It is well known that the biologically most active metabolite of vitamin D, I ,25-(0H)2DJ, is an essential hormone in the regulation of calcium homeostasis. Furthermore, evidence has accumulated to suggest that I ,25-(0H)2D3 regulates bone metabolism not only indirectly via its effect on intestinal absorption of calcium and phosphorus, but also directly through actions on bone remodelling cells and their progenitors. The aim of the present thesis has been to contribute to a better understanding of the effects of I,25-(0H)2D3 on the osteoblastic population and to investigate the cellular mechanisms in.volved in the regulation of the biological response to the hormone