Evidence map›Paper›PMID 29066728›Full record

ArticleScientific reports2017

Ghrelin rescues skeletal muscle catabolic profile in the R6/2 mouse model of Huntington's disease.

Marie Sjögren, Ana I Duarte, Andrew C McCourt, Liliya Shcherbina, Nils Wierup, Maria Björkqvist

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.8field-weighted citation impact, top 32% 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

12 citing papers in PubMed, 21 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Review
  5. Review
  6. Review
  7. Rehabilitation outcomes in Huntington disease patients with low body mass index.Journal of musculoskeletal & neuronal interactions · 2022
    Article
  8. Article
  9. Molecular Mechanisms Underlying Muscle Wasting in Huntington's Disease.International journal of molecular sciences · 2020
    Review
  10. Article
  11. Review
  12. 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 1 institution in 2 countries.

Marie SjögrenWallenberg Neuroscience Center, Department of Experimental Medical Sciences, Brain Disease Biomarker Unit, Lund University, Lund, Sweden. marie.sjogren@med.lu.se.
Ana I DuarteWallenberg Neuroscience Center, Department of Experimental Medical Sciences, Brain Disease Biomarker Unit, Lund University, Lund, Sweden.
Andrew C McCourtWallenberg Neuroscience Center, Department of Experimental Medical Sciences, Brain Disease Biomarker Unit, Lund University, Lund, Sweden.
Liliya ShcherbinaLund University Diabetes Centre, Neuroendocrine Cell Biology, Department of Clinical Sciences in Malmö, Clinical research center, Lund University, Malmö, Sweden.
Nils WierupLund University Diabetes Centre, Neuroendocrine Cell Biology, Department of Clinical Sciences in Malmö, Clinical research center, Lund University, Malmö, Sweden.
Maria BjörkqvistWallenberg Neuroscience Center, Department of Experimental Medical Sciences, Brain Disease Biomarker Unit, Lund University, Lund, Sweden.
Lund University · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Accumulating evidence suggests altered energy metabolism as a key feature in Huntington's disease (HD) pathology. Hyper-catabolism, including weight loss and muscle atrophy, is seen in HD patients and HD mouse models. Metabolic hormones are key players, not only in energy metabolism, but also in neurodegenerative processes. Ghrelin, a gut peptide-hormone, plays an important role in regulating energy metabolism, stimulating appetite, and affects brain function and increases neuronal survival. The R6/2 mouse model of HD has previously been shown to exhibit progressive weight loss, dysregulated glucose metabolism, skeletal muscle atrophy and altered body composition. In this study, we targeted energy metabolism in R6/2 mice using ghrelin administration, with the primary aim to delay weight loss and reduce muscle atrophy. We also evaluated glucose metabolism and behaviour. We here demonstrate that ghrelin administration (subcutaneous 150 μg/kg daily injections) for 4 weeks, reversed the catabolic gene expression profile (increased expression of Caspase 8, Traf-5 and Creb1) seen in R6/2 mouse skeletal muscle. Skeletal muscle morphology was also improved with ghrelin, and importantly, ghrelin administration normalized behavioural deficits in R6/2 mice. Taken together, our findings encourage further studies targeting metabolism in HD.

Indexed as

Adipose Tissue, WhiteAnimalsBiomarkersDisease Models, AnimalFatty AcidsGhrelinGlucoseHomeostasisHumansHuntington DiseaseLiverMaleMiceMuscle, SkeletalMuscular AtrophyNesting BehaviorBiomarkersFatty AcidsGhrelinGlucose

Identifiers

PMID29066728
PMCPMC5654969
OpenAlexW2766437384

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.