Evidence map›Paper›PMID 26438561›Full record

ArticleJournal of lipid research2015

PGC-1α-mediated changes in phospholipid profiles of exercise-trained skeletal muscle.

Nanami Senoo, Noriyuki Miyoshi, Naoko Goto-Inoue, Kimiko Minami, Ryoji Yoshimura, Akihito Morita, Naoki Sawada, Junichiro Matsuda, Yoshihiro Ogawa, Mitsutoshi Setou and 2 more

Open access · hybridAbstract read
In one paragraph

Article in Journal of lipid research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
3.6field-weighted citation impact, top 7% 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

34 citing papers in PubMed, 58 citations in OpenAlex.

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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

12 authors at 7 institutions in 3 countries.

Nanami SenooLaboratories of Nutritional Biochemistry Graduate School of Nutritional and Environmental Sciences, University of Shizuoka, Suruga-ku, Shizuoka 422-8526, Japan.
Noriyuki MiyoshiBiochemistry, Graduate School of Nutritional and Environmental Sciences, University of Shizuoka, Suruga-ku, Shizuoka 422-8526, Japan.
Naoko Goto-InoueDepartment of Marine Science and Resources, College of Bioresource Sciences, Nihon University, Fujisawa, Kanagawa 252-0880, Japan.
Kimiko MinamiLaboratory of Molecular Nutrition, Graduate School of Environmental and Life Science, Kyoto Prefectural University, Sakyo-ku, Kyoto, 606-8522, Japan.
Ryoji YoshimuraLaboratory of Molecular Nutrition, Graduate School of Environmental and Life Science, Kyoto Prefectural University, Sakyo-ku, Kyoto, 606-8522, Japan.
Akihito MoritaLaboratories of Nutritional Biochemistry Graduate School of Nutritional and Environmental Sciences, University of Shizuoka, Suruga-ku, Shizuoka 422-8526, Japan.
Naoki SawadaSection of Cardiology, Department of Medicine, University of Chicago, Chicago, IL 60637 Department of Molecular Endocrinology and Metabolism, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University, Bunkyo-ku, Tokyo 113-8510, Japan.
Junichiro MatsudaLaboratory of Animal Models for Human Diseases, National Institutes of Biomedical Innovation, Health, and Nutrition, Ibaraki, Osaka 567-0085, Japan.
Yoshihiro OgawaDepartment of Molecular Endocrinology and Metabolism, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University, Bunkyo-ku, Tokyo 113-8510, Japan.
Mitsutoshi SetouDepartment of Cell Biology and Anatomy, Hamamatsu University School of Medicine, Higashi-ku, Hamamatsu, Shizuoka, 431-3192, Japan Department of Anatomy, University of Hong Kong, Pokfulam, Hong Kong.
Yasutomi KameiLaboratory of Molecular Nutrition, Graduate School of Environmental and Life Science, Kyoto Prefectural University, Sakyo-ku, Kyoto, 606-8522, Japan miura@u-shizuoka-ken.ac.jp kamei@kpu.ac.jp.
Shinji MiuraLaboratories of Nutritional Biochemistry Graduate School of Nutritional and Environmental Sciences, University of Shizuoka, Suruga-ku, Shizuoka 422-8526, Japan miura@u-shizuoka-ken.ac.jp kamei@kpu.ac.jp.
University of Shizuoka · JPKyoto Prefectural University · JPHamamatsu University School of Medicine · JPNational Institute of Biomedical Innovation, Health and Nutrition · JPNihon University · JPTokyo Medical and Dental University · JPUniversity of Chicago · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Exercise training influences phospholipid fatty acid composition in skeletal muscle and these changes are associated with physiological phenotypes; however, the molecular mechanism of this influence on compositional changes is poorly understood. Peroxisome proliferator-activated receptor γ coactivator 1α (PGC-1α), a nuclear receptor coactivator, promotes mitochondrial biogenesis, the fiber-type switch to oxidative fibers, and angiogenesis in skeletal muscle. Because exercise training induces these adaptations, together with increased PGC-1α, PGC-1α may contribute to the exercise-mediated change in phospholipid fatty acid composition. To determine the role of PGC-1α, we performed lipidomic analyses of skeletal muscle from genetically modified mice that overexpress PGC-1α in skeletal muscle or that carry KO alleles of PGC-1α. We found that PGC-1α affected lipid profiles in skeletal muscle and increased several phospholipid species in glycolytic muscle, namely phosphatidylcholine (PC) (18:0/22:6) and phosphatidylethanolamine (PE) (18:0/22:6). We also found that exercise training increased PC (18:0/22:6) and PE (18:0/22:6) in glycolytic muscle and that PGC-1α was required for these alterations. Because phospholipid fatty acid composition influences cell permeability and receptor stability at the cell membrane, these phospholipids may contribute to exercise training-mediated functional changes in the skeletal muscle.

Indexed as

AnimalsHumansMaleMass SpectrometryMiceMice, TransgenicMuscle, SkeletalPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaPhospholipidsPhysical Conditioning, AnimalTranscription FactorsPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaPhospholipidsPPARGC1A protein, humanTranscription Factorsbiochemical assaysfatty acidlipidomicsmass spectrometrymolecular imagingnuclear receptorsperoxisome proliferator-activated receptor γ coactivator 1αphospholipids/phosphatidylcholinephospholipids/phosphatidylethanolaminetranscription factors

Identifiers

PMID26438561
PMCPMC4655985
OpenAlexW2188808270

What OpenQuestion holds

Textmetadata
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.