Evidence map›Paper›PMID 23274898›Full record

ArticleDiabetes2013

Electrical stimuli release ATP to increase GLUT4 translocation and glucose uptake via PI3Kγ-Akt-AS160 in skeletal muscle cells.

Cesar Osorio-Fuentealba, Ariel E Contreras-Ferrat, Francisco Altamirano, Alejandra Espinosa, Qing Li, Wenyan Niu, Sergio Lavandero, Amira Klip, Enrique Jaimovich

Open access · hybridAbstract read
In one paragraph

Article in Diabetes, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed
5.5field-weighted citation impact, top 4% 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

51 citing papers in PubMed, 119 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

9 authors at 3 institutions in 4 countries.

Cesar Osorio-FuentealbaCenter for Molecular Studies of the Cell, Biomedical Sciences Institute, Universidad de Chile, Santiago, Chile.
Ariel E Contreras-Ferrat
Francisco Altamirano
Alejandra Espinosa
Qing Li
Wenyan Niu
Sergio Lavandero
Amira Klip
Enrique Jaimovich
University of Chile · CLHospital for Sick Children · CATianjin Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Skeletal muscle glucose uptake in response to exercise is preserved in insulin-resistant conditions, but the signals involved are debated. ATP is released from skeletal muscle by contractile activity and can autocrinely signal through purinergic receptors, and we hypothesized it may influence glucose uptake. Electrical stimulation, ATP, and insulin each increased fluorescent 2-NBD-Glucose (2-NBDG) uptake in primary myotubes, but only electrical stimulation and ATP-dependent 2-NBDG uptake were inhibited by adenosine-phosphate phosphatase and by purinergic receptor blockade (suramin). Electrical stimulation transiently elevated extracellular ATP and caused Akt phosphorylation that was additive to insulin and inhibited by suramin. Exogenous ATP transiently activated Akt and, inhibiting phosphatidylinositol 3-kinase (PI3K) or Akt as well as dominant-negative Akt mutant, reduced ATP-dependent 2-NBDG uptake and Akt phosphorylation. ATP-dependent 2-NBDG uptake was also inhibited by the G protein βγ subunit-interacting peptide βark-ct and by the phosphatidylinositol 3-kinase-γ (PI3Kγ) inhibitor AS605240. ATP caused translocation of GLUT4myc-eGFP to the cell surface, mechanistically mediated by increased exocytosis involving AS160/Rab8A reduced by dominant-negative Akt or PI3Kγ kinase-dead mutants, and potentiated by myristoylated PI3Kγ. ATP stimulated 2-NBDG uptake in normal and insulin-resistant adult muscle fibers, resembling the reported effect of exercise. Hence, the ATP-induced pathway may be tapped to bypass insulin resistance.

Indexed as

Adenosine TriphosphateAnimalsAnimals, NewbornBiological TransportCell LineCells, CulturedClass Ib Phosphatidylinositol 3-KinaseElectric StimulationEnzyme InhibitorsGlucoseGlucose Transporter Type 4GTPase-Activating ProteinsHumansMaleMiceMice, Inbred C57BLAdenosine TriphosphateClass Ib Phosphatidylinositol 3-KinaseEnzyme InhibitorsGlucoseGlucose Transporter Type 4GTPase-Activating ProteinsMutant ProteinsPhosphoinositide-3 Kinase InhibitorsProto-Oncogene Proteins c-aktRecombinant Fusion ProteinsTBC1D4 protein, human

Identifiers

PMID23274898
PMCPMC3636621
OpenAlexW2163600797

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.