Evidence map›Paper›PMID 23766505›Full record

ArticleJournal of applied physiology (Bethesda, Md. : 1985)2013

Skeletal muscle signaling associated with impaired glucose tolerance in spinal cord-injured men and the effects of contractile activity.

Ceren Yarar-Fisher, C Scott Bickel, Samuel T Windham, Amie B McLain, Marcas M Bamman

Open access · greenAbstract read
In one paragraph

Article in Journal of applied physiology (Bethesda, Md. : 1985), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed, 1 pooled it
1.1field-weighted citation impact, top 23% 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

29 citing papers in PubMed, 1 synthesis or guideline pooled it, 41 citations in OpenAlex.

  1. Pooled it
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  13. Mechanisms of exercise as a preventative measure to muscle wasting.American journal of physiology. Cell physiology · 2021
    Review
  14. Article
  15. Review
  16. Exercise Interventions Targeting Obesity in Persons With Spinal Cord Injury.Topics in spinal cord injury rehabilitation · 2021
    Review
  17. Review
  18. Review
  19. Article
  20. 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 2 institutions in 1 country.

Ceren Yarar-FisherDepartment of Cell, Developmental, and Integrative Biology, University of Alabama at Birmingham, Birmingham, Alabama;
C Scott Bickel
Samuel T Windham
Amie B McLain
Marcas M Bamman
University of Alabama at Birmingham · USBirmingham VA Medical Center · US

Funding

University of Alabama at Birmingham's Diabetes Research CenterP30DK079626 · NIDDK · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI Kirk Michael Habegger · 2013 to 2026
$19.5M
UAB Center for Clinical and Translational Science (CCTS) UL1UL1TR000165 · NCATS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI KIMBERLY, ROBERT P. · 2012 to 2013
$9.6M
UAB Obesity Training ProgramT32DK062710 · NIDDK · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI James O Hill, Brooks C Wingo · 2004 to 2026
$5.5M
NIDDK NIH HHS 5T32 DK-62710NIDDK NIH HHS P30 DK079626
6 · The paper itself

Abstract

The mechanisms underlying poor glucose tolerance in persons with spinal cord injury (SCI), along with its improvement after several weeks of neuromuscular electrical stimulation-induced resistance exercise (NMES-RE) training, remain unclear, but presumably involve the affected skeletal musculature. We, therefore, investigated skeletal muscle signaling pathways associated with glucose transporter 4 (GLUT-4) translocation at rest and shortly after a single bout of NMES-RE in SCI (n = 12) vs. able-bodied (AB, n = 12) men. Subjects completed an oral glucose tolerance test during visit 1 and ≈90 NMES-RE isometric contractions of the quadriceps during visit 2. Muscle biopsies were collected before, and 10 and 60 min after, NMES-RE. We assessed transcript levels of GLUT-4 by quantitative PCR and protein levels of GLUT-4 and phosphorylated- and total AMP-activated protein kinase (AMPK)-α, CaMKII, Akt, and AS160 by immunoblotting. Impaired glucose tolerance in SCI was confirmed by higher (P < 0.05) plasma glucose concentrations than AB at all time points after glucose ingestion, despite equivalent insulin responses to the glucose load. GLUT-4 protein content was lower (P < 0.05) in SCI vs. AB at baseline. Main group effects revealed higher phosphorylation in SCI of AMPK-α, CaMKII, and Akt (P < 0.05), and Akt phosphorylation increased robustly (P < 0.05) following NMES-RE in SCI only. In SCI, low skeletal muscle GLUT-4 protein concentration may, in part, explain poor glucose tolerance, whereas heightened phosphorylation of relevant signaling proteins (AMPK-α, CaMKII) suggests a compensatory effort. Finally, it is encouraging to find (based on Akt) that SCI muscle remains both sensitive and responsive to mechanical loading (NMES-RE) even ≈22 yr after injury.

Indexed as

AdultAMP-Activated Protein KinasesBlood GlucoseCalcium-Calmodulin-Dependent Protein Kinase Type 2Electric Stimulation TherapyGlucoseGlucose IntoleranceGlucose Tolerance TestGlucose Transporter Type 4HumansInsulinMaleMiddle AgedMuscle ContractionPhosphorylationProto-Oncogene Proteins c-aktAMP-Activated Protein KinasesBlood GlucoseCalcium-Calmodulin-Dependent Protein Kinase Type 2GlucoseGlucose Transporter Type 4InsulinProto-Oncogene Proteins c-aktglucose uptake signalingneuromuscular electrical stimulationresistance exerciseskeletal musclespinal cord injury

Identifiers

PMID23766505
PMCPMC4073980
OpenAlexW2063532952

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.