Evidence map›Paper›PMID 32121211›Full record

ArticleNutrients2020

Exercise Training-Induced PPARβ Increases PGC-1α Protein Stability and Improves Insulin-Induced Glucose Uptake in Rodent Muscles.

Ju-Sik Park, John O Holloszy, Kijin Kim, Jin-Ho Koh

Open access · goldAbstract read
In one paragraph

Article in Nutrients, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
2.2field-weighted citation impact, top 12% 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

12 citing papers in PubMed, 24 citations in OpenAlex.

  1. Trial
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  4. NADInternational journal of medical sciences · 2024
    Review
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  7. Beta-hydroxy-beta-methylbutyrate associated with low-intensity exercise training improves skeletal muscle regeneration through the IGF-Akt pathway.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2022
    Article
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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

4 authors at 2 institutions in 2 countries.

Ju-Sik ParkDepartment of Taekwondo, College of Physical Education, Keimyung University, Daegu 42601, Korea.
John O HolloszyDivision of Geriatrics and Nutritional Sciences, Department of Medicine, Washington University School of Medicine, St. Louis, Missouri 63110, USA.
Kijin KimDepartment of Physical Education, College of Physical Education, Keimyung University, Daegu 42601, Korea.
Jin-Ho KohDivision of Geriatrics and Nutritional Sciences, Department of Medicine, Washington University School of Medicine, St. Louis, Missouri 63110, USA.
Keimyung University · KRWashington University in St. Louis · US

Funding

Foundation for the National Institutes of Health AG-00425National Research Foundation of Korea NRF-2019R1A2C1006334
6 · The paper itself

Abstract

This study aimed to investigate the long-term effects of training intervention and resting on protein expression and stability of peroxisome proliferator-activated receptor β/δ (PPARβ), peroxisome proliferator-activated receptor gamma coactivator 1-α (PGC1α), glucose transporter type 4 (GLUT4), and mitochondrial proteins, and determine whether glucose homeostasis can be regulated through stable expression of these proteins after training. Rats swam daily for 3, 6, 9, 14, or 28 days, and then allowed to rest for 5 days post-training. Protein and mRNA levels were measured in the skeletal muscles of these rats. PPARβ was overexpressed and knocked down in myotubes in the skeletal muscle to investigate the effects of swimming training on various signaling cascades of PGC-1α transcription, insulin signaling, and glucose uptake. Exercise training (Ext) upregulated PPARβ, PGC-1α, GLUT4, and mitochondrial enzymes, including NADH-ubiquinone oxidoreductase (NUO), cytochrome c oxidase subunit I (COX1), citrate synthase (CS), and cytochrome c (Cyto C) in a time-dependent manner and promoted the protein stability of PPARβ, PGC-1α, GLUT4, NUO, CS, and Cyto C, such that they were significantly upregulated 5 days after training cessation. PPARβ overexpression increased the PGC-1α protein levels post-translation and improved insulin-induced signaling responsiveness and glucose uptake. The present results indicate that Ext promotes the protein stability of key mitochondria enzymes GLUT4, PGC-1α, and PPARβ even after Ext cessation.

Indexed as

Physical Conditioning, AnimalAnimalsGlucoseGlucose Transporter Type 4Half-LifeInsulinMaleMiceMitochondriaMitochondrial ProteinsMuscle Fibers, SkeletalMuscle, SkeletalPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaPPAR-betaProtein BiosynthesisProtein StabilityGlucoseGlucose Transporter Type 4InsulinMitochondrial ProteinsPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaPPAR-betaexercise trainingGLUT4MitochondriaPGC-1αPPARβprotein stabilityskeletal muscle

Identifiers

PMID32121211
PMCPMC7146110
OpenAlexW3009821257

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.