Evidence map›Paper›PMID 28270443›Full record

ArticleAmerican journal of physiology. Endocrinology and metabolism2017

Skeletal muscle PGC-1β signaling is sufficient to drive an endurance exercise phenotype and to counteract components of detraining in mice.

Samuel Lee, Teresa C Leone, Lisa Rogosa, John Rumsey, Julio Ayala, Paul M Coen, Robert H Fitts, Rick B Vega, Daniel P Kelly

Open access · bronzeAbstract read
In one paragraph

Article in American journal of physiology. Endocrinology and metabolism, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.6field-weighted citation impact, top 18% 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

10 citing papers in PubMed, 16 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Article
  5. Combined effects ofFrontiers in nutrition · 2024
    Article
  6. Article
  7. Article
  8. Impaired Mitochondrial Energetics Characterize Poor Early Recovery of Muscle Mass Following Hind Limb Unloading in Old Mice.The journals of gerontology. Series A, Biological sciences and medical sciences · 2018
    Article
  9. Article
  10. Modulating Metabolism to Improve Cancer-Induced Muscle Wasting.Oxidative medicine and cellular longevity · 2018
    Review
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 1 country.

Samuel LeeCenter for Metabolic Origins of Disease, Sanford Burnham Prebys Medical Discovery Institute, Orlando, Florida.
Teresa C LeoneCenter for Metabolic Origins of Disease, Sanford Burnham Prebys Medical Discovery Institute, Orlando, Florida.
Lisa RogosaCenter for Metabolic Origins of Disease, Sanford Burnham Prebys Medical Discovery Institute, Orlando, Florida.
John RumseyCenter for Metabolic Origins of Disease, Sanford Burnham Prebys Medical Discovery Institute, Orlando, Florida.
Julio AyalaCenter for Metabolic Origins of Disease, Sanford Burnham Prebys Medical Discovery Institute, Orlando, Florida.
Paul M CoenCenter for Metabolic Origins of Disease, Sanford Burnham Prebys Medical Discovery Institute, Orlando, Florida.
Robert H FittsDepartment of Biological Sciences, Marquette University, Milwaukee, Wisconsin.
Rick B VegaCenter for Metabolic Origins of Disease, Sanford Burnham Prebys Medical Discovery Institute, Orlando, Florida.
Daniel P KellyCenter for Metabolic Origins of Disease, Sanford Burnham Prebys Medical Discovery Institute, Orlando, Florida; dkelly@sbpdiscovery.org.
Sanford Burnham Prebys Medical Discovery Institute · USDiscovery Institute · USMarquette University · USTranslational Research Institute for Metabolism and Diabetes · US

Funding

Molecular Control of Muscle Fuel MetabolismR01DK045416 · NIDDK · WASHINGTON UNIVERSITY · PI KELLY, DANIEL PATRICK · 1996 to 2020
$8.1M
Ceramide Mediated Oxidative Stress in Muscle Loss with Aging and DisuseK01AG044437 · NIA · ADVENTHEALTH ORLANDO · PI COEN, PAUL MARTIN · 2013 to 2016
$508k
NIA NIH HHS K01 AG044437NIDDK NIH HHS R01 DK045416
6 · The paper itself

Abstract

Peroxisome proliferator-activated receptor-γ coactivator (PGC)-1α and -1β serve as master transcriptional regulators of muscle mitochondrial functional capacity and are capable of enhancing muscle endurance when overexpressed in mice. We sought to determine whether muscle-specific transgenic overexpression of PGC-1β affects the detraining response following endurance training. First, we established and validated a mouse exercise-training-detraining protocol. Second, using multiple physiological and gene expression end points, we found that PGC-1β overexpression in skeletal muscle of sedentary mice fully recapitulated the training response. Lastly, PGC-1β overexpression during the detraining period resulted in partial prevention of the detraining response. Specifically, an increase in the plateau at which O

Indexed as

AnimalsMaleMiceMice, TransgenicMuscle, SkeletalMuscular Disorders, AtrophicPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaPhenotypePhysical Conditioning, AnimalPhysical EndurancePhysical FitnessRunningPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaPpargc1a protein, mouseendurance exercisemuscle detrainingPGC-1skeletal muscle

Identifiers

PMID28270443
PMCPMC5451529
OpenAlexW2594928284

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.