Evidence map›Paper›PMID 31230943›Full record

ArticleMolecular metabolism2019

Reelin is modulated by diet-induced obesity and has direct actions on arcuate proopiomelanocortin neurons.

Brandon L Roberts, Baylin J Bennett, Camdin M Bennett, Julie M Carroll, Louise S Dalbøge, Colin Hall, Wafa Hassouneh, Kristy M Heppner, Melissa A Kirigiti, Sarah R Lindsley and 10 more

Open access · goldAbstract read
In one paragraph

Article in Molecular metabolism, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed, 1 pooled it
0.4field-weighted citation impact, top 45% 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

8 citing papers in PubMed, 1 synthesis or guideline pooled it, 13 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Review
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

20 authors at 4 institutions in 3 countries.

Brandon L RobertsDivision of Cardiometabolic Health, Oregon National Primate Research Center, Beaverton, OR, 97006, USA.
Baylin J BennettDivision of Cardiometabolic Health, Oregon National Primate Research Center, Beaverton, OR, 97006, USA.
Camdin M BennettDivision of Cardiometabolic Health, Oregon National Primate Research Center, Beaverton, OR, 97006, USA.
Julie M CarrollDivision of Cardiometabolic Health, Oregon National Primate Research Center, Beaverton, OR, 97006, USA.
Louise S DalbøgeObesity Research Center, Novo Nordisk, Seattle, WA, 98109, USA.
Colin HallObesity Research Center, Novo Nordisk, Seattle, WA, 98109, USA.
Wafa HassounehObesity Research Center, Novo Nordisk, Seattle, WA, 98109, USA.
Kristy M HeppnerObesity Research Center, Novo Nordisk, Seattle, WA, 98109, USA.
Melissa A KirigitiDivision of Cardiometabolic Health, Oregon National Primate Research Center, Beaverton, OR, 97006, USA.
Sarah R LindsleyDivision of Cardiometabolic Health, Oregon National Primate Research Center, Beaverton, OR, 97006, USA.
Katherine G TennantDivision of Cardiometabolic Health, Oregon National Primate Research Center, Beaverton, OR, 97006, USA.
Cadence A TrueDivision of Cardiometabolic Health, Oregon National Primate Research Center, Beaverton, OR, 97006, USA.
Andrew WhittleObesity Research Center, Novo Nordisk, Seattle, WA, 98109, USA.
Anitra C WolfObesity Research Center, Novo Nordisk, Seattle, WA, 98109, USA.
Charles T RobertsDivision of Cardiometabolic Health, Oregon National Primate Research Center, Beaverton, OR, 97006, USA.
Mads Tang-ChristensenDiabetes Research, Novo Nordisk, Måløv, Denmark.
Mark W SleemanDepartment of Physiology, Monash University Biomedicine Discovery Institute, Clayton, Victoria, Australia.
Michael A CowleyDepartment of Physiology, Monash University Biomedicine Discovery Institute, Clayton, Victoria, Australia.
Kevin L GroveObesity Research Center, Novo Nordisk, Seattle, WA, 98109, USA.
Paul KievitDivision of Cardiometabolic Health, Oregon National Primate Research Center, Beaverton, OR, 97006, USA. Electronic address: kievitp@ohsu.edu.
Oregon National Primate Research Center · USNovo Nordisk (United States) · USMonash University · AUNovo Nordisk (Denmark) · DK

Funding

Upgrade of confocal microscopy at the Oregon National Primate Research CenterP51OD011092 · OD · OREGON HEALTH & SCIENCE UNIVERSITY · PI Bonnie J. Nagel · 2012 to 2026
$203.9M
NIH HHS P51 OD011092
6 · The paper itself

Abstract

objectiveReelin (RELN) is a large glycoprotein involved in synapse maturation and neuronal organization throughout development. Deficits in RELN signaling contribute to multiple psychological disorders, such as autism spectrum disorder, schizophrenia, and bipolar disorder. Nutritional stress alters RELN expression in brain regions associated with these disorders; however, the involvement of RELN in the neural circuits involved in energy metabolism is unknown. The RELN receptors apolipoprotein E receptor 2 (ApoER2) and very low-density lipoprotein receptor (VLDLR) are involved in lipid metabolism and expressed in the hypothalamus. Here we explored the involvement of RELN in hypothalamic signaling and the impact of diet-induced obesity (DIO) on this system.

methodsAdult male mice were fed a chow diet or maintained on a high-fat diet (HFD) for 12-16 weeks. HFD-fed DIO mice exhibited decreased ApoER2 and VLDLR expression and increased RELN protein in the hypothalamus. Electrophysiology was used to determine the mechanism by which the central fragment of RELN (CF-RELN) acts on arcuate nucleus (ARH) satiety-promoting proopiomelanocortin (POMC) neurons and the impact of DIO on this circuitry.

resultsCF-RELN exhibited heterogeneous presynaptic actions on inhibitory inputs onto ARH-POMC-EGFP neurons and consistent postsynaptic actions. Additionally, central administration of CF-RELN caused a significant increase in ARH c-Fos expression and an acute decrease in food intake and body weight.

conclusionsWe conclude that RELN signaling is modulated by diet, that RELN is involved in synaptic signaling onto ARH-POMC neurons, and that altering central CF-RELN levels can impact food intake and body weight.

Indexed as

AnimalsArcuate Nucleus of HypothalamusCell Adhesion Molecules, NeuronalDiet, High-FatExtracellular Matrix ProteinsMaleMiceMice, Inbred C57BLMice, TransgenicNerve Tissue ProteinsObesityPro-OpiomelanocortinReelin ProteinSerine EndopeptidasesCell Adhesion Molecules, NeuronalExtracellular Matrix ProteinsNerve Tissue ProteinsPro-OpiomelanocortinReelin ProteinReln protein, mouseSerine EndopeptidasesArcuate nucleusObesityProopiomelanocortinReelin

Identifiers

PMID31230943
PMCPMC6667498
OpenAlexW2950498315

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.