Introduction

Growth in childhood is heavily dependent on classical endocrine hormones such as growth hormone, thyroid hormones, glucocorticoids and insulin. Some of the trophic actions of these hormones are mediated by peptide growth factors, especially the mediation of growth hormone action on longitudinal skeletal growth by insulin-like growth factor-I (IGF-I). However, classical endocrine hormones of fetal origin, with the exception of insulin, are not major determinants of size at birth. In some instances, as in the maturational effects of thyroid hormones on the central nervous system, transplacental passage of maternal hormones is sufficient to satisfy the basic needs of the conceptus. Other hormones, such as glucocorticoids, have defined roles in late gestation as the liver and lungs mature in preparation for postnatal existence. Insulin, however, has a fundamental role as a mitogen in the early embryo, and its absence leads to severe intrauterine growth retardation. The relevance of insulin and other hormones to prenatal development has been reviewed extensively (Gluckman & Liggins, 1984; Hill & Milner, 1989; Hill, 1992).

The fundamental drive to embryonic and fetal growth appears to be orchestrated by the widespread expression, regulation of availability, and interaction of a number of peptide growth factors. Recent studies of gene manipulation have shown peptide growth factors to be obligatory for specific events of embryonic morphogenesis, and for growth of the conceptus in toto. Since the expression of most growth factors is not restricted to individual tissues, but is widespread, prenatal development can be considered mainly as an integrated network of paracrine and autocrine events.