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1 educed, as is their ability to metabolize 25-hydroxycholecalciferol [25(OH)D(3)] to its active metabo
2 holecalciferol [1alpha,25(OH)(2)D(3)] and 25-hydroxycholecalciferol [25(OH)D(3)]; the latter's effect
3 1, 1alphaOHase), the enzyme that converts 25-hydroxycholecalciferol, a circulating inactive metabolit
4 ol/L, equilibrium concentrations of serum 25-hydroxycholecalciferol changed during the winter months
5 ecalciferol input and the resulting serum 25-hydroxycholecalciferol concentration and to estimate the
6 ed to achieve or maintain any given serum 25-hydroxycholecalciferol concentration are not known, part
7 D inputs are inadequate to maintain serum 25-hydroxycholecalciferol concentration in the absence of s
8 oral input required to sustain the serum 25-hydroxycholecalciferol concentration present before the
9 ue stores) needed to sustain the starting 25-hydroxycholecalciferol concentration was estimated at ap
11 t to increase energy, calcium intake, and 25-hydroxycholecalciferol concentrations may improve bone m
12 les in the past year, lower estradiol and 25-hydroxycholecalciferol concentrations, and a higher prev
13 the interaction between serum vitamin D (25-hydroxycholecalciferol) concentrations and VDR genotype
16 is, the combination of genotype TT/Tt and 25-hydroxycholecalciferol deficiency was associated with di
18 .3-6.5], p=0.008), and undetectable serum 25-hydroxycholecalciferol (<7 nmol/L) carried a higher risk
19 als with vitamin D terms: cholecalciferol or hydroxycholecalciferols or calcifediol or dihydroxychole
21 ence of genotype ff or undetectable serum 25-hydroxycholecalciferol was strongly associated with dise