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Maternal and Fetal Amino Acid Metabolism in Gestating Sows

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Maternal and Fetal Amino Acid Metabolism in Gestating Sows Amino acids and swine reproduction 185 Maternal and fetal amino acid metabolism in gestating sows Guoyao Wu,1,2,3* Fuller W. Bazer,1,2 Gregory A. Johnson,2 Robert. C. Burghardt,2 Xilong Li,1 Zhaolai Dai,3 Junjun Wang3, and Zhenlong Wu3 1Department of Animal Science and 2Department of Veterinary Integrative Biosciences, Texas A&M University, College Station, Texas, USA 77843-2471; 3State Key Laboratory of Animal Nutrition, China Agricultural University, Beijing, China 100193 Among livestock species, swine exhibit the most severe naturally-occurring intra-uterine growth restriction (IUGR) primarily due to a reduction in net protein synthesis. Thus, new knowledge about fetal metabolism of amino acids (AA), which are building blocks for proteins and regulators of intracellular protein turnover, can provide a solution to this problem. Among all AA, requirements of glutamate and glutamine by fetal pigs are quantitatively the highest, but cannot be met through uterine uptake alone. Nearly all glutamate and ~70% glutamine in diets for gestating swine are degraded in the maternal small intestine and, therefore, do not enter the portal circulation. This necessitates interorgan AA metabolism involving maternal skeletal muscle, placenta, and fetal skeletal muscle to synthesize glutamate and glutamine from branched-chain AA, as well as storage of glutamate and glutamine in allantoic and amniotic fluids. The porcine placenta does not degrade arginine or glutamine, leading to their maximal transfer from maternal to fetal blood. Therefore, maternal sources of ornithine and proline play a major role in the placental synthesis of polyamines needed for placental growth including placental vascular growth. Likewise, during late gestation, uterine uptake of arginine, proline and aspartate/asparagine cannot meet requirements for optimal fetal growth. To provide sufficient arginine, the fetal small intestine synthesizes citrulline and arginine from glutamate and glutamine, and fetal kidneys convert citrulline into arginine. Collectively, glutamine and arginine are major sources of AA nitrogen transferred between mother and fetus. Results of recent studies indicate that dietary supplementation with these two AA can ameliorate IUGR in swine. These findings greatly advance the field of maternal-fetal AA metabolism in pigs, but also have important implications for improving reproductive efficiency in swine production worldwide. Introduction Domestic pigs have no brown adipose tissue (Satterfield & Wu 2011), but possess a high capacity for synthesizing triacylglycerides in white adipose tissue after birth (Smith et al. 1999). Excess white fat in the body causes insulin resistance, metabolic disorders, and impaired lactation performance in animals, including swine (Jobgen et al. 2006; Wu 2010a). Thus, during gestation, gilts or multiparous sows are usually fed a substantially reduced amount of E-mail: [email protected] 186 G. Wu et al. diet (e.g., 2 to 2.2 kg/day that is approximately 50% of their ad libitum feed consumption) to reduce energy intake and prevent females from becoming overweight (Ashworth 1991; Kim et al. 2009; Pond et al. 1969, 1981). This strategy, however, results in inadequate provision of dietary amino acids (AA) to both mother and fetus (Wu et al. 2010). Amino acids are the building blocks for proteins in cells and, importantly, they are also precursors for synthesis of glucose and nitrogenous substances [e.g., nitric oxide (NO), polyamines, creatine, dopamine, thyroid hormones, and catecholamines] essential for whole body homeostasis (Wu 2009). Thus, AA have nutritional, physiological, and regulatory roles in animals (Fig. 1). Current feeding programs for gestating swine remain suboptimal due, in part, to inadequate knowledge about maternal and fetal AA nutrition (Kim et al. 2009). Thus, among livestock species, swine suffer the greatest prenatal loss (up to 50%) and exhibit the most severe naturally- occurring intra-uterine growth restriction (IUGR) primarily because of a reduction in net protein synthesis (Vallet et al. 2002; Wu et al. 2006). This provides an impetus to develop novel and effective strategies to improve pregnancy outcome in pigs. The major objectives of this article are to highlight maternal-fetal AA metabolism and nutrition in gestating swine. Readers are referred to the work of Bazer et al. (2013) for recent advances in the roles of AA in regulating embryonic growth, survival and development during early pregnancy. Sources of AA for the fetus The porcine