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1 e reduced, as is their ability to metabolize 25-hydroxycholecalciferol [25(OH)D(3)] to its active met
2 xycholecalciferol [1alpha,25(OH)(2)D(3)] and 25-hydroxycholecalciferol [25(OH)D(3)]; the latter's eff
3 27B1, 1alphaOHase), the enzyme that converts 25-hydroxycholecalciferol, a circulating inactive metabo
4 nmol/L, equilibrium concentrations of serum 25-hydroxycholecalciferol changed during the winter mont
5 holecalciferol input and the resulting serum 25-hydroxycholecalciferol concentration and to estimate
6 uired to achieve or maintain any given serum 25-hydroxycholecalciferol concentration are not known, p
7 in D inputs are inadequate to maintain serum 25-hydroxycholecalciferol concentration in the absence o
8 ted oral input required to sustain the serum 25-hydroxycholecalciferol concentration present before t
9 issue stores) needed to sustain the starting 25-hydroxycholecalciferol concentration was estimated at
11 port to increase energy, calcium intake, and 25-hydroxycholecalciferol concentrations may improve bon
12 cycles in the past year, lower estradiol and 25-hydroxycholecalciferol concentrations, and a higher p
13 ted the interaction between serum vitamin D (25-hydroxycholecalciferol) concentrations and VDR genoty
16 losis, the combination of genotype TT/Tt and 25-hydroxycholecalciferol deficiency was associated with
18 I 1.3-6.5], p=0.008), and undetectable serum 25-hydroxycholecalciferol (<7 nmol/L) carried a higher r
20 resence of genotype ff or undetectable serum 25-hydroxycholecalciferol was strongly associated with d