ABSTRACT
Vitamin D is a secosteroid hormone classically involved in the regulation of phosphocalcic homeostasis and osteogenesis (Annweiler et al. 2010e; Kalueff and Tuohimaa 2007). The past decade was characterized by an increased number of publications highlighting the adverse effects of hypovitaminosis D not only on bone diseases but also on non-bone health outcomes (Zittermann 2003; Sutra Del Galy et al. 2009; Bouvard et al. 2011), including immunosuppression, cancer, infections, or cardiovascular diseases, as described in previous chapters. These observations could be explained by the fact that vitamin D exhibits multiple biological targets mediated by the vitamin D receptor (VDR), which is present in numerous cells and tissues (Annweiler et al. 2010e; Kalueff and Tuohimaa 2007).
