AdipoRon, a new therapeutic prospect for Duchenne muscular dystrophy
Open accessAbstract
Background: Adiponectin (ApN) is a hormone known to exhibit insulin‐sensitizing, fat‐burning, and anti‐inflammatory properties in several tissues, including the skeletal muscle. Duchenne muscular dystrophy (DMD) is a devastating disease characterized by dystrophin deficiency with subsequent chronic inflammation, myofiber necrosis, and impaired regeneration. Previously, we showed that transgenic up‐regulation of ApN could significantly attenuate the dystrophic phenotype in mdx mice (model of DMD). Recently, an orally active ApN receptor agonist, AdipoRon, has been identified. This synthetic small molecule has the advantage of being more easily produced and administrable than ApN. The aim of this study was to investigate the potential effects of AdipoRon on the dystrophic muscle. Methods: Four‐week‐old mdx mice (n = 6–9 per group) were orally treated with AdipoRon (mdx‐AR) for 8 weeks and compared with untreated (mdx) mice and to control (wild‐type) mice. In vivo functional tests were carried out to measure the global force and endurance of mice. Ex vivo biochemical and molecular analyses were performed to evaluate the pathophysiology of the skeletal muscle. Finally, in vitro tests were conducted on primary cultures of healthy and DMD human myotubes. Results: AdipoRon treatment mitigated oxidative stress (−30% to 45% for 4‐hydroxy‐2‐nonenal and peroxiredoxin 3, P < 0.0001) as well as inflammation in muscles of mdx mice (−35% to 65% for interleukin 1 beta, tumour necrosis factor alpha, and cluster of differentiation 68, a macrophage maker, P < 0.0001) while increasing the anti‐inflammatory cytokine, interleukin 10 (~5‐fold, P < 0.0001). AdipoRon also improved the myogenic programme as assessed by a ~2‐fold rise in markers of muscle proliferation and differentiation (P < 0.01 or less vs. untreated mdx). Plasma lactate dehydrogenase and creatine kinase were reduced by 30–40% in mdx‐AR mice, reflecting less sarcolemmal damage (P < 0.0001). When compared with untreated mdx mice, mdx‐AR mice exhibited enhanced physical performance with an increase in both muscle force and endurance and a striking restoration of the running capacity during eccentric exercise. AdipoRon mainly acted through ApN receptor 1 by increasing AMP‐activated protein kinase signalling, which led to repression of nuclear factor‐kappa B, up‐regulation of utrophin (a dystrophin analogue), and a switch towards an oxidative and more resistant fibre phenotype. The effects of AdipoRon were then recapitulated in human DMD myotubes. Conclusions: These results demonstrate that AdipoRon exerts several beneficial effects on the dystrophic muscle. This molecule could offer promising therapeutic prospect for managing DMD or other muscle and inflammatory disorders.
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AdipoRon reproduced the beneficial effects of ApN in young mdx mice when given orally for 2 months.
“All these beneficial effects of ApN have recently been reproduced by AdipoRon, an agonist of ApN receptor given orally for 2 months to young mdx mice [103] (see Section 6.3).”
From Adiponectin and Its Mimics on Skeletal Muscle: Insulin Sensitizers, Fat Burners, Exercise Mimickers, Muscling Pills … or Everything Together? (2020) · cites this paper as [103]
The mechanisms leading to protective effects of ApN/AdipoRon in DMD involved activation of the AdipoR1-AMPK-SIRT1-PGC-1α axis both in vivo (mdx mice) and in vitro (human dystrophic myotubes).
“As in healthy muscle, the mechanisms leading to the protective effects of ApN/AdipoRon in DMD involved the activation of the AdipoR1-AMPK-SIRT1-PGC-1α axis both in vivo (mdx mice) or in vitro (human dystrophic myotubes) [56,57,103]”
From Adiponectin and Its Mimics on Skeletal Muscle: Insulin Sensitizers, Fat Burners, Exercise Mimickers, Muscling Pills … or Everything Together? (2020) · cites this paper as [103]
Silencing each component of the AdipoR1-AMPK-SIRT1-PGC-1α cascade abrogated the effects of ApN/AdipoRon.
