Evidence map›Paper›PMID 29968251›Full record

ReviewThe Journal of physiology2019

The impact of immobilisation and inflammation on the regulation of muscle mass and insulin resistance: different routes to similar end-points.

Hannah Crossland, Sarah Skirrow, Zudin A Puthucheary, Dumitru Constantin-Teodosiu, Paul L Greenhaff

Open access · hybridAbstract readReview
In one paragraph

Review in The Journal of physiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed, 1 pooled it
2.9field-weighted citation impact, top 8% 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

42 citing papers in PubMed, 1 synthesis or guideline pooled it, 75 citations in OpenAlex.

  1. Pooled it
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  7. MuRF1 Partners With TRIM72 to Impair Insulin Signaling in Skeletal Muscle Cells.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
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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

5 authors at 2 institutions in 1 country.

Hannah CrosslandMRC/Arthritis Research UK Centre for Musculoskeletal Ageing Research, Arthritis Research UK Centre for Sport, Exercise and Osteoarthritis, National Institute for Health Research Nottingham Biomedical Research Centre, School of Life Sciences, University of Nottingham, UK.
Sarah SkirrowMRC/Arthritis Research UK Centre for Musculoskeletal Ageing Research, Arthritis Research UK Centre for Sport, Exercise and Osteoarthritis, National Institute for Health Research Nottingham Biomedical Research Centre, School of Life Sciences, University of Nottingham, UK.
Zudin A PuthuchearyInstitute of Sport, Exercise and Health, London, UK.
Dumitru Constantin-TeodosiuMRC/Arthritis Research UK Centre for Musculoskeletal Ageing Research, Arthritis Research UK Centre for Sport, Exercise and Osteoarthritis, National Institute for Health Research Nottingham Biomedical Research Centre, School of Life Sciences, University of Nottingham, UK.ORCID 0000-0002-8448-5564
Paul L GreenhaffMRC/Arthritis Research UK Centre for Musculoskeletal Ageing Research, Arthritis Research UK Centre for Sport, Exercise and Osteoarthritis, National Institute for Health Research Nottingham Biomedical Research Centre, School of Life Sciences, University of Nottingham, UK.ORCID 0000-0003-4403-0490
University of Nottingham · GBEnglish Institute of Sport · GB

Funding

Arthritis Research UK 19891Arthritis Research UK 21595Medical Research Council MR/K00414X/1Medical Research Council MR/P021220/1Versus Arthritis 19891
6 · The paper itself

Abstract

Loss of muscle mass and insulin sensitivity are common phenotypic traits of immobilisation and increased inflammatory burden. The suppression of muscle protein synthesis is the primary driver of muscle mass loss in human immobilisation, and includes blunting of post-prandial increases in muscle protein synthesis. However, the mechanistic drivers of this suppression are unresolved. Immobilisation also induces limb insulin resistance in humans, which appears to be attributable to the reduction in muscle contraction per se. Again mechanistic insight is missing such that we do not know how muscle senses its "inactivity status" or whether the proposed drivers of muscle insulin resistance are simply arising as a consequence of immobilisation. A heightened inflammatory state is associated with major and rapid changes in muscle protein turnover and mass, and dampened insulin-stimulated glucose disposal and oxidation in both rodents and humans. A limited amount of research has attempted to elucidate molecular regulators of muscle mass loss and insulin resistance during increased inflammatory burden, but rarely concurrently. Nevertheless, there is evidence that Akt (protein kinase B) signalling and FOXO transcription factors form part of a common signalling pathway in this scenario, such that molecular cross-talk between atrophy and insulin signalling during heightened inflammation is believed to be possible. To conclude, whilst muscle mass loss and insulin resistance are common end-points of immobilisation and increased inflammatory burden, a lack of understanding of the mechanisms responsible for these traits exists such that a substantial gap in understanding of the pathophysiology in humans endures.

Indexed as

Bed RestInsulin ResistanceAnimalsHumansInflammationMuscle ProteinsMuscle, SkeletalMuscle Proteinsbed-restcarbohydrate metabolisminactivitymuscle atrophymuscle fuel selectionmuscle protein breakdownmuscle protein synthesis

Identifiers

PMID29968251
PMCPMC6395472
OpenAlexW2889606947

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.