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The Journal of Nutrition Vol. 128 No. 10 October 1998,
pp. 1752-1759
, **, 
, , , and, **, , , 4
* Department of Human Biology and Nutritional Sciences and Department of Animal and Poultry Science, University of Guelph, Guelph, ON, Canada N1G 2W1; ** Department of Agricultural, Food, and Nutritional Sciences, University of Alberta, Edmonton, AB, Canada T6G 2P5; The Research Institute, The Hospital for Sick Children, Toronto; and Department of Paediatrics and Department of Nutritional Sciences, University of Toronto, Toronto, ON, Canada M5G 1X8
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ABSTRACT |
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Abstract
Introduction
Methods
Results
Discussion
References
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Evidence is accumulating that the amino acid requirements for neonates receiving total parenteral nutrition (TPN) are significantly different than those for oral feeding and need to be determined. The parenteral threonine requirement was determined in 3-d-old male Yorkshire piglets (n = 25) by examining the effect of varying dietary threonine intakes [0.05-0.6 g/(kg·d)] on phenylalanine oxidation. The diet included adequate energy, total amino acids and phenylalanine, with excess tyrosine. Phenylalanine kinetics were determined from a primed, continuous intravenous infusion of L-[1-14C]phenylalanine. Phenylalanine oxidation, estimated from the rate of 14CO2 released in expired air during isotope infusion, decreased (P < 0.05) as threonine intake increased from 0.05 to 0.15 g/(kg·d) and was low and constant for threonine intakes >0.15 g/(kg·d). Using breakpoint analysis with 95% confidence interval (CI), mean requirement and safe level of parenteral threonine intake were estimated to be 0.19 and 0.21 g/(kg·d), respectively (equivalent to 13 and 14 mg/g amino acids, respectively). To compare these data with those of orally fed controls, we then repeated the experiment by infusing identical diets intragastrically to piglets (n = 25); the varying dietary threonine intakes were 0.1-1.2 g/(kg·d). Employing identical kinetics and analyses, the mean requirement and safe level of oral threonine intake were estimated to be 0.42 and 0.51 g/(kg·d), respectively (equivalent to 28 and 34 mg/g amino acids, respectively). These data demonstrate that the threonine requirement of neonates during TPN is ~45% of the mean oral requirement.
KEY WORDS: total parenteral nutrition · piglets · threonine · amino acid kinetics · indicator amino acid oxidation
Part of the nutritional strategy for neonates fed enterally or parenterally is to provide indispensable amino acids at a level sufficient to meet the demands for protein synthesis while avoiding an excessive supply. The accumulation of an amino acid or its degradative products in body pools may stress immature enzymatic systems and lead to further accumulation and possible toxicity. The threonine requirement is affected by the ontogenic development of metabolic enzymes. In both preterm (Schanler and Garza 1987 The amino acid profile and concentrations in parenteral nutrition solutions generally reflect those in oral diets. However, there is evidence that parenteral amino acid requirements are lower than enteral requirements (House et al. 1998 No reports were found in the literature in which the threonine requirement was determined directly in either orally or parenterally fed premature infants. The objective of this study was to determine threonine requirement in a neonatal piglet model receiving total parenteral nutrition (TPN)5 by employing the indicator amino acid oxidation technique using L-[1-14C]phenylalanine. Discovery of a threonine requirement different from current practice would justify direct studies in the human infant. This study contributes to our overall goal of designing an optimal amino acid profile for neonates.
Animals and study protocol.
All procedures used in this study were approved by the Animal Care Committee of the University of Guelph. A total of 50 male Yorkshire piglets, ~3 d of age, were transferred from a specific pathogen-free herd (Arkell Swine Research Unit, University of Guelph, Guelph, Canada) to the animal holding facilities in the Department of Animal and Poultry Science, University of Guelph. On arrival, the piglets were weighed, anesthetized and fitted with catheters (Ed-Art, Don Mills, Canada) by using modified methods of Wykes et al. (1993) Tracer infusion, 14CO2 collection and analytical procedures.
Phenylalanine flux and oxidation were determined in Experiment 1 by a primed [260 kBq (7 µCi)/kg], constant infusion [130 kBq (3.5 µCi)/(kg·h)] of a tracer solution containing 85.1 MBq (2.3 mCi)/L of L-[1-14C]phenylalanine [200 MBq (54 mCi)/mmol; Dupont Canada, Mississauga, Canada]. In Experiment 2, the prime infusion was reduced [186 kBq (5 µCi)/kg]; furthermore, because of the uncertainty of our new intragastric model, we extended the constant infusion to 6 h to ensure that adequate plateaux were achieved. Details of the infusion protocol, 14CO2 and blood collection procedures have been described previously (House et al. 1997a Statistical analyses.
