Evidence map›Paper›PMID 35484130›Full record

ArticleNature communications2022

Enhancement of anaerobic glycolysis - a role of PGC-1α4 in resistance exercise.

Jin-Ho Koh, Mark W Pataky, Surendra Dasari, Katherine A Klaus, Ivan Vuckovic, Gregory N Ruegsegger, Arathi Prabha Kumar, Matthew M Robinson, K Sreekumaran Nair

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed, 3 pooled it
5.4field-weighted citation impact, top 3% 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

35 citing papers in PubMed, 3 syntheses or guidelines pooled it, 47 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 4 institutions in 2 countries.

Jin-Ho Koh *Division of Endocrinology and Metabolism, Mayo Clinic, Rochester, MN, United States.
Mark W Pataky *Division of Endocrinology and Metabolism, Mayo Clinic, Rochester, MN, United States.ORCID 0000-0003-3273-7886
Surendra DasariDepartment of Health Sciences Research, Mayo Clinic, Rochester, MN, United States.
Katherine A KlausDivision of Endocrinology and Metabolism, Mayo Clinic, Rochester, MN, United States.
Ivan VuckovicMayo Clinic Regional Comprehensive Metabolomics Core, Mayo Clinic, Rochester, MN, United States.ORCID 0000-0001-7806-7238
Gregory N RuegseggerDivision of Endocrinology and Metabolism, Mayo Clinic, Rochester, MN, United States.
Arathi Prabha KumarDivision of Endocrinology and Metabolism, Mayo Clinic, Rochester, MN, United States.
Matthew M RobinsonSchool of Biological and Population Health Sciences, College of Public Health and Human Sciences, Oregon State University, Corvallis, OR, 97331, United States.
K Sreekumaran NairDivision of Endocrinology and Metabolism, Mayo Clinic, Rochester, MN, United States. nair@mayo.edu.ORCID 0000-0002-0649-9469
Mayo Clinic in Arizona · USMayo Clinic · USMayo Clinic in Florida · USOregon State University · US

Funding

Mayo Clinic Center for Translational Science ActivitiesUL1TR000135 · NCATS · MAYO CLINIC ROCHESTER · PI KHOSLA, SUNDEEP · 2012 to 2015
$41.2M
DIABETES AND METABOLISMT32DK007352 · NIDDK · MAYO CLINIC ROCHESTER · PI MICHAEL D. JENSEN · 1986 to 2026
$9.4M
Molecular Mechanisms of Exercise Benefits to Insulin Resistant PeopleR01AG062859 · NIA · MAYO CLINIC ROCHESTER · PI K Sreekumaran Nair · 2019 to 2026
$5.1M
NCATS NIH HHS UL1 TR000135NIA NIH HHS R01 AG062859NIDDK NIH HHS T32 DK007352
6 · The paper itself

Abstract

Resistance exercise training (RET) is an effective countermeasure to sarcopenia, related frailty and metabolic disorders. Here, we show that an RET-induced increase in PGC-1α4 (an isoform of the transcriptional co-activator PGC-1α) expression not only promotes muscle hypertrophy but also enhances glycolysis, providing a rapid supply of ATP for muscle contractions. In human skeletal muscle, PGC-1α4 binds to the nuclear receptor PPARβ following RET, resulting in downstream effects on the expressions of key glycolytic genes. In myotubes, we show that PGC-1α4 overexpression increases anaerobic glycolysis in a PPARβ-dependent manner and promotes muscle glucose uptake and fat oxidation. In contrast, we found that an acute resistance exercise bout activates glycolysis in an AMPK-dependent manner. These results provide a mechanistic link between RET and improved glucose metabolism, offering an important therapeutic target to counteract aging and inactivity-induced metabolic diseases benefitting those who cannot exercise due to many reasons.

Indexed as

PPAR-betaResistance TrainingAnaerobiosisGlycolysisHumansTranscription FactorsPPAR-betaTranscription Factors

Identifiers

PMID35484130
PMCPMC9050893
OpenAlexW4225153356

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.