TY - JOUR
T1 - Maternal-fetal-infant dynamics of the C3-epimer of 25-hydroxyvitamin D
AU - Bailey, Dana
AU - Perumal, Nandita
AU - Yazdanpanah, Mehrdad
AU - Al Mahmud, Abdullah
AU - Baqui, Abdullah H.
AU - Adeli, Khosrow
AU - Roth, Daniel E.
PY - 2014/6
Y1 - 2014/6
N2 - Background: Poor vitamin D status (i.e. low serum 25-hydroxyvitamin D (25(OH)D)) has been associated with adverse clinical outcomes during pregnancy and childhood. However, the interpretation of serum 25(OH)D levels may be complicated by the presence of the C3-epimer of 25(OH)D. We aimed to quantify C3-epi-25(OH)D3 in pregnant women and fetuses, to explore the relationship of the C3-epimer between maternal and cord samples, and to establish whether infant C3-epimer abundance is explained by prenatal formation. Methods: In a sub-study of a randomized trial of prenatal vitamin D3, 25(OH)D3 and C3-epi-25(OH)D3 were quantified by LC-MS/MS in 71 sets of mother-fetus-infant serum samples, including maternal delivery specimens, cord blood, and infant specimens acquired at 3-28weeks of age. Results: Without supplementation, median concentrations of C3-epi-25(OH)D3 were higher in infants (6.80nmol/L) than mothers (0.45nmol/L) and cord blood (0nmol/L). However, there was substantial variation such that C3-epi-25(OH)D3 accounted for up to 11% (maternal), 14% (cord), and 25% (infant) of the total 25(OH)D3. Supplemental vitamin D3 significantly increased maternal-fetal C3-epi-25(OH)D3, and was a preferential source of C3-epi-25(OH)D3 compared to basal vitamin D, possibly due to C3-epi-cholecalciferol in the supplement. Multivariate regression did not suggest transplacental transfer of C3-epi-25(OH)D3, but rather indicated its generation within the fetal-placental unit from maternally-derived 25(OH)D3. Neither maternal nor fetal C3-epi-25(OH)D3 is accounted for the relatively high concentrations of infant C3-epi-25(OH)D3, suggesting rapid postnatal generation. Conclusions: C3-epi-25(OH)D3 is present in some pregnant women and fetuses, but does not appear to be efficiently transferred transplacentally. High C3-epimer concentrations in infancy are probably due to postnatal formation rather than fetal stores.
AB - Background: Poor vitamin D status (i.e. low serum 25-hydroxyvitamin D (25(OH)D)) has been associated with adverse clinical outcomes during pregnancy and childhood. However, the interpretation of serum 25(OH)D levels may be complicated by the presence of the C3-epimer of 25(OH)D. We aimed to quantify C3-epi-25(OH)D3 in pregnant women and fetuses, to explore the relationship of the C3-epimer between maternal and cord samples, and to establish whether infant C3-epimer abundance is explained by prenatal formation. Methods: In a sub-study of a randomized trial of prenatal vitamin D3, 25(OH)D3 and C3-epi-25(OH)D3 were quantified by LC-MS/MS in 71 sets of mother-fetus-infant serum samples, including maternal delivery specimens, cord blood, and infant specimens acquired at 3-28weeks of age. Results: Without supplementation, median concentrations of C3-epi-25(OH)D3 were higher in infants (6.80nmol/L) than mothers (0.45nmol/L) and cord blood (0nmol/L). However, there was substantial variation such that C3-epi-25(OH)D3 accounted for up to 11% (maternal), 14% (cord), and 25% (infant) of the total 25(OH)D3. Supplemental vitamin D3 significantly increased maternal-fetal C3-epi-25(OH)D3, and was a preferential source of C3-epi-25(OH)D3 compared to basal vitamin D, possibly due to C3-epi-cholecalciferol in the supplement. Multivariate regression did not suggest transplacental transfer of C3-epi-25(OH)D3, but rather indicated its generation within the fetal-placental unit from maternally-derived 25(OH)D3. Neither maternal nor fetal C3-epi-25(OH)D3 is accounted for the relatively high concentrations of infant C3-epi-25(OH)D3, suggesting rapid postnatal generation. Conclusions: C3-epi-25(OH)D3 is present in some pregnant women and fetuses, but does not appear to be efficiently transferred transplacentally. High C3-epimer concentrations in infancy are probably due to postnatal formation rather than fetal stores.
KW - 25-Hydroxyvitamin D
KW - C3-epi-25-hydroxyvitamin D
KW - Cord
KW - LC-MS/MS
KW - Maternal
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U2 - 10.1016/j.clinbiochem.2014.01.015
DO - 10.1016/j.clinbiochem.2014.01.015
M3 - Article
C2 - 24462965
AN - SCOPUS:84902676692
SN - 0009-9120
VL - 47
SP - 816
EP - 822
JO - Clinical Biochemistry
JF - Clinical Biochemistry
IS - 9
ER -