Evidence map›Paper›PMID 27550988›Full record

ArticlePhysiological reports2016

Acute resistance exercise-induced IGF1 expression and subsequent GLUT4 translocation.

Kohei Kido, Satoru Ato, Takumi Yokokawa, Yuhei Makanae, Koji Sato, Satoshi Fujita

Open access · goldAbstract read
In one paragraph

Article in Physiological reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
4.2field-weighted citation impact, top 6% 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

32 citing papers in PubMed, 61 citations in OpenAlex.

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  8. Exercise: a non-drug strategy of NK cell activation.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2024
    Review
  9. βFrontiers in physiology · 2024
    Article
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  20. The Effects of Exogenous Lactate Administration on the IGF1/Akt/mTOR Pathway in Rat Skeletal Muscle.International journal of environmental research and public health · 2020
    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

6 authors at 4 institutions in 1 country.

Kohei KidoFaculty of Sport and Health Science, Ritsumeikan University, Kusatsu, Japan.
Satoru AtoFaculty of Sport and Health Science, Ritsumeikan University, Kusatsu, Japan.
Takumi YokokawaLaboratory of Sports and Exercise Medicine, Graduate School of Human and Environmental Studies, Kyoto University, Kyoto, Japan.
Yuhei MakanaeDepartment of Physical Education, National Defense Academy, Yokosuka, Japan.
Koji SatoGraduate School of Human Development and Environment, Kobe University, Kobe, Japan.
Satoshi FujitaFaculty of Sport and Health Science, Ritsumeikan University, Kusatsu, Japan safujita@fc.ritsumei.ac.jp.
Ritsumeikan University · JPKobe University · JPKyoto University · JPNational Defense Academy of Japan · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Acute aerobic exercise (AE) is a major physiological stimulus for skeletal muscle glucose uptake through activation of 5' AMP-activated protein kinase (AMPK). However, the regulation of glucose uptake by acute resistance exercise (RE) remains unclear. To investigate the intracellular regulation of glucose uptake after acute RE versus acute AE, male Sprague-Dawley rats were divided into three groups: RE, AE, or nonexercise control. After fasting for 12 h overnight, the right gastrocnemius muscle in the RE group was exercised at maximum isometric contraction via percutaneous electrical stimulation (3 × 10 sec, 5 sets). The AE group ran on a treadmill (25 m/min, 60 min). Muscle samples were taken 0, 1, and 3 h after completion of the exercises. AMPK, Ca(2+)/calmodulin-dependent protein kinase II, and TBC1D1 phosphorylation were increased immediately after both forms of exercise and returned to baseline levels by 3 h. Muscle IGF1 expression was increased by RE but not AE, and maintained until 3 h after RE Additionally, Akt and AS160 phosphorylation were sustained for 3 h after RE, whereas they returned to baseline levels by 3 h after AE Similarly, GLUT4 translocation remained elevated 3 h after RE, although it returned to the baseline level by 3 h after AE Overall, this study showed that AMPK/TBC1D1 and IGF1/Akt/AS160 signaling were enhanced by acute RE, and that GLUT4 translocation after acute RE was more prolonged than after acute AE These results suggest that acute RE-induced increases in intramuscular IGF1 expression might be a distinct regulator of GLUT4 translocation.

Indexed as

Abnormalities, MultipleAMP-Activated Protein KinasesAnimalsCalcium-Calmodulin-Dependent Protein Kinase Type 2GlucoseGlucose Transporter Type 4Growth DisordersGTPase-Activating ProteinsInsulin-Like Growth Factor IMaleMuscle, SkeletalPhosphorylationPhysical Conditioning, AnimalProteinsProtein Translocation SystemsRatsAMP-Activated Protein KinasesCalcium-Calmodulin-Dependent Protein Kinase Type 2GlucoseGlucose Transporter Type 4GTPase-Activating Proteinsinsulin-like growth factor-1, ratInsulin-Like Growth Factor IProteinsProtein Translocation SystemsTBC1D1 protein, ratTBC1D4 protein, ratAerobic exerciseglucose transporter type 4insulin‐like growth factor 1resistance exercise

Identifiers

PMID27550988
PMCPMC5002915
OpenAlexW2507620686

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Registered trials

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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.