fetus receives AA from its mother via placental transport and can synthesize some AA, including alanine, arginine, asparagine, aspartate, cysteine, glutamate, glutamine, glycine, proline, serine, and tyrosine (Wu et al. 2010). Fetal blood, which contains relatively high concentrations of glutamine and glycine, is the parenteral source of all AA for the fetus. In addition, allantoic fluid, which is derived from both maternal and fetal sources, is a reservoir of AA for the fetus and contains unusually high concentrations of arginine (e.g., 4 to 6 mM) Fig. 1 Nutritional, physiological and regulatory roles of AA in animals. Reprinted from Wu (2010) with permission from American Society of Nutrition. Amino acids and swine reproduction 187 and glycine (4 to 5 mM) during early and late gestation, respectively (Table 1). Nutrients in the allantoic fluid are transported through the allantoic epithelium, enter the fetal-placental circulation, and are utilized by fetal-placental tissues (Figure 2). During early pregnancy, marked increases in concentrations of each AA in allantoic fluid are not accounted for by changes in allantoic fluid volume (Table 1) or by changes in concentrations of AA in maternal and fetal plasma (Wu et al. 1995). AA may play an important role in regulating osmolality in allantoic fluid. Amniotic fluid is derived from both the fetus (kidneys, lungs, epidermis, and fetal blood vessels in the placenta and umbilical cord) and the mother (blood vessels via amniotic membranes) (Schmidt 1992). This fluid is removed by both the fetus and the mother through the same Table 1. Amino acid composition in the body and allantoic fluid of fetal pigs AA composition in fetal pigs on different AA composition in allantoic fluid of fetal 1 2 Amino acid days of gestation (mg AA/g wet weight) pigs on different days of gestation (µM) 40 60 90 110 114 30 40 60 90 110 Alanine4 3.63 3.01 4.26 5.87 6.46 233 281 92 396 669 Arginine5 3.77 3.24 4.58 5.85 6.47 185 4103 642 128 465 Aspartate4 2.90 2.34 3.01 3.92 4.25 16 164 85 170 195 Asparagine4 2.41 1.94 2.50 3.25 3.53 61 280 56 83 139 Citrulline4 0.023 0.024 0.032 0.046 0.054 10 72 46 96 30 Cysteine 4 0.78 0.67 0.92 1.19 1.28 70 220 308 230 604 Glutamate4 4.94 4.21 5.34 6.81 7.72 112 2383 609 1182 1056 Glutamine5 3.19 2.72 3.44 4.39 4.98 638 3442 273 652 701 Glycine5 3.69 3.60 6.53 9.23 10.8 803 360 195 4227 3054 Histidine3 1.54 1.05 1.42 1.85 2.07 76 687 61 73 78 Hydroxyproline4 0.50 0.91 2.08 3.01 3.48 61 49 28 41 82 Isoleucine3 2.18 1.71 2.08 2.61 2.89 28 80 31 10 13 Leucine3 5.04 3.83 4.82 6.13 6.75 63 153 38 14 33 Lysine3 5.15 3.42 4.14 5.19 5.77 362 1950 390 214 617 Methionine3 1.39 1.05 1.34 1.71 1.86 17 31 16 15 273 Ornithine4 0.08 0.075 0.09 0.12 0.13 124 2524 645 76 85 Phenylalanine3 2.78 2.03 2.52 3.14 3.44 36 40 34 195 51 Proline5 3.68 4.07 5.42 7.06 7.82 261 144 46 117 336 Serine4 3.05 2.35 2.96 3.98 4.33 553 902 79 603 1218 Taurine4 0.28 0.23 0.28 0.36 0.38 457 641 298 450 658 Threonine3 2.52 1.90 2.42 2.95 3.24 218 1780 89 343 545 Tryptophan3 0.72 0.61 0.82 1.03 1.11 13 53 69 164 574 Tyrosine4 2.13 1.58 1.85 2.27 2.43 45 70 22 42 39 Valine3 3.40 2.41 3.13 3.88 4.21 80 163 66 57 144 1Adapted from Wu et al. (1999). 2Adapted from Wu et (1995) and Wu et al (1996). 3Traditionally classified as “nutritionally essential AA” (EAA). 4Traditionally classified as “nutritionally nonessential AA” (NEAA). 5Currently classified as “conditionally essential AA” (CEAA; Wu 2013). 188 G. Wu et al. Uterus Placenta Fetus Orn BCAA Pro Met Asn PA Blood PA flow (NO) Uterine artery GSH GSH Umbilical vein Ala Glu Asp AA AA, Gluc, O2 BCAA Skeletal Gluc Pro Gln muscle O2 Protein Orn Gln ATP Uterine AA Blood Met micro- Fruc Cit Small CO2 flow (NO) + vascula- PA intestine NH4 ture Arg Gln Arg Cit Ser GlcN6P AA Gly + + + CO2 + NH4 CO2 + NH4 CO2 + NH4 Tyr CO GSH Uterine vein Blood Umbilical artery 2 + NH + flow (NO) AA 4 Fig. 2 Provision of AA from mother to fetus in gestating swine. Uterine artery delivers AA, glucose, and oxygen from maternal arterial blood to the uterus and, through the uterine microvasculature, to the placenta. Umbilical vein supplies AA, glucose, and oxygen from the placenta to the fetus. Adapted from Wu (2013). channels, along with the participation of the fetal intestine following swallowing. Thus, with the development of intestinal amino acid transport systems during gestation, the drinking of amniotic fluid provides the enteral source of AA for fetal utilization. The nutritional significance of amniotic fluid is graphically illustrated by the finding that esophageal ligation, which prevents the entry of this fluid into the small intestine, results in IUGR in the fetus (Trahair & Harding 1995).
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