Evidence map›Paper›PMID 30206270›Full record

ArticleScientific reports2018

Integrative effects of dystrophin loss on metabolic function of the mdx mouse.

Jana Strakova, Forum Kamdar, Debra Kulhanek, Maria Razzoli, Daniel J Garry, James M Ervasti, Alessandro Bartolomucci, DeWayne Townsend

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.7field-weighted citation impact, top 9% 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

25 citing papers in PubMed, 46 citations in OpenAlex.

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  8. Aging reveals a sex-dependent susceptibility of sarcospan-deficient mice to cardiometabolic disease.American journal of physiology. Heart and circulatory physiology · 2024
    Article
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  11. Review
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  15. Science advances · 2022
    Article
  16. Article
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  18. Reducing sarcolipin expression improves muscle metabolism inAmerican journal of physiology. Cell physiology · 2022
    Article
  19. Review
  20. 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

8 authors at 1 institution in 1 country.

Jana StrakovaDepartment of Integrative Biology and Physiology, Medical School, University of Minnesota, Minneapolis, MN, USA.
Forum KamdarDepartment of Medicine, Cardiovascular Division, Medical School, University of Minnesota, Minneapolis, MN, USA.
Debra KulhanekDepartment of Medicine, Cardiovascular Division, Medical School, University of Minnesota, Minneapolis, MN, USA.
Maria RazzoliDepartment of Integrative Biology and Physiology, Medical School, University of Minnesota, Minneapolis, MN, USA.
Daniel J GarryDepartment of Medicine, Cardiovascular Division, Medical School, University of Minnesota, Minneapolis, MN, USA.
James M ErvastiDepartment of Biochemistry, Molecular Biology, and Biophysics, Medical School, University of Minnesota, Minneapolis, MN, USA.
Alessandro BartolomucciDepartment of Integrative Biology and Physiology, Medical School, University of Minnesota, Minneapolis, MN, USA.
DeWayne TownsendDepartment of Integrative Biology and Physiology, Medical School, University of Minnesota, Minneapolis, MN, USA. town0045@umn.edu.
University of Minnesota Medical Center · US

Funding

CYTOSKELETAL INTERACTIONS OF DYSTROPHINR01AR042423 · NIAMS · UNIVERSITY OF WISCONSIN MADISON · PI ERVASTI, JAMES M · 1994 to 2025
$9.3M
Improving dystrophin gene therapy through understanding dystrobrevin functionR01HL114832 · NHLBI · UNIVERSITY OF MINNESOTA · PI TOWNSEND, DEWAYNE · 2013 to 2017
$1.8M
Molecular dissection of TLQP-21 peptide functions in obesityR01DK102496 · NIDDK · UNIVERSITY OF MINNESOTA · PI BARTOLOMUCCI, ALESSANDRO · 2014 to 2018
$1.7M
Coronary Regulation in Dystrophic CardiomyopathyK08HL102066 · NHLBI · UNIVERSITY OF MINNESOTA · PI TOWNSEND, DEWAYNE · 2010 to 2014
$641k
Muscular Dystrophy Association (Muscular Dystrophy Association Inc.) 351960NHLBI NIH HHS K08 HL102066NHLBI NIH HHS R01 HL114832NIAMS NIH HHS R01 AR042423NIDDK NIH HHS R01 DK102496
6 · The paper itself

Abstract

Duchenne muscular dystrophy (DMD) is a disease marked by the development of skeletal muscle weakness and wasting. DMD results from mutations in the gene for the cytoskeletal protein dystrophin. The loss of dystrophin expression is not limited to muscle weakness but has multiple systemic consequences. Managing the nutritional requirements is an important aspect of the clinical care of DMD patients and is complicated by the poor understanding of the role of dystrophin, and dystrophic processes, in regulating metabolism. Here, we show that mdx mice, a genetic model of DMD, have significantly reduced fat mass relative to wild type C57BL/10. The alteration in body composition is independent of the presence of skeletal muscle disease, as it is still present in mice with transgenic expression of a fully-functional dystrophin in skeletal muscle. Furthermore, mdx mice do not increase their fat mass or body weight when housed under thermoneutral conditions, in marked contrast to C57BL/10 mice. We also demonstrated that mdx mice have significantly reduced fat metabolism and altered glucose uptake. These significant metabolic changes in dystrophic mice implicate dystrophin as an important regulator of metabolism. Understanding the metabolic functions of dystrophin is important for managing the nutritional needs of DMD patients.

Indexed as

AnimalsBody CompositionDisease Models, AnimalDystrophinGene Expression RegulationGlucoseHumansMiceMice, Inbred mdxMice, TransgenicMuscle ContractionMuscle, SkeletalMuscular Dystrophy, AnimalMuscular Dystrophy, DuchenneMutationDystrophinGlucose

Identifiers

PMID30206270
PMCPMC6134145
OpenAlexW2892051905

What OpenQuestion holds

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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.