Evidence map›Paper›PMID 31527314›Full record

ArticleJCI insight2019

Mss51 deletion enhances muscle metabolism and glucose homeostasis in mice.

Yazmin I Rovira Gonzalez, Adam L Moyer, Nicolas J LeTexier, August D Bratti, Siyuan Feng, Congshan Sun, Ting Liu, Jyothi Mula, Pankhuri Jha, Shama R Iyer and 7 more

Open access · goldAbstract read
In one paragraph

Article in JCI insight, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.0field-weighted citation impact, top 24% 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

15 citing papers in PubMed, 28 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

17 authors at 4 institutions in 1 country.

Yazmin I Rovira GonzalezThe Hugo W. Moser Research Institute, Kennedy Krieger Institute, Baltimore, Maryland, USA.
Adam L MoyerThe Hugo W. Moser Research Institute, Kennedy Krieger Institute, Baltimore, Maryland, USA.
Nicolas J LeTexierThe Hugo W. Moser Research Institute, Kennedy Krieger Institute, Baltimore, Maryland, USA.
August D BrattiThe Hugo W. Moser Research Institute, Kennedy Krieger Institute, Baltimore, Maryland, USA.
Siyuan FengThe Hugo W. Moser Research Institute, Kennedy Krieger Institute, Baltimore, Maryland, USA.
Congshan SunThe Hugo W. Moser Research Institute, Kennedy Krieger Institute, Baltimore, Maryland, USA.
Ting LiuDivision of Cardiology, Johns Hopkins School of Medicine, Baltimore, Maryland, USA.
Jyothi MulaThe Hugo W. Moser Research Institute, Kennedy Krieger Institute, Baltimore, Maryland, USA.
Pankhuri JhaThe Hugo W. Moser Research Institute, Kennedy Krieger Institute, Baltimore, Maryland, USA.
Shama R IyerDepartment of Orthopaedics, University of Maryland School of Medicine, Baltimore, Maryland, USA.
Richard M LoveringDepartment of Orthopaedics, University of Maryland School of Medicine, Baltimore, Maryland, USA.
Brian O'RourkeDivision of Cardiology, Johns Hopkins School of Medicine, Baltimore, Maryland, USA.
Hye Lim NohProgram in Molecular Medicine, University of Massachusetts Medical School, Worcester, Massachusetts, USA.
Sujin SukProgram in Molecular Medicine, University of Massachusetts Medical School, Worcester, Massachusetts, USA.
Jason K KimProgram in Molecular Medicine, University of Massachusetts Medical School, Worcester, Massachusetts, USA.
George K Essien UmanahDepartment of Neurology.
Kathryn R WagnerThe Hugo W. Moser Research Institute, Kennedy Krieger Institute, Baltimore, Maryland, USA.
University of Massachusetts Chan Medical School · USUniversity of Maryland, Baltimore · USJohns Hopkins Medicine · USJohns Hopkins University · US

Funding

Interdisciplinary Training Program Muscle BiologyT32AR007592 · NIAMS · UNIVERSITY OF MARYLAND BALTIMORE · PI Aikaterini Kontrogianni-Konstantopoulos · 1996 to 2026
$11.7M
Training Program in Cellular and Molecular MedicineT32GM008752 · NIGMS · JOHNS HOPKINS UNIVERSITY · PI RAO, RAJINI · 2000 to 2019
$11.7M
UMass Mouse Metabolic Phenotyping Center - Metabolism CoreU2CDK093000 · NIDDK · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI KIM, JASON K · 2016 to 2021
$4.6M
UMass Mouse Metabolic Phenotyping CenterU24DK093000 · NIDDK · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI KIM, JASON K · 2011 to 2015
$2.1M
Targeting Metabo-Redox Network Vulnerability in Heart Failure and Sudden DeathR01HL134821 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI FOSTER, D BRIAN, O'ROURKE, BRIAN · 2018 to 2021
$2.1M
Molecular Determinants of Mitochondrial Instability and ArrhythmiasR01HL137259 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI AKAR, FADI GABRIEL, O'ROURKE, BRIAN · 2017 to 2020
$2.0M
NHLBI NIH HHS R01 HL134821NHLBI NIH HHS R01 HL137259NIAMS NIH HHS T32 AR007592NIDDK NIH HHS U24 DK093000NIDDK NIH HHS U2C DK093000NIGMS NIH HHS T32 GM008752
6 · The paper itself

Abstract

Myostatin is a negative regulator of muscle growth and metabolism and its inhibition in mice improves insulin sensitivity, increases glucose uptake into skeletal muscle, and decreases total body fat. A recently described mammalian protein called MSS51 is significantly downregulated with myostatin inhibition. In vitro disruption of Mss51 results in increased levels of ATP, β-oxidation, glycolysis, and oxidative phosphorylation. To determine the in vivo biological function of Mss51 in mice, we disrupted the Mss51 gene by CRISPR/Cas9 and found that Mss51-KO mice have normal muscle weights and fiber-type distribution but reduced fat pads. Myofibers isolated from Mss51-KO mice showed an increased oxygen consumption rate compared with WT controls, indicating an accelerated rate of skeletal muscle metabolism. The expression of genes related to oxidative phosphorylation and fatty acid β-oxidation were enhanced in skeletal muscle of Mss51-KO mice compared with that of WT mice. We found that mice lacking Mss51 and challenged with a high-fat diet were resistant to diet-induced weight gain, had increased whole-body glucose turnover and glycolysis rate, and increased systemic insulin sensitivity and fatty acid β-oxidation. These findings demonstrate that MSS51 modulates skeletal muscle mitochondrial respiration and regulates whole-body glucose and fatty acid metabolism, making it a potential target for obesity and diabetes.

Indexed as

AnimalsCRISPR-Cas SystemsDiabetes Mellitus, Type 2Diet, High-FatDisease Models, AnimalFatty AcidsFemaleGlucoseHumansInsulinInsulin ResistanceMaleMiceMice, KnockoutMitochondriaMitochondrial ProteinsFatty AcidsGlucoseInsulinMitochondrial ProteinsMss51 protein, mouseTranscription FactorsDiabetesFatty acid oxidationGlucose metabolismMetabolismMuscle Biology

Identifiers

PMID31527314
PMCPMC6824300
OpenAlexW2973651406

What OpenQuestion holds

Textmetadata
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.