The first recognized homoeostatic function of Vitamin D was its
regulation of whole body Ca2þ homoeostasis by promoting Ca2þ
absorption by the kidney and the intestine. Vitamin D acts by
increasing the expression of the main components responsible for
epithelial Ca2þ transport such as TRPV5, TRPV6, calbindin D-9k,
calbindin D-28k, Naþ/Ca2þ exchanger (NCX) and plasma membrane
Ca2þ-ATPase 1b (PMCA1b) [21e25]. A defect in these Vitamin Ddependent Ca2þ homoeostatic mechanisms causes rickets in infants and osteomalacia in adults [26,27]. Vitamin D deficiency is
now recognized as a major risk factor in many other human desease