Evidence map›Paper›PMID 16916907›Full record

ArticleThe Journal of physiology2006

Akt signalling through GSK-3beta, mTOR and Foxo1 is involved in human skeletal muscle hypertrophy and atrophy.

Bertrand Léger, Romain Cartoni, Manu Praz, Séverine Lamon, Olivier Dériaz, Antoinette Crettenand, Charles Gobelet, Paul Rohmer, Michel Konzelmann, François Luthi and 1 more

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in The Journal of physiology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 157 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
157citing papers in PubMed, 4 pooled it
5.8field-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

157 citing papers in PubMed, 4 syntheses or guidelines pooled it, 377 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Pooled it
  5. Trial
  6. Trial
  7. Trial
  8. Countering disuse atrophy in older adults with low-volume leucine supplementation.Journal of applied physiology (Bethesda, Md. : 1985) · 2020
    Trial
  9. Trial
  10. Trial
  11. Trial
  12. Trial
  13. Trial
  14. Trial
  15. Trial
  16. Article
  17. Review
  18. Article
  19. Article
  20. Article

97 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

11 authors at 2 institutions in 1 country.

Bertrand LégerSchool of Exercise and Nutrition Sciences, Deakin University, 221 Burwood Highway 3125, Australia.
Romain Cartoni
Manu Praz
Séverine Lamon
Olivier Dériaz
Antoinette Crettenand
Charles Gobelet
Paul Rohmer
Michel Konzelmann
François Luthi
Aaron P Russell
Clinique Romande de Réadaptation · CHHôpital de Sion · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Skeletal muscle size is tightly regulated by the synergy between anabolic and catabolic signalling pathways which, in humans, have not been well characterized. Akt has been suggested to play a pivotal role in the regulation of skeletal muscle hypertrophy and atrophy in rodents and cells. Here we measured the amount of phospho-Akt and several of its downstream anabolic targets (glycogen synthase kinase-3beta (GSK-3beta), mTOR, p70(s6k) and 4E-BP1) and catabolic targets (Foxo1, Foxo3, atrogin-1 and MuRF1). All measurements were performed in human quadriceps muscle biopsies taken after 8 weeks of both hypertrophy-stimulating resistance training and atrophy-stimulating de-training. Following resistance training a muscle hypertrophy ( approximately 10%) and an increase in phospho-Akt, phospho-GSK-3beta and phospho-mTOR protein content were observed. This was paralleled by a decrease in Foxo1 nuclear protein content. Following the de-training period a muscle atrophy (5%), relative to the post-training muscle size, a decrease in phospho-Akt and GSK-3beta and an increase in Foxo1 were observed. Atrogin-1 and MuRF1 increased after the hypertrophy and decreased after the atrophy phases. We demonstrate, for the first time in human skeletal muscle, that the regulation of Akt and its downstream signalling pathways GSK-3beta, mTOR and Foxo1 are associated with both the skeletal muscle hypertrophy and atrophy processes.

Indexed as

Adaptor Proteins, Signal TransducingAdultAtrophyCell Cycle ProteinsForkhead Box Protein O1Forkhead Box Protein O3Forkhead Transcription FactorsGene Expression RegulationGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaHumansHypertrophyMaleMuscle ProteinsMuscle, SkeletalPhosphoproteinsAdaptor Proteins, Signal TransducingCell Cycle ProteinsEIF4EBP1 protein, humanFBXO32 protein, humanForkhead Box Protein O1Forkhead Box Protein O3Forkhead Transcription FactorsFOXO1 protein, humanFOXO3 protein, humanGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaGSK3B protein, humanMTOR protein, humanMuscle ProteinsPhosphoproteinsProtein KinasesProto-Oncogene Proteins c-aktRibosomal Protein S6 Kinases, 70-kDaRNA, MessengerSKP Cullin F-Box Protein LigasesTOR Serine-Threonine KinasesTRIM63 protein, humanTripartite Motif ProteinsUbiquitin-Protein Ligases

Identifiers

PMID16916907
PMCPMC1890416
OpenAlexW2160030455

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.