"It is therefore quite futile to inject some substance . . . into the maternal circulation of
the rat at the end of pregnancy, and then, if it goes through into the foetal circulation,
to report that 'the placenta is permeable to' whatever it was that was injected.
Early studies of amino acid transport across the ovine placenta suggested that
amino acids taken up by the placenta from the maternal circulation are delivered to
the fetus with no major loss (placental amino acid utilization) or addition (placental
amino acid production) (1).
The placenta possesses features allowing it to modify the maternal reproductive
tract into a hospitable and nutritive environment for the developing embryo and
fetus. These fundamental tasks are accomplished through the differentiation of the
trophoblast cell lineage.
Fetal physiologists have centered their attention on the endocrine system when
considering the potential interaction of one fetal organ with another or one fetal
organ with the placenta.
The placenta is classically considered to be a source of hormones that play an
important role in the establishment and maintenance of pregnancy. Because of its
hemochorial structure, the human placenta produces hormones and easily secretes
them into the maternal circulation.
The placenta of mammals is a very adaptable organ that accomplishes many
critical functions necessary for the well-being of the host and developing fetus. For
example, the placenta serves as an attachment site to secure the developing fetus to
the uterus, and it transports nutrients from the maternal to the fetal compartment.
Many factors affect the rate of fetal growth and development in addition to overall
fetal well-being. In eutherian mammals, the placenta serves as the primary mediator
and modulator of those factors that ultimately determine development rate.
The regulation of specific gene expression in response to changes of nutrition has
become a major focus of modern nutritional research, owing to the emergence of
techniques of molecular biology that have allowed the cloning of a number of genes
involved in the regulation of carbohydrate and fat metabolism.
Oxygen is an essential substrate for life before birth; it is required to produce
energy, maintain tissues already laid down, and support accretion of new tissues.
Fetal oxygen requirements are therefore ultimately determined by the rate of fetal
growth and the factors that regulate this process.
The factors responsible for retarding fetal growth are numerous and not completely
understood. Although it is reasonable to assume that altered placental handling and
transport of metabolic fuels can affect fetal growth, little is known about the precise
relation between these changes and the numerous aspects of fetal growth (1).
The importance of lipid metabolism in intrauterine growth retardation (IUGR)
has not been extensively studied. Although little is known of the effect of marginal
dietary intakes of essential fatty acids on fetal lipid metabolism, there is evidence
that placental lipids of infants that are small for gestational age (SGA) are low in
20:4 n-6 and 22:6 n-3.
During gestation, the mother has to adapt her own metabolism to support a continuous
extraction of nutrients through the placenta to sustain fetal development. Quantitatively,
glucose and amino acids are the most abundant of these nutrients crossing
the placenta (1,2), and the continuous dependence of the fetus on these compounds
is well-known. However, the placenta is practically impermeable to lipids, except
for free fatty acids (FFA) and ketone bodies (3).
Much of what we know about placental physiology and biochemistry has come
from studies carried out in animals, particularly the guinea pig, rabbit, and sheep.
Much less information is available concerning metabolism of the human fetus, for
obvious reasons—both ethical and practical.
Our ability to understand the physiology of the fetus in utero and the metabolic
changes associated with pregnancy has increased in the last 10 years because of the
development of fetal blood sampling techniques and the application of stable isotope
Maternal vascular diseases are known to influence fetal growth by reducing the
availability of nutrients through the impaired uteroplacental circulation. Intrauterine
fetal growth retardation (IUGR) is related to an increased risk for perinatal morbidity
Fetal growth and development are primarily determined by genetic information
in the fetus, but the genetic regulation of fetal growth is influenced by various factors
that can exert a stimulatory or inhibitory effect.
Substance abuse in pregnancy is generally believed to be on the increase in many
of the developed countries of the world. Pregnant women who expose themselves
to toxic substances are at risk for adverse outcome. However, it is not entirely clear
to what degree any one specific substance abused may affect either the mother or
the baby during the course of pregnancy.
The adverse effect of maternal smoking on fetal birth weight is a well-established
fact, but the role of the placenta in this phenomenon is not fully understood. During
the last 4 years, we have determined the effects of smoking on placental structure
and function in Aberdeen women.
Dr. Battaglia: From my point of view, this conference has been very successful.
It was timely to bring people together from basic research and clinical research. We
covered a variety of new areas in methodology, ranging from molecular biology to
clinically applicable techniques, that can be applied to learn much more about placental
function and fetal nutrition.