Proceedings of The Physiological Society

Mitochondria: Form and function (London, UK) (2017) Proc Physiol Soc 38, PC12

Poster Communications

Reduction in the vitamin D receptor results in impaired mitochondrial function in C2C12 Myoblasts

S. P. Ashcroft1, J. Bass2, N. J. Szewczyk2, P. Atherton2, A. Philp1

1. Sport, Exercise & Rehabilitation Sciences, University of Birmingham, Birmingham, United Kingdom. 2. School of Medicine, University of Nottingham, Derby, United Kingdom.


Approximately 25% of the world's population is affected by vitamin D (VitD) deficiency. It has been reported to play a role in maintaining skeletal muscle function. Large scale epidemiological studies have established a link between VitD deficiency and sarcopenia [1]. The biological functions of VitD and its active metabolites are mediated by the VitD Receptor (VDR) and its control over nuclear transcription. The treatment of cholecalciferol in VitD deficient humans resulted in improvements in skeletal muscle phosphocreatine recovery suggesting VitD or its metabolites alter skeletal muscle oxidative capacity [2]. Despite this little is known about the precise role of the VDR in mediating these adaptations. Following the knock down of the VDR (VDR-KD) in the myogenic C2C12 cell line mitochondrial function was assessed using the Seahorse XFe24 extracellular flux analyser. Scramble control and VDR-KD cells were plated at 30,000 cells/well (n=10). Following assays cells were lysed and data normalised to protein content. Values are means ± SD., and compared by T.Test. VDR-KD resulted in impaired rates of both basal (6.93 ± 1.02 vs. 9.86 ± 3.42 pmol/min/mg, p<0.05) and maximal respiration (19.65 ± 1.24 vs. 30.76 ± 10.42 pmol/min/mg, p<0.05) compared to scramble control. Further analysis revealed a reduction in total ATP production (45.0 ± 3.0 vs. 55.2 ± 8.1 pmolATP/min/mg, p<0.05) as well as a reduction in the contribution from oxidative phosphorylation (39.9 ± 3.5 vs. 46.1 ± 8.4 pmolATP/min/mg, p<0.05) in VDR-KD compared to scramble control. These data highlight an important role for the VDR in maintaining skeletal muscle mitochondrial function, specifically that related to oxidative metabolism.

Where applicable, experiments conform with Society ethical requirements