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Abstract
Replacing body stores of vitamin D in pregnant rats with radiolabelled cholecalciferol,
enabled the measurement of cholecalciferol and its hydroxylated metabolites in fetal
tissue. Elevated levels of 24, 25-dihydroxycholecalciferol were found to be present
in fetuses, with highest accumulation in the skeleton. A similar finding was observed
when tritiated 24,25-dihydroxycholecalciferol was administered continuously to pregnant
rats. When tritiated 1,25-dihydroxycholecalciferol was administered, very little was
transported into the fetuses, and out of the transported fraction a major portion
was found to be esterified. A selectivity pattern was established for the lacteal
transport of cholecalciferol and its hydroxylated metabolites, in the order: cholecalciferol
> 25-hydroxycholecalciferol > 24,25-dihydroxycholecalciferol > 1,25-dihydroxycholecalciferol.
Vitamin D sulfoconjugates were not detected in suckling rat pups, and over 80% of
the lacteal-transported 1,25-dihydroxycholecalciferol in suckling pups was found to
be esterified. It is suggested that rat fetuses and newborn pups do not require 1,25-dihydroxycholecalciferol,
that a protective mechanism against vitamin D intoxication operates in fetuses and
pups in the form of esterifying enzymes, and that 24,25-dihydroxycholecalciferol might
be associated with bone metabolism.