Evidence map›Paper›PMID 30252210›Full record

ArticlePhysiological reports2018

Myostatin inhibits glucose uptake via suppression of insulin-dependent and -independent signaling pathways in myoblasts.

Xin-Hua Liu, William A Bauman, Christopher P Cardozo

Open access · goldAbstract read
In one paragraph

Article in Physiological reports, 2018. 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
1.9field-weighted citation impact, top 13% 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, 60 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Trial
  4. Review
  5. Review
  6. Article
  7. Review
  8. Review
  9. Inflammation-Insulin Resistance Crosstalk and the Central Role of Myokines.International journal of molecular sciences · 2025
    Review
  10. Review
  11. Article
  12. Review
  13. Review
  14. Potential Vitamin E Signaling Mediators in Skeletal Muscle.Antioxidants (Basel, Switzerland) · 2024
    Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. TelmisartanFrontiers in pharmacology · 2023
    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

3 authors at 2 institutions in 1 country.

Xin-Hua LiuNational Center for the Medical Consequences of Spinal Cord Injury, James J. Peter VA Medical Center, Bronx, New York.
William A BaumanNational Center for the Medical Consequences of Spinal Cord Injury, James J. Peter VA Medical Center, Bronx, New York.
Christopher P CardozoNational Center for the Medical Consequences of Spinal Cord Injury, James J. Peter VA Medical Center, Bronx, New York.
Icahn School of Medicine at Mount Sinai · USJames J. Peters VA Medical Center · US

Funding

RRD VA B2020CRRD VA B9212C
6 · The paper itself

Abstract

The glucose transporter 4 (Glut4) mediates insulin-dependent glucose uptake. Glut4 expression levels are correlated with whole-body glucose homeostasis. Insulin signaling is known to recruit Glut4 to the cell surface. Expression of Glut4 is subject to tissue-specific hormonal and metabolic regulation. The molecular mechanisms regulating skeletal muscle Glut4 expression remain to be elucidated. Myostatin (Mstn) is reported to be involved in the regulation of energy metabolism. While elevated Mstn levels in muscle are associated with obesity and type-2 diabetes in both human and mouse models, Mstn null mice exhibit immunity to dietary-induced obesity and insulin resistance. The molecular mechanisms by which Mstn initiates the development of insulin resistance and disorders of glucose disposal are not well delineated. Here we investigated effects of Mstn on insulin action in C2C12 cells. Mstn significantly reduced basal and insulin-induced IRS-1 tyrosine (Tyr495) phosphorylation, and expression and activation of PI3K, associated with diminished AKT phosphorylation and elevated GSK3β phosphorylation at Ser9. In addition, Mstn inhibited Glut4 mRNA and protein expression, and reduced insulin-induced Glut4 membrane translocation and glucose uptake. Conversely, SB431542, a Smad2/3 inhibitor, significantly increased cellular response to insulin. Mstn decreased AMP-activated protein kinase (AMPK) activity accompanied by reduced Glut4 gene expression and glucose uptake, which were partially reversed by AICAR, an AMPK activator. These data suggest that Mstn inhibits Glut4 expression and insulin-induced Glut4 integration into cytoplasmic membranes and glucose uptake and that these changes are mediated by direct insulin-desensitizing effect and indirect suppression of AMPK activation.

Indexed as

Signal TransductionAMP-Activated Protein Kinase KinasesAnimalsCell LineGlucoseGlucose Transporter Type 4Glycogen Synthase Kinase 3 betaInsulinInsulin Receptor Substrate ProteinsMiceMyoblastsMyostatinPhosphatidylinositol 3-KinasesProtein KinasesSmad ProteinsAMP-Activated Protein Kinase KinasesGlucoseGlucose Transporter Type 4Glycogen Synthase Kinase 3 betaInsulinInsulin Receptor Substrate ProteinsIrs1 protein, mouseMyostatinPhosphatidylinositol 3-KinasesProtein KinasesSlc2a4 protein, mouseSmad ProteinsGlut4insulin resistancemuscle cellsmyostatin

Identifiers

PMID30252210
PMCPMC6121119
OpenAlexW2890592215

What OpenQuestion holds

Textmetadata
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.