Evidence map›Paper›PMID 26384382›Full record

ArticleDiabetes2016

Obesity Impairs Skeletal Muscle Regeneration Through Inhibition of AMPK.

Xing Fu, Meijun Zhu, Shuming Zhang, Marc Foretz, Benoit Viollet, Min Du

Open access · bronzeAbstract read
In one paragraph

Article in Diabetes, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 99 papers.

0numbers the graph read from it
0cells of the map it votes in
99citing papers in PubMed
5.9field-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

99 citing papers in PubMed, 148 citations in OpenAlex.

  1. Trial
  2. A Myocyte-Enriched Long Non-Coding RNA NRMLncR Enhances Myogenesis in Mouse.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
  3. Deletion of Tgf-β1 From CD206Journal of cachexia, sarcopenia and muscle · 2026
    Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. bioRxiv : the preprint server for biology · 2026
    Article
  9. Article
  10. Insights into intramuscular adipose-muscle signaling in the diabetic lower extremity.Journal of clinical & translational endocrinology · 2025
    Article
  11. Article
  12. Article
  13. Article
  14. International journal of molecular sciences · 2025
    Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. Review

39 more citing papers are in PubMed but not listed here.

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 3 institutions in 2 countries.

Xing FuWashington Center for Muscle Biology, Department of Animal Sciences and Department of Pharmaceutical Sciences, Washington State University, Pullman, WA.
Meijun ZhuSchool of Food Science, Washington State University, Pullman, WA.
Shuming ZhangSchool of Food Science, Washington State University, Pullman, WA.
Marc ForetzINSERM U1016, Institut Cochin, Paris, France Université Paris Descartes, Sorbonne Paris Cité, Paris, France CNRS UMR 8104, Paris, France.
Benoit ViolletINSERM U1016, Institut Cochin, Paris, France Université Paris Descartes, Sorbonne Paris Cité, Paris, France CNRS UMR 8104, Paris, France.
Min DuWashington Center for Muscle Biology, Department of Animal Sciences and Department of Pharmaceutical Sciences, Washington State University, Pullman, WA min.du@wsu.edu.
Washington State University · USUniversité Paris Cité · FRWashington Center · US

Funding

Maternal obesity, AMPK and fetal brown adipogenesisR01HD067449 · NICHD · WASHINGTON STATE UNIVERSITY · PI MIN DU · 2010 to 2026
$4.6M
NICHD NIH HHS 1R01-HD-067449NICHD NIH HHS R01 HD067449
6 · The paper itself

Abstract

Obesity is increasing rapidly worldwide and is accompanied by many complications, including impaired muscle regeneration. The obese condition is known to inhibit AMPK activity in multiple tissues. We hypothesized that the loss of AMPK activity is a major reason for hampered muscle regeneration in obese subjects. We found that obesity inhibits AMPK activity in regenerating muscle, which was associated with impeded satellite cell activation and impaired muscle regeneration. To test the mediatory role of AMPKα1, we knocked out AMPKα1 and found that both proliferation and differentiation of satellite cells are reduced after injury and that muscle regeneration is severely impeded, reminiscent of hampered muscle regeneration seen in obese subjects. Transplanted satellite cells with AMPKα1 deficiency had severely impaired myogenic capacity in regenerating muscle fibers. We also found that attenuated muscle regeneration in obese mice is rescued by AICAR, a drug that specifically activates AMPK, but AICAR treatment failed to improve muscle regeneration in obese mice with satellite cell-specific AMPKα1 knockout, demonstrating the importance of AMPKα1 in satellite cell activation and muscle regeneration. In summary, AMPKα1 is a key mediator linking obesity and impaired muscle regeneration, providing a convenient drug target to facilitate muscle regeneration in obese populations.

Indexed as

Aminoimidazole CarboxamideAMP-Activated Protein KinasesAnimalsCell DifferentiationCell ProliferationDiet, High-FatFlow CytometryHypoglycemic AgentsImmunoblottingImmunohistochemistryMiceMice, KnockoutMuscle DevelopmentMuscle, SkeletalObesityRegenerationAICA ribonucleotideAminoimidazole CarboxamideAMP-Activated Protein KinasesHypoglycemic AgentsPrkaa1 protein, mouseRibonucleotides

Identifiers

PMID26384382
PMCPMC4686944
OpenAlexW2229640146

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.