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Fetal energy and nitrogen requirements are met mostly by placental transfer of glucose and amino acids; fatty acids may contribute additional energy in some species. Placental metabolism accounts for much of the total net consumption of oxygen and macronutrients by the conceptus, and alters the composition of nutrients delivered to the fetus. The molecular basis for the facilitated transport of glucose by the placenta is well described; molecular characterization of the more complex systems for the active transport of most amino acids is under way. Maternal and placental macronutrient supply is a powerful regulator of fetal metabolism and growth, especially in late gestation. Endocrine mediation of these responses matures as gestation advances, adding to the influences of locally expressed regulators throughout gestation. Insulin, thyroid hormones, and, near term, corticosteroids, are especially influential in the direct and indirect control of fetal nutrient disposal and tissue growth. Prenatal growth retardation does not necessarily constrain the rate of neonatal growth, but at any given postnatal body weight, low-birth-weight lambs are fatter and have smaller muscles. Experimental evidence is accumulating for longer-term influences of prenatal nutrition through fetal programming of propensity for mature-onset diseases such as hypertension and type II diabetes. |
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