Evidence map›Paper›PMID 32407314›Full record

ArticlePloS one2020

Rev-erbα heterozygosity produces a dose-dependent phenotypic advantage in mice.

Ryan D Welch, Cyrielle Billon, Amina Kameric, Thomas P Burris, Colin A Flaveny

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.4field-weighted citation impact, top 48% 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

7 citing papers in PubMed, 10 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Circadian regulator REV-ERBα is a master regulator of tumor lineage plasticity and an effective therapeutic target.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  5. Article
  6. Article
  7. 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

5 authors at 4 institutions in 1 country.

Ryan D WelchThe Salk Institute for Biological Sciences, La Jolla, CA, United States of America.
Cyrielle BillonThe Center for Clinical Pharmacology, Saint Louis College of Pharmacy, Saint Louis, MO, United States of America.
Amina KamericThe Department of Pharmacology and Physiology, Saint Louis University School of Medicine, Saint Louis, MO, United States of America.
Thomas P BurrisThe Center for Clinical Pharmacology, Saint Louis College of Pharmacy, Saint Louis, MO, United States of America.
Colin A FlavenyThe Department of Pharmacology and Physiology, Saint Louis University School of Medicine, Saint Louis, MO, United States of America.ORCID 0000-0002-5391-715X
University of Health Sciences and Pharmacy · USJewish Hospital · USSaint Louis University · USSalk Institute for Biological Studies · US

Funding

TRAINING PROGRAM IN DIABETES RESEARCHT32DK007494 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI SALTIEL, ALAN R. · 1986 to 2021
$4.7M
NIDDK NIH HHS T32 DK007494
6 · The paper itself

Abstract

Numerous mutational studies have demonstrated that circadian clock proteins regulate behavior and metabolism. Nr1d1(Rev-erbα) is a key regulator of circadian gene expression and a pleiotropic regulator of skeletal muscle homeostasis and lipid metabolism. Loss of Rev-erbα expression induces muscular atrophy, high adiposity, and metabolic syndrome in mice. Here we show that, unlike knockout mice, Nr1d1 heterozygous mice are not susceptible to muscular atrophy and in fact paradoxically possess larger myofiber diameters and improved neuromuscular function, compared to wildtype mice. Heterozygous mice lacked dyslipidemia, a characteristic of Nr1d1 knockout mice and displayed increased whole-body fatty-acid oxidation during periods of inactivity (light cycle). Heterozygous mice also exhibited higher rates of glucose uptake when fasted, and had elevated basal rates of gluconeogenesis compared to wildtype and knockout littermates. Rev-erbα ablation suppressed glycolysis and fatty acid-oxidation in white-adipose tissue (WAT), whereas partial Rev-erbα loss, curiously stimulated these processes. Our investigations revealed that Rev-erbα dose-dependently regulates glucose metabolism and fatty acid oxidation in WAT and muscle.

Indexed as

Adipose Tissue, WhiteAdiposityAnimalsBehavior, AnimalCircadian ClocksDyslipidemiasFatty AcidsGluconeogenesisGlucoseHeterozygoteHumansLipid MetabolismMetabolic SyndromeMiceMice, KnockoutMuscle, SkeletalFatty AcidsGlucoseNr1d1 protein, mouseNuclear Receptor Subfamily 1, Group D, Member 1

Identifiers

PMID32407314
PMCPMC7224546
OpenAlexW3024486335

What OpenQuestion holds

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LicenceCC BY
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.