Factors Affecting Fetal Growth

Numerous factors influence the growth of the fetus. The fetus derives nutrients from the maternal plasma through the placenta. Mothers on a high plane of nutrition give birth to larger offspring than those with nutritional limitations. Any restriction of blood supply to the placenta and fetus will hinder fetal growth. When competition for available maternal nutrients becomes greater, such as when a multiparous animal produces a larger than average litter, the placenta is generally smaller and the average birthweight more variable than when a litter of average size is produced.[1] Growth of a fetus in a region of the uterine horn with restricted blood supply may result in a runt, which is much smaller than its littermates at birth. Skeletal muscles are particularly small in growth-retarded animals, whereas the brain of the runt is nearly as large as that of its littermates.[6] Since fewer muscle fibers form during fetal development of runts compared to larger littermates, runts tend to grow slower, become fatter, and remain lighter muscled postnatally than offspring of normal birthweight.[3]

The size of the fetus is also controlled by the size of the dam, which may be even more important than nutrition of the dam. Reciprocal crosses between large Shire horses and Shetland ponies, in which the size of the foal follows that of the dam, have demonstrated this. The size of the dam's uterus limits the size of the placenta and subsequently the nutrition and size of the foal.[1]

In addition to maternal nutrition and obvious genetic factors associated with breed or body frame size, fetal development of specific tissues is regulated by a variety of endocrine and local growth factors. Perhaps the dominant fetal growth regulator in late gestation is insulin-like growth factor-1 (IGF-1), which is produced by the fetal liver and other tissues.[7] Fetal IGF-I promotes fetal substrate uptake and inhibits tissue catabolic pathways. In contrast to regulation of IGF-1 by growth hormone during postnatal life, fetal IGF-1 is stimulated by fetal insulin, which is predominantly controlled by fetal glucose concentration. Thus, fetal IGF-1 is sensitive to maternal nutrition, and reduction in fetal growth due to nutrient restriction is associated with reduced fetal IGF-1.

The importance of local growth factors on fetal development is highlighted by the discovery of myostatin, a member of the transforming growth factor-beta superfamily. Myostatin is an inhibitor of skeletal muscle development, and defects in this growth factor lead to increases in myoblast proliferation and subsequent increases in muscle fiber number that characterize the double-muscled condition of cattle. This again illustrates the important effects of fetal development on postnatal growth.

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