Maternal to fetal transfer of phylloquinone

The transfer of phylloquinone from the maternal to
fetal circulation is poor. Despite a 500-fold increase in
maternal plasma phylloquinone concentration following
the intravenous administration of 1 mg of phylloquinone
to pregnant women at term, the corresponding
increase in cord plasma was only about fi ve-fold. The
levels attained in cord plasma (0.10–0.14 ng mL–1) after
injection were at most near the lower end of the normal
fasting adult range (0.10–0.66 ng mL–1) (Shearer et al.,
1982). When pregnant women were given daily oral
doses of 20 mg phylloquinone for at least 3 days, cord
plasma levels of phylloquinone were boosted 30-fold at
mid-trimester and 60-fold at term. Again, these levels
were substantially lower than corresponding supplemented
maternal levels (Mandelbrot et al., 1988). The
large concentration gradient of phylloquinone between
maternal and neonatal plasma suggests that phylloquinone
does not cross the placenta readily. Alternatively,
uptake by fetal plasma is low, perhaps because of low
levels of transporting lipoproteins.
The cord plasma of premature infants increased
by an average of 2.3-fold after their mothers received
5 mg of phylloquinone intramuscularly several hours
to 35 min before delivery (Yang et al., 1989). Thus
supplemental phylloquinone given to the mother antenatally
can be transferred to premature infants, but
to a lesser degree than to term babies.
10.4.6 Storage and catabolism in the liver
Storage
The liver has a limited capacity for long-term storage
of vitamin K compared to vitamin A. Surprisingly,
phylloquinone comprises only about 10% of the total
liver stores of vitamin K. Menaquinones ranging from
MK-4 to MK-13 make up the bulk of stores with the
long-chain forms (MK-9 to MK-13), constituting
73% of total vitamin K (Usui et al., 1990). Unlike
phylloquinone, which undergoes rapid turnover, the
hepatic turnover of long-chain menaquinones is low,
presumably because of their high affi nity for membranes
(Shearer, 1992). The contrasting turnovers of
phylloquinone and menaquinones may account for
the predominance of the latter in liver. Whether the
menaquinones originate from the diet or from bacterial
synthesis, their strong retention relative to phylloquinone
would enable concentrations to gradually
build up while phylloquinone is being constantly
utilized and metabolized. In support of this concept,
hepatic stores of phylloquinone are rapidly depleted
during dietary restriction of vitamin K, but hepatic
stores of menaquinones are not (Usui et al., 1990).
Also, the common hepatic menaquinones (MK-9 to
MK-13) are not detectable in plasma, suggesting that
they are not easily mobilized. It appears, therefore,
that the large hepatic pool of menaquinones does
not contribute signifi cantly to vitamin K nutriture
but represents a very slow turnover of the extremely
lipophilic long-chain menaquinones. Further work is
needed to establish the origin of hepatic menaquinones
and their nutritional relevance.
In the liver of the human fetus, phylloquinone is detectable
as early as 10 weeks gestation, and at term the
concentration is about one-fi fth the value in adults.
Hepatic concentrations of menaquinones are usually
undetectable at birth and in the fi rst week of life. The
gradual build-up of hepatic stores of menaquinones
is consistent with the colonization of the neonatal gut
by enteric bacteria.