Searchable abstracts of presentations at key conferences in endocrinology
Endocrine Abstracts (2012) 30 OC2.3

BSPED2012 Oral Communications Oral Communications 2 (10 abstracts)

Does vitamin D modulate mitochondrial oxidative phosphorylation?

Akash Sinha , Steve Ball , Kieren Hollingsworth & Tim Cheetham


Newcastle University, Newcastle Upon Tyne, UK.


Introduction: Mitochondria are critical organelles which generate most of the energy (ATP) in the eukaryotic cell by oxidative phosphorylation. Impaired mitochondrial function will, therefore, restrict myocellular function. Vitamin D deficiency is widely prevalent with fatigue amongst its commonest manifestation. 31P-MRS is a non-invasive technique used to measure skeletal muscle bioenergetics in vivo. We have examined the relationship between vitamin D and mitochondrial oxidative capacity.

Methods: We evaluated skeletal muscle bioenergetics using 31P-MRS in 64 volunteers. Resting metabolites and parameters of oxidative phosphorylation and peripheral vascular supply – τ1/2 PCr and proton efflux – were calculated using a validated exercise protocol. Regression analysis was undertaken to determine the predictors of oxidative phosphorylation (Minitab v16). Serum 25OHD was used as a surrogate of vitamin D status. Body fat assessment was undertaken using bio-impedance.

Results: Only serum 25OHD was a significant predictor of τ1/2PCr (P=0.012) in multiple regression analysis. In order to describe the relationship between serum 25OHD and τ1/2 PCr, a fitted line model was created. A negative correlation between serum 25OHD and τ1/2 PCr (r=−0.42, P=0.009) suggests that mitochondrial oxidative phosphorylation potential decreases with diminishing serum 25OHD levels. Vitamin D was negatively correlated with body fat% (r=−0.36, P=0.019) but no relationship existed between τ1/2 PCr and body fat%. There was no relationship between serum 25OHD and proton efflux.

Conclusion: Serum 25OHD may facilitate mitochondrial oxidative phosphorylation. The coupling efficiency of oxidative phosphorylation is correlated with many factors including hormone-responsive elements on the mitochondrial genome and our data suggest that vitamin D may modulate mitochondrial energy transduction. This may represent the bioenergetic basis for the fatigue experienced by vitamin D deficient adolescents and adults, although further studies are required to establish causality.

Volume 30

40th Meeting of the British Society for Paediatric Endocrinology and Diabetes

British Society for Paediatric Endocrinology and Diabetes 

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