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Corrigendum Free access | 10.1172/JCI138278

RANKL inhibition improves muscle strength and insulin sensitivity and restores bone mass

Nicolas Bonnet, Lucie Bourgoin, Emmanuel Biver, Eleni Douni, and Serge Ferrari

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Published June 1, 2020 - More info

Published in Volume 130, Issue 6 on June 1, 2020
J Clin Invest. 2020;130(6):3329–3329. https://doi.org/10.1172/JCI138278.
© 2020 American Society for Clinical Investigation
Published June 1, 2020 - Version history
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RANKL inhibition improves muscle strength and insulin sensitivity and restores bone mass
Nicolas Bonnet, … , Eleni Douni, Serge Ferrari
Nicolas Bonnet, … , Eleni Douni, Serge Ferrari
Research Article Bone Biology Muscle biology

RANKL inhibition improves muscle strength and insulin sensitivity and restores bone mass

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Abstract

Receptor activator of NF-κB ligand (RANKL) activates, while osteoprotegerin (OPG) inhibits, osteoclastogenesis. A neutralizing Ab against RANKL, denosumab, improves bone strength in osteoporosis. OPG also improves muscle strength in mouse models of Duchenne’s muscular dystrophy (mdx) and denervation-induced atrophy, but its role and mechanisms of action on muscle weakness in other conditions remain to be investigated. We investigated the effects of RANKL inhibitors on muscle in osteoporotic women and mice that either overexpress RANKL (HuRANKLTg+), or lack Pparb and concomitantly develop sarcopenia (Pparb–/–). In women, taking denosumab for more than 3 years improved appendicular lean mass and handgrip strength compared with no treatment, whereas bisphosphonate did not. HuRANKLTg+ mice displayed lower limb force and maximal speed, while their leg muscle mass was diminished, with a lower number of type I and II fibers. Both OPG and denosumab increased limb force proportionally to the increase in muscle mass. They markedly improved muscle insulin sensitivity and glucose uptake, and decreased antimyogenic and inflammatory gene expression in muscle, such as myostatin and protein tyrosine phosphatase receptor-γ. Similarly, in Pparb–/–, OPG increased muscle volume and force while also normalizing insulin signaling and higher expression of inflammatory genes in skeletal muscle. In conclusion, RANKL deteriorates while its inhibitors improve muscle strength and insulin sensitivity in osteoporotic mice and humans. Hence, denosumab could represent a novel therapeutic approach for sarcopenia.

Authors

Nicolas Bonnet, Lucie Bourgoin, Emmanuel Biver, Eleni Douni, Serge Ferrari

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Original citation: J Clin Invest. 2019;129(8):3214–3223. https://doi.org/10.1172/JCI125915

Citation for this corrigendum: J Clin Invest. 2020;130(6):3329. https://doi.org/10.1172/JCI138278

Following the publication of this article, errors were noted in Figure 1, B and C. The authors were able to provide the original data, and a corrected version of Figure 1 appears below.

The online version of the article has been updated with the corrected information.

The authors regret the errors.

Footnotes

See the related article at RANKL inhibition improves muscle strength and insulin sensitivity and restores bone mass.

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  • Version 1 (June 1, 2020): Print issue publication

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