Evidence map›Paper›PMID 21508135›Full record

ArticleThe Journal of clinical endocrinology and metabolism2011

Impaired muscle AMPK activation in the metabolic syndrome may attenuate improved insulin action after exercise training.

Andrew S Layne, Sami Nasrallah, Mark A South, Mary E A Howell, Melanie P McCurry, Michael W Ramsey, Michael H Stone, Charles A Stuart

Registry-linked trialOpen access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in The Journal of clinical endocrinology and metabolism, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT00727779 (Mechanisms by Which Strength Training Ameliorates the Metabolic Syndrome), which is not on this map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.7field-weighted citation impact, top 16% 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.

NCT00727779 nacompletednot on this map

Mechanisms by Which Strength Training Ameliorates the Metabolic Syndrome

TypeinterventionalSponsorEast Tennessee State UniversityRan2008 to 2013Enrolled50ConditionsMetabolic SyndromeArmsstrength training
3 · Its place in the literature

Who cites it

24 citing papers in PubMed, 43 citations in OpenAlex.

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  14. Muscle hypertrophy in prediabetic men after 16 wk of resistance training.Journal of applied physiology (Bethesda, Md. : 1985) · 2017
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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

8 authors at 2 institutions in 2 countries.

Andrew S LayneCenter of Excellence for Sport Science and Coach Education, Department of Kinesiology, Leisure, and Sports Science, Clemmer College of Education, East Tennessee State University, Johnson City, Tennessee 37614, USA.
Sami Nasrallah
Mark A South
Mary E A Howell
Melanie P McCurry
Michael W Ramsey
Michael H Stone
Charles A Stuart
East Tennessee State University · USInstitute for Sports Medicine · DE

Funding

Mechanisms by which strength training ameliorates the Metabolic SyndromeR15DK080488 · NIDDK · EAST TENNESSEE STATE UNIVERSITY · PI STUART, CHARLES A · 2008 to 2011
$607k
NIDDK NIH HHS DK080488NIDDK NIH HHS R15 DK080488
6 · The paper itself

Abstract

contextStrength training induces muscle remodeling and may improve insulin responsiveness.

objectiveThis study will quantify the impact of resistance training on insulin sensitivity in subjects with the metabolic syndrome and correlate this with activation of intramuscular pathways mediating mitochondrial biogenesis and muscle fiber hypertrophy.

designTen subjects with the metabolic syndrome (MS) and nine sedentary controls underwent 8 wk of supervised resistance exercise training with pre- and posttraining anthropometric and muscle biochemical assessments.

settingResistance exercise training took place in a sports laboratory on a college campus.

main outcome measuresPre- and posttraining insulin responsiveness was quantified using a euglycemic clamp. Changes in expression of muscle 5-AMP-activated protein kinase (AMPK) and mammalian target of rapamycin (mTOR) pathways were quantified using immunoblots.

resultsStrength and stamina increased in both groups. Insulin sensitivity increased in controls (steady-state glucose infusion rate = 7.0 ± 2.0 mg/kg · min pretraining training vs. 8.7 ± 3.1 mg/kg · min posttraining; P < 0.01) but did not improve in MS subjects (3.3 ± 1.3 pre vs. 3.1 ± 1.0 post). Muscle glucose transporter 4 increased 67% in controls and 36% in the MS subjects. Control subjects increased muscle phospho-AMPK (43%), peroxisome proliferator-activated receptor γ coactivator 1α (57%), and ATP synthase (60%), more than MS subjects (8, 28, and 21%, respectively). In contrast, muscle phospho-mTOR increased most in the MS group (57 vs. 32%).

conclusionFailure of resistance training to improve insulin responsiveness in MS subjects was coincident with diminished phosphorylation of muscle AMPK, but increased phosphorylation of mTOR, suggesting activation of the mTOR pathway could be involved in inhibition of exercise training-related increases in AMPK and its activation and downstream events.

Indexed as

Adenylate KinaseAdultAnalysis of VarianceExerciseFemaleGlucose Clamp TechniqueGlucose Transporter Type 4Glucose Transporter Type 5HumansInsulinInsulin ResistanceMaleMetabolic SyndromeMiddle AgedMitochondriaMuscle, SkeletalAdenylate KinaseGlucose Transporter Type 4Glucose Transporter Type 5InsulinSLC2A4 protein, humanSLC2A5 protein, humanTOR Serine-Threonine Kinases

Identifiers

PMID21508135
PMCPMC3100747
OpenAlexW2086957024

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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.