Evidence map›Paper›PMID 28251839›Full record

ArticleJournal of cachexia, sarcopenia and muscle2017

Urolithin B, a newly identified regulator of skeletal muscle mass.

Julie Rodriguez, Nicolas Pierre, Damien Naslain, Françoise Bontemps, Daneel Ferreira, Fabian Priem, Louise Deldicque, Marc Francaux

Open access · goldAbstract read
In one paragraph

Article in Journal of cachexia, sarcopenia and muscle, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed, 1 pooled it
3.4field-weighted citation impact, top 7% 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

36 citing papers in PubMed, 1 synthesis or guideline pooled it, 64 citations in OpenAlex.

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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.

Julie RodriguezInstitute of Neuroscience, Université catholique de Louvain, 1 place Pierre de Coubertin, 1348, Louvain-la-Neuve, Belgium.
Nicolas PierreInstitute of Neuroscience, Université catholique de Louvain, 1 place Pierre de Coubertin, 1348, Louvain-la-Neuve, Belgium.
Damien NaslainInstitute of Neuroscience, Université catholique de Louvain, 1 place Pierre de Coubertin, 1348, Louvain-la-Neuve, Belgium.
Françoise BontempsDe Duve Institute, Université catholique de Louvain, 75 Avenue Hippocrate, 1200, Brussels, Belgium.
Daneel FerreiraDepartment of Biomolecular Sciences, Division of Pharmacognosy, Research Institute of Pharmaceutical Sciences, University of Mississippi, Medicinal Plant Garden, RM 104, University, MS, 38677, USA.
Fabian PriemPROCELL nutrition sprl, 2 Rue Jean Burgers, 7850, Enghien, Belgium.
Louise DeldicqueInstitute of Neuroscience, Université catholique de Louvain, 1 place Pierre de Coubertin, 1348, Louvain-la-Neuve, Belgium.
Marc FrancauxInstitute of Neuroscience, Université catholique de Louvain, 1 place Pierre de Coubertin, 1348, Louvain-la-Neuve, Belgium.
UCLouvain · BEde Duve Institute · BEUniversity of Mississippi · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe control of muscle size is an essential feature of health. Indeed, skeletal muscle atrophy leads to reduced strength, poor quality of life, and metabolic disturbances. Consequently, strategies aiming to attenuate muscle wasting and to promote muscle growth during various (pathological) physiological states like sarcopenia, immobilization, malnutrition, or cachexia are needed to address this extensive health issue. In this study, we tested the effects of urolithin B, an ellagitannin-derived metabolite, on skeletal muscle growth.

methodsC2C12 myotubes were treated with 15 μM of urolithin B for 24 h. For in vivo experiments, mice were implanted with mini-osmotic pumps delivering continuously 10 μg/day of urolithin B during 28 days. Muscle atrophy was studied in mice with a sciatic nerve denervation receiving urolithin B by the same way.

resultsOur experiments reveal that urolithin B enhances the growth and differentiation of C2C12 myotubes by increasing protein synthesis and repressing the ubiquitin-proteasome pathway. Genetic and pharmacological arguments support an implication of the androgen receptor. Signalling analyses suggest a crosstalk between the androgen receptor and the mTORC1 pathway, possibly via AMPK. In vivo experiments confirm that urolithin B induces muscle hypertrophy in mice and reduces muscle atrophy after the sciatic nerve section.

conclusionsThis study highlights the potential usefulness of urolithin B for the treatment of muscle mass loss associated with various (pathological) physiological states.

Indexed as

AnimalsCell DifferentiationCells, CulturedCoumarinsFemaleMaleMiceMice, Inbred C57BLMuscle Fibers, SkeletalMuscle ProteinsMuscle, SkeletalMuscular AtrophyProteasome Endopeptidase ComplexReceptors, AndrogenSignal TransductionUbiquitin-Protein LigasesCoumarinsMuscle ProteinsProteasome Endopeptidase ComplexReceptors, AndrogenUbiquitin-Protein Ligasesurolithin BAndrogen receptorHypertrophymTORC1 signallingPolyphenols

Identifiers

PMID28251839
PMCPMC5566634
OpenAlexW2593660669

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.