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Placental function and fetal nutrition. Frederick C Battaglia, ed. [Pp 263, hardback]. Nestlé UK Ltd, 1997. ISBN 0-7817-1406-0.
How is it that hibernating mother bears don’t eat and drink, but still produce baby bears that are not growth retarded? When there is some restriction of nutrient supply to the human fetus, what are the adaptive mechanisms that are made successfully in one pregnancy and not so successfully in another? These are among the many challenging questions considered by expert contributors to this 1996 workshop on placental function and fetal nutrition. Much of the work reported is from animal studies, and species differences and developmental considerations inevitably complicate our understanding of the relation between fetal growth and placental function. However, the advent of novel techniques such as stable isotope methodology have permitted new insight into human physiology. For example, rather than the fetus being a major drain on the resources of maternal metabolism, the rate of transfer of amino acids from the mother indicate that in well nourished women the needs of the fetus ought to be supplied by very small increases in protein intake (or whole body protein breakdown).
One essential role for the placenta is to modify the maternal reproductive tract into a hospitable and nutritive environment for the developing embryo, a role for which paternal genes seem to be essential. Subsequently, placenta and fetus function as an integrated unit. The supply of some amino acids (such as branched chain) depends not only on placental transport but also on placental metabolism, and studies in sheep show that gluconeogenesis in the fetal liver increases only when placental delivery of glucose falls to a low level. The trophoblast secretes steroids and trophic peptides that are essential for fetal growth and development, among them human growth hormone variant which may have a role in mediating the metabolic demands of pregnancy, and in preparing the breast for lactation. In conjunction with hormones, dietary constituents also have a role in the regulation of gene expression. In the hyperglycaemic diabetic mother, for example, there is a fourfold increase in messenger RNA for the glucose transporter GLUT-3, which probably has a major role in placental glucose uptake and metabolism.
Chronic oxygen deficiency restricts and modifies the pattern of fetal growth, altering fetal plasma amino acid profiles, while anabolic hormones decrease and catabolic hormones increase. Although the possibility exists that the induction of maternal hyperoxia might be an appropriate intervention for intrauterine growth retardation, its safety and effectiveness are not established. Other factors known to reduce the transport of specific amino acids include prolonged alcohol consumption, cocaine use, and excessive smoking.
There is now considerable evidence pointing to an association between poor growth in early life and the risk of age related disease in adulthood. Intrauterine growth retardation affects 4–10% of deliveries and an understanding of the metabolic perturbations underlying this heterogeneous condition may ultimately lead to the development of therapeutic strategies which will improve both short and long term outcomes. Those caring for the newborn or their mothers, and anyone intrigued by the Barker hypothesis will find that this series of scientific papers gives a fascinating overview of a burgeoning area of nutritional research.