Evidence map›Paper›PMID 25547587›Full record

ArticleJournal of negative results in biomedicine2014

Skeletal muscle atrophy in sedentary Zucker obese rats is not caused by calpain-mediated muscle damage or lipid peroxidation induced by oxidative stress.

Nancy Pompeani, Emma Rybalka, Heidy Latchman, Robyn M Murphy, Kevin Croft, Alan Hayes

Open access · hybridAbstract read
In one paragraph

Article in Journal of negative results in biomedicine, 2014. 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
1.1field-weighted citation impact, top 25% 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, 17 citations in OpenAlex.

  1. Article
  2. Review
  3. Genome Editing to Abrogate Muscle Atrophy.Advances in experimental medicine and biology · 2023
    Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
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 1 country.

Nancy PompeaniCentre for Chronic Disease, College of Health and Biomedicine, Victoria University, Melbourne, Australia. nancycapitanio@hotmail.com.
Emma RybalkaCentre for Chronic Disease, College of Health and Biomedicine, Victoria University, Melbourne, Australia. emma.rybalka@vu.edu.au.
Heidy LatchmanDepartment of Zoology, La Trobe University, Melbourne, Australia. H.Latchman@latrobe.edu.au.
Robyn M MurphyDepartment of Zoology, La Trobe University, Melbourne, Australia. R.Murphy@latrobe.edu.au.
Kevin CroftSchool of Medicine and Pharmacology, University of Western Australia, Perth, Australia. kevin.croft@uwa.edu.au.
Alan HayesCentre for Chronic Disease, College of Health and Biomedicine, Victoria University, Melbourne, Australia. alan.hayes@vu.edu.au.
Victoria University · AULa Trobe University · AUUniversity of Western Australia · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundSkeletal muscle undergoes significant atrophy in Type 2 diabetic patients and animal models. We aimed to determine if atrophy of Zucker rat skeletal muscle was due to the activation of intracellular damage pathways induced by excess reactive oxygen species production (specifically those associated with the peroxidation of lipid membranes) and calpain activity. 14 week old obese Zucker rats and littermate lean controls were injected with 1% Evan's Blue Dye. Animals were anaesthetised and extensor digitorum longus and soleus muscles were dissected, snap frozen and analysed for ROS-mediated F2-isoprostane production and calpain activation/autolysis. Contralateral muscles were histologically analysed for markers of muscle membrane permeability and atrophy.

resultsMuscle mass was lower in extensor digitorum longus and soleus of obese compared with lean animals, concomitant with reduced fibre area. Muscles from obese rats had a higher proportional area of Evan's Blue Dye fluorescence, albeit this was localised to the interstitium/external sarcolemma. There were no differences in F2-isoprostane production when expressed relative to arachidonic acid content, which was lower in the obese EDL and soleus muscles. There were no differences in the activation of either μ-calpain or calpain-3.

conclusionsThis study highlights that atrophy of Zucker rat skeletal muscle is not related to sarcolemmal damage, sustained hyperactivation of the calpain proteases or excessive lipid peroxidation. As such, establishing the correct pathways involved in atrophy is highly important so as to develop more specific treatment options that target the underlying cause. This study has eliminated two of the potential pathways theorised to be responsible.

Indexed as

AnimalsBlood GlucoseBody WeightCalpainLipid PeroxidationMaleMuscle, SkeletalMuscular AtrophyObesityOxidative StressRatsRats, ZuckerBlood GlucoseCalpain

Identifiers

PMID25547587
PMCPMC4296544
OpenAlexW2123773654

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.