Vitamin D status modulates mitochondrial oxidative capacities in skeletal muscle: role in sarcopenia

Jérôme Salles, Audrey Chanet, Christelle Guillet, Anouk Mm Vaes, Elske M. Brouwer-Brolsma, Christophe Rocher, Christophe Giraudet, Véronique Patrac, Emmanuelle Meugnier, Christophe Montaurier, Philippe Denis, Olivier Le Bacquer, Adeline Blot, Marion Jourdan, Yvette Luiking, Matthew Furber, Miriam van Dijk, Nicolas Tardif, Y. Boirie, Stéphane Walrand*

*Corresponding author for this work

Research output: Contribution to journalArticleAcademicpeer-review

11 Citations (Scopus)


Skeletal muscle mitochondrial function is the biggest component of whole-body energy output. Mitochondrial energy production during exercise is impaired in vitamin D-deficient subjects. In cultured myotubes, loss of vitamin D receptor (VDR) function decreases mitochondrial respiration rate and ATP production from oxidative phosphorylation. We aimed to examine the effects of vitamin D deficiency and supplementation on whole-body energy expenditure and muscle mitochondrial function in old rats, old mice, and human subjects. To gain further insight into the mechanisms involved, we used C2C12 and human muscle cells and transgenic mice with muscle-specific VDR tamoxifen-inducible deficiency. We observed that in vivo and in vitro vitamin D fluctuations changed mitochondrial biogenesis and oxidative activity in skeletal muscle. Vitamin D supplementation initiated in older people improved muscle mass and strength. We hypothesize that vitamin D supplementation is likely to help prevent not only sarcopenia but also sarcopenic obesity in vitamin D-deficient subjects.

Original languageEnglish
Article number1288
JournalCommunications Biology
Issue number1
Publication statusPublished - 24 Nov 2022


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