Hormonal
Treatment with 1α,25-dihydroxyvitamin D3 (calcitriol) increases mitochondrial oxygen consumption rate (OCR), volume, and branching in human skeletal muscle cells by modulating the expression of fusion/fission proteins and pyruvate dehydrogenase kinases.
This research highlights that muscle mitochondrial health is specifically regulated by the active form of Vitamin D (calcitriol), not just precursor forms. For individuals with muscle weakness or myopathy, ensuring adequate Vitamin D status is critical, but the underlying mechanism involves complex genomic regulation of mitochondrial fusion and energy consumption. This does not imply that everyone needs active Vitamin D medication, but it explains why Vitamin D deficiency is linked to muscle weakness and why restoring levels can improve mitochondrial function.
The mitochondrial oxygen consumption rate (OCR) increased in 1α,25(OH)2D3-treated cells... In 1α,25(OH)2D3-treated cells, mitochondrial volume and branching and expression of the pro-fusion protein OPA1... increased, whereas expression of the pro-fission proteins Fis1... and Drp1... decreased.
Why this rating
High-quality in vitro mechanistic study using primary human cells, transcriptomics, and functional assays, but lacks clinical efficacy data on muscle performance.
Source
1α,25-Dihydroxyvitamin D3 Regulates Mitochondrial Oxygen Consumption and Dynamics in Human Skeletal Muscle Cells
Zachary C. Ryan et al. · Journal of Biological Chemistry · 2015
DOI 10.1074/jbc.m115.684399
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