Evidence map›Paper›PMID 38124345›Full record

ArticleJournal of cachexia, sarcopenia and muscle2024

Effect of insulin insufficiency on ultrastructure and function in skeletal muscle.

Chantal Kopecky, Michael Haug, Barbara Reischl, Nandan Deshpande, Bikash Manandhar, Thomas W King, Victoria Lee, Marc R Wilkins, Margaret Morris, Patsie Polly and 3 more

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

Article in Journal of cachexia, sarcopenia and muscle, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
1.4field-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

4 citing papers in PubMed, 8 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

13 authors at 3 institutions in 2 countries.

Chantal KopeckySchool of Biomedical Sciences, Faculty of Medicine & Health, UNSW Sydney, Sydney, Australia.
Michael HaugDepartment of Chemical and Biological Engineering, Institute of Medical Biotechnology, Friedrich-Alexander University Erlangen-Nürnberg, Erlangen, Germany.
Barbara ReischlDepartment of Chemical and Biological Engineering, Institute of Medical Biotechnology, Friedrich-Alexander University Erlangen-Nürnberg, Erlangen, Germany.
Nandan DeshpandeSydney Informatics Hub, University of Sydney, Sydney, Australia.
Bikash ManandharSchool of Biomedical Sciences, Faculty of Medicine & Health, UNSW Sydney, Sydney, Australia.
Thomas W KingSchool of Biomedical Sciences, Faculty of Medicine & Health, UNSW Sydney, Sydney, Australia.
Victoria LeeSchool of Biomedical Sciences, Faculty of Medicine & Health, UNSW Sydney, Sydney, Australia.
Marc R WilkinsSystems Biology Initiative, Faculty of Science, UNSW Sydney, Sydney, Australia.
Margaret MorrisSchool of Biomedical Sciences, Faculty of Medicine & Health, UNSW Sydney, Sydney, Australia.
Patsie PollySchool of Biomedical Sciences, Faculty of Medicine & Health, UNSW Sydney, Sydney, Australia.
Oliver FriedrichSchool of Biomedical Sciences, Faculty of Medicine & Health, UNSW Sydney, Sydney, Australia.
Kerry-Anne RyeSchool of Biomedical Sciences, Faculty of Medicine & Health, UNSW Sydney, Sydney, Australia.
Blake J CochranSchool of Biomedical Sciences, Faculty of Medicine & Health, UNSW Sydney, Sydney, Australia.ORCID 0000-0002-9615-7939
UNSW Sydney · AUFriedrich-Alexander-Universität Erlangen-Nürnberg · DEThe University of Sydney · AU

Funding

DAAD - Universities Australia Co-operation Scheme 57443180
6 · The paper itself

Abstract

backgroundDecreased insulin availability and high blood glucose levels, the hallmark features of poorly controlled diabetes, drive disease progression and are associated with decreased skeletal muscle mass. We have shown that mice with β-cell dysfunction and normal insulin sensitivity have decreased skeletal muscle mass. This project asks how insulin deficiency impacts on the structure and function of the remaining skeletal muscle in these animals.

methodsSkeletal muscle function was determined by measuring exercise capacity and specific muscle strength prior to and after insulin supplementation for 28 days in 12-week-old mice with conditional β-cell deletion of the ATP binding cassette transporters ABCA1 and ABCG1 (β-DKO mice). Abca1 and Abcg1 floxed (fl/fl) mice were used as controls. RNAseq was used to quantify changes in transcripts in soleus and extensor digitorum longus muscles. Skeletal muscle and mitochondrial morphology were assessed by transmission electron microscopy. Myofibrillar Ca

resultsRNA transcripts were significantly altered in β-DKO mice compared with fl/fl controls (32 in extensor digitorum longus and 412 in soleus). Exercise capacity and muscle strength were significantly decreased in β-DKO mice compared with fl/fl controls (P = 0.012), and a loss of structural integrity was also observed in skeletal muscle from the β-DKO mice. Supplementation of β-DKO mice with insulin restored muscle integrity, strength and expression of 13 and 16 of the dysregulated transcripts in and extensor digitorum longus and soleus muscles, respectively.

conclusionsInsulin insufficiency due to β-cell dysfunction perturbs the structure and function of skeletal muscle. These adverse effects are rectified by insulin supplementation.

Indexed as

InsulinMuscle, SkeletalAnimalsMiceMitochondriaMuscle Fibers, SkeletalInsulinInsulinMuscle functionMuscle structureSkeletal muscle

Identifiers

PMID38124345
PMCPMC10834341
OpenAlexW4390055289

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.