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Recent studies have suggested that vitamin D activities involve vitamin D receptor (VDR)-dependent and VDR-independent effects of 1α,25-dihydroxyvitamin D 3  (1,25(OH) 2 D 3 ) and 25-hydroxyvitamin D 3  (25(OH)D 3 ) and ligand-independent effects of the VDR. Here, we describe a novel  in vivo  system using genetically modified rats deficient in the  Cyp27b1  or  Vdr  genes. Type II rickets model rats with a mutant  Vdr  (R270L), which recognizes 1,25(OH) 2 D 3  with an affinity equivalent to that for 25(OH)D 3 , were also generated. Although  Cyp27b1 -knockout (KO),  Vdr- KO, and  Vdr  (R270L) rats each showed rickets symptoms, including abnormal bone formation, they were significantly different from each other. Administration of 25(OH)D 3  reversed rickets symptoms in  Cyp27b1 -KO and  Vdr  (R270L) rats. Interestingly, 1,25(OH) 2 D 3  was synthesized in  Cyp27b1 -KO rats, probably by Cyp27a1. In contrast, the effects of 25(OH)D 3  on  Vdr  (R270L) rats strongly suggested a direct action of 25(OH)D 3  via VDR-genomic pathways. These results convincingly suggest the usefulness of our  in vivo  system.

Generation of novel genetically modified rats to reveal the molecular mechanisms of vitamin D actions