Cited by 52Adipokines, Inflammation, and Metabolic DiseasesMuscle Physiology and DisordersAdipose Tissue and Metabolism

Adiponectin and Skeletal Muscle

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Jortay, Julie, Senou, Maximin, Abou-Samra, Michel, Noel, Laurence, Robert, Annie, Many, Marie-Christine, Brichard, Sonia M.·2012·The American Journal of Pathology

Abstract

Upregulation of muscular adiponectin could act as a local protective mechanism to counteract cellular damage in obesity by weakening inflammation, oxidative stress, and apoptosis. To test this hypothesis, adiponectin-knockout (KO) and wild-type (WT) mice were fed a Western diet (WD). WT mice under WD conditions displayed 63% higher adiponectin expression in myocytes than those under standard laboratory diet (SLD) conditions (P = 0.011). WD-fed KO mice exhibited approximately threefold larger myocyte degeneration than WT mice (P = 0.003). Even under SLD conditions, myotubes of KO mice displayed already moderate immunolabeling for markers of oxidative stress (peroxiredoxin-3/5) and for a lipid peroxidation product (hydroxynonenal). Expression of tumor necrosis factor-α (TNF-α) and caspase-6, a marker of apoptosis, was also present. After WD challenge, immunoreactivity for these markers was strong in muscle of KO mice, although it was detected to a lesser extent in WT mice. Activation of NF-κB and caspase-6 doubled in myocytes of WD-fed KO mice when compared to WT mice (P < 0.001). Furthermore, muscle electrotransfer of the adiponectin gene prevented these abnormalities in WD-fed KO mice. Finally, gene abrogation of the adiponectin receptor 1 (AdipoR1) by siRNA recapitulated a pro-inflammatory state in C2C12 myotubes. Thus, upregulation of muscular adiponectin may be triggered by obesity and be crucial locally to counteract oxidative stress, inflammation, and apoptosis. These effects operate in an autocrine/paracrine manner via AdipoR1 and down-regulation of NF-κB signaling.

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Crossref · 10.1016/j.ajpath.2012.03.035

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Authors
Jortay, J., Senou, M., Abou-Samra, M., Noel, L., Robert, A., Many, M.-C., & Brichard, S. M.
Affiliations
UCLouvain (BE)
Corresponding author
Brichard, Sonia M.
Venue
The American Journal of Pathology
Publisher
Elsevier BV
Published
2012-07
Volume
181
Issue
1
Pages
245-256
ISSN
0002-9440 (ISSN-L)
OpenAlex
W1813443405
Cited by
52
References
33
Citations by year
2026: 2 · 2025: 2 · 2024: 4 · 2023: 4 · 2022: 3 · 2021: 6 · 2020: 3 · 2019: 3 · 2018: 7 · 2017: 6 · 2016: 2 · 2015: 4 · 2014: 3 · 2013: 3
FWCI
2.39
Type
journal article
Language
en
Open access
Locations
  • American Journal Of Pathology (publishedVersion)
  • PubMed (publishedVersion)
  • Digital Access to Libraries (Université catholique de Louvain (UCL), l'Université de Namur (UNamur) and the Université Saint-Louis (USL-B)) (submittedVersion)
Topics
  • Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Muscle Physiology and Disorders
  • Health Sciences › Medicine › Physiology › Adipose Tissue and Metabolism
Keywords
adiponectin, skeletal muscle, obesity, AdipoR1, NF-κB signaling, oxidative stress, inflammation, apoptosis, Western diet, TNF-α, caspase-6, peroxiredoxin, 4-hydroxynonenal, autocrine and paracrine signaling, adiponectin knockout mice
MeSH terms
Animals, Body Composition, Body Weight, Diet, Obesity, Stress, Physiological, Tumor Necrosis Factor-alpha, NF-kappa B, Apoptosis, Gene Transfer Techniques, Mice, Knockout, Oxidative Stress, Muscle, Skeletal, Muscle Fibers, Skeletal, Muscle Cells, Mice, Adiponectin, Caspase 6

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