“Silencing each component of this cascade abrogated the effects of ApN/AdipoRon.”
From Adiponectin and Its Mimics on Skeletal Muscle: Insulin Sensitizers, Fat Burners, Exercise Mimickers, Muscling Pills … or Everything Together? (2020) · cites this paper as [103]
ApN/AdipoRon supplementation induced a shift in the secretion of downstream myokines toward a less inflammatory profile in DMD human myotubes.
“and induced a shift in the secretion of downstream myokines toward a less inflammatory profile.”
From Adiponectin and Its Mimics on Skeletal Muscle: Insulin Sensitizers, Fat Burners, Exercise Mimickers, Muscling Pills … or Everything Together? (2020) · cites this paper as [103]
ApN/AdipoRon supplementation retained its anti-inflammatory properties in DMD human myotubes.
“We found that ApN/AdipoRon supplementation retained its anti-inflammatory properties in DMD human myotubes [56,57,103]”
From Adiponectin and Its Mimics on Skeletal Muscle: Insulin Sensitizers, Fat Burners, Exercise Mimickers, Muscling Pills … or Everything Together? (2020) · cites this paper as [103]
AdipoRon has beneficial and protective effects on dystrophic skeletal muscle in mdx mice and in human DMD myotubes.
“Our latest study has brought to light the beneficial and protective effects of AdipoRon on the dystrophic skeletal muscle in mdx mice and in human DMD myotubes.”
From Adiponectin and Its Mimics on Skeletal Muscle: Insulin Sensitizers, Fat Burners, Exercise Mimickers, Muscling Pills … or Everything Together? (2020) · cites this paper as [103]
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- Authors
- Abou‐Samra, M., Selvais, C. M., Boursereau, R., Lecompte, S., Noel, L., & Brichard, S. M.
- Affiliations
- UCLouvain (BE)
- Endocrinology, Diabetes and Nutrition Unit, Institute of Experimental and Clinical Research, Medical Sector Université Catholique de Louvain Brussels Belgium
- Corresponding author
- Abou‐Samra, Michel
- Venue
- Journal of Cachexia, Sarcopenia and Muscle
- Publisher
- Wiley
- Published
- 2020-01-21
- Volume
- 11
- Issue
- 2
- Pages
- 518-533
- ISSN
- 2190-5991 (ISSN-L)
- 2190-6009
- PMC
- PMC7113498
- OpenAlex
- W3001361857
- Cited by
- 44
- References
- 65
- Citations by year
- 2026: 3 · 2025: 7 · 2024: 7 · 2023: 6 · 2022: 10 · 2021: 9 · 2020: 2
- FWCI
- 2.19
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Journal of Cachexia Sarcopenia and Muscle (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Digital Access to Libraries (Université catholique de Louvain (UCL), l'Université de Namur (UNamur) and the Université Saint-Louis (USL-B)) (submittedVersion, other-oa)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- Koning Boudewijnstichting
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Muscle Physiology and Disorders
- Health Sciences › Medicine › Genetics › Neurogenetic and Muscular Disorders Research
- Health Sciences › Medicine › Physiology › Adipose Tissue and Metabolism
- Keywords
- AdipoRon, adiponectin receptor agonist, Duchenne muscular dystrophy, mdx mice, oxidative stress, muscle inflammation, myogenesis, muscle regeneration, muscle strength and endurance, eccentric exercise, IL-10, peroxiredoxin 3, 4-hydroxynonenal, creatine kinase, lactate dehydrogenase
- MeSH terms
- Animals, Female, Humans, Male, Piperidines, Survival Analysis, Mice, Inbred mdx, Muscular Dystrophy, Duchenne, Mice
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