Evidence map›Paper›PMID 31506484›Full record

ArticleScientific reports2019

Glycine administration attenuates progression of dystrophic pathology in prednisolone-treated dystrophin/utrophin null mice.

Daniel J Ham, Anastasia Gardner, Tahnee L Kennedy, Jennifer Trieu, Timur Naim, Annabel Chee, Francesca M Alves, Marissa K Caldow, Gordon S Lynch, René Koopman

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
0.8field-weighted citation impact, top 29% 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

15 citing papers in PubMed, 24 citations in OpenAlex.

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  6. A fat- and sucrose-enriched diet causes metabolic alterations in mdx mice.American journal of physiology. Regulatory, integrative and comparative physiology · 2023
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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

10 authors at 1 institution in 3 countries.

Daniel J HamCentre for Muscle Research, Department of Physiology, The University of Melbourne, Melbourne, Australia.
Anastasia GardnerCentre for Muscle Research, Department of Physiology, The University of Melbourne, Melbourne, Australia.
Tahnee L KennedyCentre for Muscle Research, Department of Physiology, The University of Melbourne, Melbourne, Australia.
Jennifer TrieuCentre for Muscle Research, Department of Physiology, The University of Melbourne, Melbourne, Australia.
Timur NaimCentre for Muscle Research, Department of Physiology, The University of Melbourne, Melbourne, Australia.
Annabel CheeCentre for Muscle Research, Department of Physiology, The University of Melbourne, Melbourne, Australia.
Francesca M AlvesCentre for Muscle Research, Department of Physiology, The University of Melbourne, Melbourne, Australia.
Marissa K CaldowCentre for Muscle Research, Department of Physiology, The University of Melbourne, Melbourne, Australia.
Gordon S LynchCentre for Muscle Research, Department of Physiology, The University of Melbourne, Melbourne, Australia.ORCID http://orcid.org/0000-0001-9220-9810
René KoopmanCentre for Muscle Research, Department of Physiology, The University of Melbourne, Melbourne, Australia. rkoopman@unimelb.edu.au.ORCID http://orcid.org/0000-0001-5359-0284
The University of Melbourne · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Duchenne muscular dystrophy (DMD) is an X-linked genetic disease characterized by progressive muscle wasting and weakness and premature death. Glucocorticoids (e.g. prednisolone) remain the only drugs with a favorable impact on DMD patients, but not without side effects. We have demonstrated that glycine preserves muscle in various wasting models. Since glycine effectively suppresses the activity of pro-inflammatory macrophages, we investigated the potential of glycine treatment to ameliorate the dystrophic pathology. Dystrophic mdx and dystrophin-utrophin null (dko) mice were treated with glycine or L-alanine (amino acid control) for up to 15 weeks and voluntary running distance (a quality of life marker and strong correlate of lifespan in dko mice) and muscle morphology were assessed. Glycine increased voluntary running distance in mdx mice by 90% (P < 0.05) after 2 weeks and by 60% (P < 0.01) in dko mice co-treated with prednisolone over an 8 week treatment period. Glycine treatment attenuated fibrotic deposition in the diaphragm by 28% (P < 0.05) after 10 weeks in mdx mice and by 22% (P < 0.02) after 14 weeks in dko mice. Glycine treatment augmented the prednisolone-induced reduction in fibrosis in diaphragm muscles of dko mice (23%, P < 0.05) after 8 weeks. Our findings provide strong evidence that glycine supplementation may be a safe, simple and effective adjuvant for improving the efficacy of prednisolone treatment and improving the quality of life for DMD patients.

Indexed as

Disease Models, AnimalAnimalsAnti-Inflammatory AgentsGlycineGlycine AgentsMaleMiceMice, Inbred C57BLMice, Inbred mdxMice, KnockoutMuscular Dystrophy, AnimalMuscular Dystrophy, DuchennePrednisoloneAnti-Inflammatory AgentsGlycineGlycine AgentsPrednisolone

Identifiers

PMID31506484
PMCPMC6736947
OpenAlexW2972722461

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.