The central role of the vitamin D endocrine system in calcium homeostasis is now well established [DeLuca and Schnoes, 1983; Kumar, 19841. Research during the early part of this century demonstrated the critical role of the fat-soluble vitamin, vitamin D, in preventing rickets [Mellanby, 1919; McCollum et al., 19221. The pioneering experiments of Nicolaysen showed that vitamin D was essential for the maintenance of a positive calcium balance when dietary calcium was reduced [Nicolaysen and Eeg-Larsen, 19531. DeLuca and colleagues at the University of Wisconsin and Kodicek and colleagues at Cambridge defined the metabolic processes needed for the biotransformation of vitamin D to its biologically active metabolite, la,25-dihydroxyvitamin D3 [DeLuca and Schnoes, 1983; Kumar, 19841. It is now well established that vitamin D3 is metabolized to an essential intermediary metabolite, 25-hydro*tamin D3, by hepatic, microsomal, and mitochondrial cytochrome P-450 containing vitamin D3 25-hydroxylases [DeLuca and Schnoes, 1983; Kumar, 1984, 19901. 25-hydroxyvitamin D3 itself is metabolized to the bioactive metabolite of la,25-dihydroxyvitamin D3, in kidney proximal