Partition of Maternal Nutrient Supply Between Maternal and Conceptus Tissues

The progressive gestational increases in fetal and placental demand for nutrients results in the consumption

Maternal non-uterine

Gravid uterus

Placenta

Fetus

Placenta

Fetus

Uterine

Umbilical

artery t

__ I

artery

r

^ c

A

J ! V

t

Uterine

I i

Umbilical

vein

vein

Fig. 1 Schematic representation of the pregnant ewe and its conceptus, illustrating the approach to estimating the partition of nutrients in vivo.

Fig. 1 Schematic representation of the pregnant ewe and its conceptus, illustrating the approach to estimating the partition of nutrients in vivo.

soon after birth and is characterized by very high plasma concentrations of growth hormone and low levels of insulin-like growth factor (IGF) I during fetal life.[6] Circulating levels of IGF-II are much higher in the fetus than in the dam, related to the relatively high expression of this growth factor in multiple fetal tissues.

Fetal adrenal responsiveness to ACTH accelerates dramatically as term approaches, and the resulting exponential increase in fetal cortisol concentrations, independent of maternal levels, is a key factor in induction of the cascade of events leading to parturition.[7]

of a progressively greater fraction of the maternal nutrient supply by conceptus tissues. Thus, as term approaches, the gravid uterus consumes 30 50% of maternal glucose supply in well-fed ewes, depending on fetal number and maternal nutrition.[3] Maternal glucose production increases concomitantly through increased voluntary feed intake, if diet quantity and quality allow, and increased mobilization of endogenous glucogenic precursors. However, the rate of increase in maternal production lags behind the rate of increase in conceptus consumption. Accordingly, the fetus becomes increasingly sensitive to changes in maternal glucose supply as gestation advances.

Partition between maternal and conceptus tissues of other important nutrients, including amino acids, is less well-described. However, we have estimated that net consumption by the gravid uterus accounts for 60 70% of the protein absorbed by well-fed ewes carrying twins in late pregnancy.[5]

Maternal and Fetal Endocrine Relationships

During late gestation, fetal endocrine systems rapidly mature, and fetal concentrations of most important hormones are regulated independently of those of the mother. This separation is enabled by placental impermeability to most maternal protein and steroid hormones. Nevertheless, the dam can indirectly influence the endocrine status of her fetus(es) in several ways. Examples include the tendency for maternal and fetal insulinemia to be associated through the independent responses of the maternal and fetal pancreas to parallel changes in blood glucose concentrations, and the association between maternal and fetal thyroid hormone concentrations commonly mediated by maternal iodine status.

Other fetal endocrine systems are essentially uninfluenced by the dam during late pregnancy, including the somatotropic and adrenocorticotropic axes. In sheep (and presumably in other large domestic animal species) the somatotropic axis does not become fully engaged until

PLACENTAL INFLUENCES ON MATERNAL-FETAL COMMUNICATION

Placental Nutrient Transport

Major functions of the placenta, comprising transport of nutrients and excreta, production of hormones and other bioactive signaling molecules, and immune protection of the fetus, are discussed elsewhere in this encyclopedia. The selective ability of the placenta to transport nutrients from maternal to fetal circulations is an important aspect of maternal fetal communication. Ultimately, maternal fetal nutrient transfer is determined by the complex integration of fetal demand and is dictated by genetic capacity for growth, placental transport capacity, and maternal nutrient supply, which are regulated in an interdependent manner. For example, moderate maternal undernutrition and reduction in glucose supply can lead to upregulation of placental capacity for glucose transport, whereas more severe nutrient deprivation decreases both placental transport capacity and fetal demand for energy substrates such as glucose.[8]

Maternal plasma glucose (mmol/l)

Fig. 2 Relations between fetal and maternal arterial concen trations of plasma glucose in sheep (!), cow (•), pig (A), and horse (O) during late gestation. (Reproduced from Ref. [4] with permission of the publisher.)

Maternal plasma glucose (mmol/l)

Fig. 2 Relations between fetal and maternal arterial concen trations of plasma glucose in sheep (!), cow (•), pig (A), and horse (O) during late gestation. (Reproduced from Ref. [4] with permission of the publisher.)

Differences among the molecular mechanisms for nutrient transport account for different patterns of association between maternal and fetal nutrient concentrations. Placental glucose transport is accomplished by facilitated diffusion through actions of the glucose transporter molecules GLUT1 and GLUT3.[8] It is therefore not surprising that this concentration-dependent process results in strong association between maternal and fetal glucose concentrations1-4-1 (Fig. 2). In contrast, maternal fetal transfer of calcium and most amino acids is achieved by active transport, which explains how it is possible both for fetal concentrations of these nutrients to exceed those of the dam and for the general lack of correlation between maternal and fetal concentrations.1-8-1 Placental transfer of oxygen is influenced more by a combination of uterine and umbilical blood flows and by maternal and fetal hemoglobin concentrations than by placental diffusion characteristics. Nevertheless, the adaptability of the system is such that, in the sheep, placental blood flows must be reduced substantially

(> 50%) before clear decreases in fetal oxygenation occur.[2]

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