$44.0M
Yale Mouse Metabolic Phenotyping CenterU24DK059635 · NIDDK · YALE UNIVERSITY · PI SHULMAN, GERALD I · 2001 to 2015
$8.9M
Melanocortin Signaling in Feeding BehaviorR01DK070332 · NIDDK · VANDERBILT UNIVERSITY · PI CONE, ROGER D. · 2004 to 2017
$6.1M
Mechanisms of Lipid-Induced Hepatic Insulin ResistanceR01DK040936 · NIDDK · YALE UNIVERSITY · PI SHULMAN, GERALD I · 1989 to 2015
$5.1M
NIDDK NIH HHS P30 DK045735NIDDK NIH HHS R01 DK040936NIDDK NIH HHS R01 DK070332NIDDK NIH HHS R01 DK-40936NIDDK NIH HHS U24 DK059635
6 · The paper itself

Abstract

Defective melanocortin signaling causes hyperphagic obesity in humans and the melanocortin-4 receptor knockout mouse (MC4R(-/-)). The human disease most commonly presents, however, as haploinsufficiency of the MC4R. This study validates the MC4R(+/-) mouse as a model of the human disease in that, like the MC4R(-/-), the MC4R(+/-) mouse also exhibits a sustained hyperphagic response to dietary fat. Furthermore, both saturated and monounsaturated fats elicit this response. N-acylphosphatidylethanolamine (NAPE) is a signaling lipid induced after several hours of high-fat feeding, that, if dysregulated, might explain the feeding behavior in melanocortin obesity syndrome. Remarkably, however, MC4R(-/-) mice produce elevated levels of NAPE and are fully responsive to the anorexigenic activity of NAPE and oleoylethanolamide. Interestingly, additional differences in N-acylethanolamine (NAE) biochemistry were seen in MC4R(-/-) animals, including reduced plasma NAE levels and elevated hypothalamic levels of fatty acid amide hydrolase expression. Thus, while reduced expression of NAPE or NAE does not explain the high-fat hyperphagia in the melanocortin obesity syndrome, alterations in this family of signaling lipids are evident. Analysis of the microstructure of feeding behavior in response to dietary fat in the MC4R(-/-) and MC4R(+/-) mice indicates that the high-fat hyperphagia involves defective satiation and an increased rate of food intake, suggesting defective satiety signaling and enhanced reward value of dietary fat.

Indexed as

AmidohydrolasesAnimalsBasic Helix-Loop-Helix ProteinsDietary FatsFatty Acid Amide HydrolasesFemaleGene Expression RegulationHeterozygoteHyperphagiaMaleMiceMice, KnockoutMutationReceptor, Melanocortin, Type 1Receptor, Melanocortin, Type 4Repressor ProteinsAmidohydrolasesBasic Helix-Loop-Helix ProteinsDietary FatsFatty Acid Amide HydrolasesReceptor, Melanocortin, Type 1Receptor, Melanocortin, Type 4Repressor ProteinsSim1 protein, mouse

Identifiers

PMID21239438
PMCPMC3040060
OpenAlexW2121465211

What OpenQuestion holds

Textmetadata
Read underepoch 390

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.