Amino acids for fetal growth and birth weight

Maternal intake is an important amino acid source for fetal growth and litter birth weight. Amino acids are needed for synthesizing necessary elements for fetal growth such as hormones and nucleotides (Reeds and Hutchens, 1994) as well as for building fetal tissue proteins and peptides. Amino acids are also an important energy source for fetal growth (Bell et ai, 1989).

Dwyer and Stickland (1994) investigated the effect of supplemental protein and energy on fetal growth from severely underfed sows during gestation and found that protein supplementation rehabilitated fetal growth more than the effects obtained from energy supplementation. This result agrees with the previous finding from Atinmo et ai (1974) who showed that protein restriction caused greater impairment of fetus growth than energy restriction. Pond et ai (1991) also demonstrated that severe protein restriction reduced fetus weight at day 50 of gestation as well as birth weight. Maternal body weight was also reduced whereas backfat thickness increased for protein-restricted sows. This result indicates that the effect of maternal protein restriction on fetal growth can be initiated by early- and mid-gestation that is even before the period of most rapid fetal growth (late-gestation). Protein deficiency during early- and mid-gestation affects the fetal growth more detrimentally than during the late-gestation (Pond et ai, 1992). Effect of protein restriction on reduced fetal growth can be explained by decreased amino acid concentration in fetal plasma whereas maternal plasma amino acid concentration was not affected (Wu et ai, 1998a). Atinmo et ai (1976) also demonstrated that maternal protein restriction decreased plasma growth hormone level in the fetus.

Placental development is an important factor in supporting fetal growth. The fetus receives nutrients through placental blood vessels (Ford, 1995; Ott et ai, 1997). Placental angiogenesis occurs rapidly during placental development (Reynolds et ai, 1992). Knight et ai (1977) demonstrated that placental growth was maximized by day 60 of gestation.

Placental growth is affected by maternal protein intake. Wu et al. (1998b) showed that severe protein restriction to gilts during gestation decreased placental amino acid content.

The number of fetal muscle fibres is one of key determinants for postnatal growth (Handel and Stickland, 1987; Rehfeldt et al., 1993). Development of fetal muscle fibre is well reviewed by Lefaucheur and Gerrard (1998) and Wigmore and Dunglison (1998). Nutritional modification can alter the number of secondary muscle fibres whereas primary fibre numbers are resistant to environmental influences (Wigmore and Stickland, 1983). It was shown that hyperplasia of muscle fibre was completed by day 90 of gestation. Secondary fibre hyperplasia began at approximately day 50 of gestation in the pig and continues until day 85-90 (Wigmore and Stickland, 1983). Dwyer et al. (1994) showed that increasing maternal nutrient intake from day 25 to 50 of gestation increased muscle fibre hyperplasia by 13% and suggested that increasing sow feed intake in early pregnancy may improve the mean postnatal growth rate of the litter in the later growth phases to slaughter. Several other investigators also agree that providing sufficient amino acids before day 60 of gestation is critical for fetal and placental growth (Bazer, 1992; Pond et al., 1992; Scholknecht et al., 1994)

Arginine may be important for fetal growth. Sparks et al. (1985) and Wu et al. (1999) demonstrated that the rate of arginine deposition to fetal tissue proteins was one of the greatest among amino acids. Arginine was efficiently metabolized to nitric oxide. The metabolic importance of nitric oxide to the fetal growth as an endothelium-derived relaxing factor, a neurotransmitter, and a modulator of the immune response (Wu et al., 1996) makes the role of arginine significant. Reducing the maternal dietary protein level decreased placental free arginine concentration and, therefore, reduced nitric oxide synthesis (Wu et al., 1998c) that may impair placental and endometrial angio-genesis and growth. Wu et al. (1998c) suggested that reduced arginine concentration in placenta leads to reduction in placental-fetal blood flow, nutrient supply from mother to fetus, and ultimately fetal growth retardation. Conventional maize and soybean meal-based diets normally contain arginine abundantly. Whether increasing dietary arginine content raises placental arginine uptake is not known yet.

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