2 Maternal-Fetal Transfer of Vitamin A …
31
Fig. 2.2 Maternal circulating forms of retinoids and carotenoids available to the developing embryo.
The mammalian embryo is entirely dependent on maternal circulating retinoids for its VA supply. In
the maternal bloodstream, two major retinoid forms can be identified: 1. retinol bound to RBP, the
major form in the fasting state, when most of the retinol is secreted into the circulation from the liver
stores, and 2. retinyl esters packaged in chylomicrons and their remnants, which may account for the
majority of circulating retinoids upon dietary VA intake. Although at lower concentrations, other
forms of VA circulate in the bloodstream, such as the VA precursor β-carotene in chylomicrons
and lipoprotein particles, and its metabolites (apocarotenoids). ROH, retinol; RE, retinyl ester;
RA, retinoic acid; RBP, retinol-binding protein. Figure reprinted from (Spiegler et al. 2012) with
permission from Elsevier
while cows did not miscarry and birthed healthy offspring when they were fed yellow
corn [described without citation in (Bushue and Wan 2010)]. McCollum and Davis
subsequently discovered that a rat fed a purified diet could not conceive until the
diet was supplemented with egg extract. The authors concluded that certain nutrients
could not be synthesized by the offspring, but needed to be obtained from the maternal
diet (McCollum and Davis 1913). In the 1920s, the first studies were published
specifically mentioning VA as the essential nutrient for reproduction. Sherman and
MacLeod (Sherman and MacLeod 1925) and Sure (Sure 1928) reported that female
rats fed a VA-deficient diet were sterile or resorbed their fetuses. It is noteworthy
that Sure’s studies were performed on second-generation VA-deficient rats because
this extended regimen of dietary VA deprivation (across two generations) ensures
the depletion of hepatic VA stores. Under such conditions, the liver can no longer
buffer the absence of VA in the diet, resulting in VA deficiency. Cannon confirmed
that VA induced infertility in 1940 (Cannon 1940).
In addition to describing the effects of VA on embryonic development, early studies also pointed to its influence on placental development. Mason (Mason 1935) made
31
Fig. 2.2 Maternal circulating forms of retinoids and carotenoids available to the developing embryo.
The mammalian embryo is entirely dependent on maternal circulating retinoids for its VA supply. In
the maternal bloodstream, two major retinoid forms can be identified: 1. retinol bound to RBP, the
major form in the fasting state, when most of the retinol is secreted into the circulation from the liver
stores, and 2. retinyl esters packaged in chylomicrons and their remnants, which may account for the
majority of circulating retinoids upon dietary VA intake. Although at lower concentrations, other
forms of VA circulate in the bloodstream, such as the VA precursor β-carotene in chylomicrons
and lipoprotein particles, and its metabolites (apocarotenoids). ROH, retinol; RE, retinyl ester;
RA, retinoic acid; RBP, retinol-binding protein. Figure reprinted from (Spiegler et al. 2012) with
permission from Elsevier
while cows did not miscarry and birthed healthy offspring when they were fed yellow
corn [described without citation in (Bushue and Wan 2010)]. McCollum and Davis
subsequently discovered that a rat fed a purified diet could not conceive until the
diet was supplemented with egg extract. The authors concluded that certain nutrients
could not be synthesized by the offspring, but needed to be obtained from the maternal
diet (McCollum and Davis 1913). In the 1920s, the first studies were published
specifically mentioning VA as the essential nutrient for reproduction. Sherman and
MacLeod (Sherman and MacLeod 1925) and Sure (Sure 1928) reported that female
rats fed a VA-deficient diet were sterile or resorbed their fetuses. It is noteworthy
that Sure’s studies were performed on second-generation VA-deficient rats because
this extended regimen of dietary VA deprivation (across two generations) ensures
the depletion of hepatic VA stores. Under such conditions, the liver can no longer
buffer the absence of VA in the diet, resulting in VA deficiency. Cannon confirmed
that VA induced infertility in 1940 (Cannon 1940).
In addition to describing the effects of VA on embryonic development, early studies also pointed to its influence on placental development. Mason (Mason 1935) made