“…The fluoro groups on the 24-position preclude metabolism of 1,25-(OH) 2 D 3 to 24-hydroxylated metabolites [101]. When vitamin D-deficient rats were maintained on 24,24 difluoro-25-OH-D 3 as their sole source of vitamin D 3 , growth, reproduction, and skeletal mineralization remained normal when compared to rats maintained on 25-OH-D 3 or 1,25-(OH) 2 D 3 [19,100,102]. Thus, it is clear that 24-hydroxylation of vitamin D plays no significant role in the functions of vitamin D. The CYP-24 null mouse has been produced with a phenotype of high plasma levels of 1,25-(OH) 2 D 3 and defective mineralization [103].…”