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Gestational age (days)

Figure 6 Dry weight (A) and fat content (B) plotted against gestational age in the same newborn human infants shown in

Figure 3 for LGA (■. . •••), AGA (O, —), and SGA (♦,---)

infants. (Reproduced with permission from Sparks JW (1992) Intrauterine growth and nutrition. In: Polin RA and Fox WW (eds.) Fetal and Neonatal Physiology, p. 184. Philadelphia: W. B. Saunders.)

over the last third of gestation, there is a bias towards thinner, SGA infants with less fat relative to nonfat weight and nitrogen content, raising the possibility that in a species that does lay down considerable fetal fat during late gestation, differences in intrauterine growth rate may reflect fat deposition more than the growth of nonfat, protein-containing tissues.

Mineral Accretion in the Fetus

Fetal calcium content is best correlated with fetal body length; this is true for both AGA and SGA infants. Using this index, fetal calcium content increases exponentially with a linear increase in length. Using this estimate, the human fetal rate of calcium accretion is about 85 mg kg-1 day-1. Accretion of other minerals varies more directly with body weight, and according to the distribution of the minerals into extracellular (e.g., sodium) or intracellular (e.g., potassium) spaces.

Regulation of Fetal Growth

Fetal growth is the result of interaction among maternal, placental, and fetal factors, representing a mix of genetic mechanisms and environmental influences through which the genetic factors are expressed and modulated. The single most important environmental influence that affects fetal growth is the nutrition of the fetus. Nutrient supply to the fetus and the resulting increases in fetal tissue and plasma concentrations of anabolic hormones and growth factors are regulated by maternal health, maternal nutrition, uterine growth (including uterine blood flow and endometrial surface area), and placental growth and function.

Genetic Factors

Many genes contribute to fetal growth and birth weight of the normal term fetus. Maternal genotype is more important than fetal genotype in the overall regulation of fetal growth. Table 4 presents estimates of the quantitative contribution of fetal and parental factors to fetal growth and birth weight at term. The more modest regulation by the paternal genotype, acting through the fetal genotype, is essential for trophoblast development. In fact, overexpression of the paternal genotype can produce trophoblast tumors. More specific gene targeting studies have shown the importance of genomic imprinting on fetal growth. For example, in mice normal fetal and placental growth require that the IGF2 gene be paternal and the IGF2 receptor gene be maternal, and paternal disomy producing IGF2 gene overexpression results in fetal overgrowth while

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