Evidence map›Paper›PMID 30093355›Full record

ArticleMolecular metabolism2018

AMPK activation negatively regulates GDAP1, which influences metabolic processes and circadian gene expression in skeletal muscle.

David G Lassiter, Rasmus J O Sjögren, Brendan M Gabriel, Anna Krook, Juleen R Zierath

Open access · goldAbstract read
In one paragraph

Article in Molecular metabolism, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed, 1 pooled it
1.8field-weighted citation impact, top 15% 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

13 citing papers in PubMed, 1 synthesis or guideline pooled it, 25 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Review
  5. Review
  6. Article
  7. Article
  8. Exercise as a Peripheral Circadian Clock Resynchronizer in Vascular and Skeletal Muscle Aging.International journal of environmental research and public health · 2021
    Review
  9. Article
  10. Article
  11. Review
  12. Exercise Timing and Circadian Rhythms.Current opinion in physiology · 2019
    Article
  13. Review
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

5 authors at 1 institution in 2 countries.

David G LassiterDepartment of Molecular Medicine and Surgery, Integrative Physiology, Karolinska Institutet, Stockholm, Sweden.
Rasmus J O SjögrenDepartment of Molecular Medicine and Surgery, Integrative Physiology, Karolinska Institutet, Stockholm, Sweden.
Brendan M GabrielDepartment of Physiology and Pharmacology, Integrative Physiology, Karolinska Institutet, Stockholm, Sweden.
Anna KrookDepartment of Physiology and Pharmacology, Integrative Physiology, Karolinska Institutet, Stockholm, Sweden.
Juleen R ZierathDepartment of Molecular Medicine and Surgery, Integrative Physiology, Karolinska Institutet, Stockholm, Sweden; Department of Physiology and Pharmacology, Integrative Physiology, Karolinska Institutet, Stockholm, Sweden; Section of Integrative Physiology, The Novo Nordisk Foundation Center for Basic Metabolic Research, Faculty of Health and Medical Science, University of Copenhagen, Copenhagen, Denmark. Electronic address: Juleen.Zierath@ki.se.
Karolinska Institutet · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveWe sought to identify AMPK-regulated genes via bioinformatic analysis of microarray data generated from skeletal muscle of animal models with genetically altered AMPK activity. We hypothesized that such genes would play a role in metabolism. Ganglioside-induced differentiation-associated protein 1 (GDAP1), a gene which plays a role in mitochondrial fission and peroxisomal function in neuronal cells but whose function in skeletal muscle is undescribed, was identified and further validated. AMPK activation reduced GDAP1 expression in skeletal muscle. GDAP1 expression was elevated in skeletal muscle from type 2 diabetic patients but decreased after acute exercise.

methodsThe metabolic impact of GDAP1 silencing was determined in primary skeletal muscle cells via siRNA-transfections. Confocal microscopy was used to visualize whether silencing GDAP1 impacted mitochondrial network morphology and membrane potential.

resultsGDAP1 silencing increased mitochondrial protein abundance, decreased palmitate oxidation, and decreased non-mitochondrial respiration. Mitochondrial morphology was unaltered by GDAP1 silencing. GDAP1 silencing and treatment of cells with AMPK agonists altered several genes in the core molecular clock machinery.

conclusionWe describe a role for GDAP1 in regulating mitochondrial proteins, circadian genes, and metabolic flux in skeletal muscle. Collectively, our results implicate GDAP1 in the circadian control of metabolism.

Indexed as

AMP-Activated Protein KinasesAnimalsCircadian RhythmComputational BiologyDiabetes Mellitus, Type 2Gene ExpressionGlucoseHumansMaleMetabolismMiceMice, Inbred C57BLMice, KnockoutMitochondriaMuscle, SkeletalNerve Tissue ProteinsAMP-Activated Protein KinasesGDAP proteinGlucoseNerve Tissue ProteinsAMPKCircadianDiabetesGDAP1MitochondriaSkeletal muscle

Identifiers

PMID30093355
PMCPMC6157647
OpenAlexW2884098388

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.