Evidence map›Paper›PMID 26399516›Full record

ArticleJournal of physiology and biochemistry2015

Irisin, a unique non-inflammatory myokine in stimulating skeletal muscle metabolism.

Roger A Vaughan, Nicholas P Gannon, Christine M Mermier, Carole A Conn

Abstract read
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In one paragraph

Article in Journal of physiology and biochemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed, 2 pooled it
4.0field-weighted citation impact, top 6% 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

37 citing papers in PubMed, 2 syntheses or guidelines pooled it, 75 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Myokines and mitochondrial function in cardiometabolic diseases.Journal of physiology and biochemistry · 2026
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  17. CombinedNutrients · 2022
    Article
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  20. Biological Aspects of Selected Myokines in Skeletal Muscle: Focus on Aging.International journal of molecular sciences · 2021
    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

4 authors at 2 institutions in 1 country.

Roger A VaughanDepartment of Exercise Science, High Point University, 833 Montlieu Ave., High Point, NC, 27268, USA. rvaughan@highpoint.edu.
Nicholas P GannonDepartment of Biochemistry and Molecular Biology, School of Medicine, University of New Mexico Health Sciences Center, Albuquerque, NM, 87131, USA. ngannon@mcw.edu.
Christine M MermierDepartment of Health, Exercise and Sports Science, University of New Mexico, Albuquerque, NM, 87131, USA. cmermier@unm.edu.
Carole A ConnDepartment of Individual, Family, and Community Education: Nutrition, University of New Mexico, Albuquerque, NM, 87131, USA. cconn@unm.edu.
University of New Mexico · USHigh Point University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Exercise offers several benefits for health, including increased lean body mass and heightened energy expenditure, which may be partially attributable to secretory factors known as myokines. Irisin, a recently identified myokine, was shown to increase metabolic rate and mitochondrial content in both myocytes and adipocytes; however, the mechanism(s) of action still remain largely unexplained. This work investigated if irisin functions by acting as an inflammatory myokine leading to cellular stress and energy expenditure. C2C12 myotubes were treated with various concentrations of irisin, TNFα, or IL6 for various durations. Glycolytic and oxidative metabolism, as well as mitochondrial uncoupling, were quantified by measurement of acidification and oxygen consumption, respectively. Metabolic gene and protein expression were measured by quantitative real-time polymerase chain reaction (qRT-PCR) and immunoblotting, respectively. Mitochondrial content was assessed by fluorescent imaging. NFκB activity was assessed using an NFκB GFP-linked reporter system. Consistent with previous findings, irisin significantly increased expression of several genes including peroxisome proliferator-activated receptor γ coactivator-1α (PGC-1α) leading to increased mitochondrial content and oxygen consumption. Despite some similarities between TNFα and irisin treatment, irisin failed to activate the NFκB pathway like TNFα, suggesting that irisin may not act as an inflammatory signal. Irisin has several effects on myotube metabolism which appear to be dependent on substrate availability; however, the precise mechanism(s) by which irisin functions in skeletal muscle remain unclear. Our observations support the hypothesis that irisin does not function through inflammatory NFκB activation like other myokines (such as TNFα).

Indexed as

AnimalsCell LineFibronectinsGene ExpressionMiceMuscle Fibers, SkeletalMuscle, SkeletalNF-kappa BOxygen ConsumptionFibronectinsFNDC5 protein, mouseNF-kappa BFibronectin type III domain containing protein 5 (FNDC5)Interleukin 6 (IL6)Peroxisome proliferator-activated receptor γ coactivator-1α (PGC-1α)SecretomeTumor necrosis factor α (TNFα)

Identifiers

PMID26399516
OpenAlexW1693278100

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.