The principal function of vitamin D in the maintenance of calcium homeostasis is to increase intestinal calcium absorption. This conclusion was made from studies in vitamin D receptor (VDR) null mice which showed that rickets and osteomalacia were prevented when VDR null mice were fed a rescue diet that included high calcium, indicating that the skeletal abnormalities of the VDR null mice are primarily the result of impaired intestinal calcium absorption. Although vitamin D is critical for controlling intestinal calcium absorption, the mechanisms involved have remained incomplete. This chapter reviews studies, including studies in genetically modified mice, that have provided new insight and have challenged the traditional model of VDR-mediated calcium absorption.
Keywords: 1,25-Dihydroxyvitamin D3; Bone; Calbindin-D9k; Calcium; Intestine; Kidney; Parathyroid hormone; Transient receptor potential vanilloid type 6 (TRPV6); Vitamin D; Vitamin D receptor.