Each experiment was a completely randomized design, with intake of threonine serving as the main treatment effect. Differences among treatments were determined by ANOVA (SAS/STAT, version 6.09, SAS Institute, Cary, NC). If P values were <0.05 for the F-value of the ANOVA model, significant differences between treatment means were assessed by using the Student-Newman-Keuls multiple comparisons procedure. Threonine requirements were established using a two-phase linear regression crossover model, as described previously (Ball and Bayley 1984 The piglets remained healthy and were interested in the environment during the course of both trials. The weight upon arrival (1.75 kg, pooled SD = 0.14) and final weight (2.57 kg, pooled SD = 0.20) were not significantly different among diet levels or between feeding routes. Rates of body weight gain for the 5 d after adaptation and before diet treatment initiation were not different (145 and 146 g/d for parenterally fed and intragastrically fed piglets, respectively).
Experiment 1: Parenteral threonine requirement.
Threonine intake significantly influenced plasma phenylalanine concentration, which declined from 119 to 77 µmol/L as threonine intake increased from 0.05 to 0.10 g/(kg·d), respectively (P < 0.05); no significant changes in phenylalanine concentration were observed with further increases in threonine intake (not shown). Plasma threonine concentration increased significantly from 88 to 647 µmol/L as threonine intake increased from 0.05 to 0.60 g/(kg·d) (P < 0.0001) (not shown).
Experiment 2: Oral threonine requirement.
As in the parenteral requirement study, plasma phenylalanine concentration declined as threonine intake increased [146 µmol/L at 0.1 g threonine/(kg·d) to 82 µmol/L at 0.2 g threonine/(kg·d); P < 0.05)]; phenylalanine concentration did not change with further increases in threonine intake (not shown). Plasma threonine concentration increased from 27 to 1732 µmol/L with increasing threonine intakes from 0.1 to 1.2 g/(kg·d) (P < 0.001) (not shown).
The indicator amino acid oxidation technique has been successfully applied to determine amino acid requirements in piglets and humans (Zello et al. 1995
INTRODUCTION
Abstract
Introduction
Methods
Results
Discussion
References
) and term infants (Janas et al. 1985), threonine intake positively correlated with plasma threonine, suggesting that oxidation of excess threonine was not sufficient. Furthermore, in preterm infants fed formula, the highest serum threonine concentrations were observed in the infants with the lowest gestational ages (Rigo and Senterre 1980). In growing rats, hepatic threonine dehydratase (EC 4.2.1.16) activity was low during most of the postnatal period, compared with adult rats (Grogan et al. 1988). High plasma concentrations of threonine are of potential concern in infants because of the possible neurotoxic effects of threonine. Because threonine concentrations in cerebrospinal fluid correlate with increasing plasma concentrations and because of the extensive neurologic development occurring during the early life of infants, high threonine intakes represent a possible danger to the developing brain (Anderson and Raiten 1992). Therefore, excess threonine intakes might be hazardous to the premature infant fed orally or parenterally due to the immature metabolic system of these infants.
). Parenterally administered threonine, in particular, may be in excess because gastrointestinal requirements are diminished as a result of gut atrophy. In low birth weight infants receiving intravenous infusions containing threonine, increased plasma threonine concentrations were observed even when total nitrogen and energy intakes were low (Anderson et al. 1977). High threonine intakes, such as those provided by intravenous solutions (Anderson et al. 1977) and whey protein-predominant formulas (Janas et al. 1985), appear to exceed the capacity of the low birth weight infant to metabolize this amino acid (Rigo et al. 1994, Scott et al. 1985). Given a reduced capacity to metabolize threonine during early infancy, threonine intakes in excess of requirement should be avoided in both oral and intravenous formulations.
MATERIALS AND METHODS
Abstract
Introduction
Methods
Results
Discussion
References
for the venous catheters and Rombeau et al. (1984) for the stomach catheter. Briefly, catheters were tunnelled under the skin from the point of exit on the left side of the chest to the points of entry into the blood vessels or stomach. In Experiment 1 (parenteral threonine requirement), an infusion catheter was inserted into the left jugular vein and advanced to the superior vena cava just cranial to the heart. In Experiment 2 (oral threonine requirement), the infusion catheter was inserted into the stomach using a Stamm gastrostomy. A sampling catheter was introduced into the left femoral vein of all pigs and advanced into the inferior vena cava just caudal to the heart. Catheter positions were verified at necropsy. After surgery, the piglets were fitted with an adjustable cotton jacket with an attached anchoring button attached to a tether. The laboratory conditions and piglet housing have been described previously (Wykes et al. 1993).
). In Experiment 1, TPN was administered using pressure-sensitive infusion pumps and lipid (Intralipid 20%, Pharmacia-Upjohn, Stockholm, Sweden) was infused simultaneously using syringe pumps. In Experiment 2, water (1.5-fold dilution to lower osmolarity) and the appropriate amount of lipid were added to the final solutions, which were infused continuously by using the same pressure-sensitive infusion pumps. The infusion regimen (continuous, 24 h) was designed to supply all nutrients required by piglets (Wykes et al. 1993); piglets received 15 g amino acids/(kg·d) and 1.1 MJ metabolizable energy/(kg·d) with glucose and lipid each supplying 50% of nonprotein energy intake. Full infusion rates for Experiment 1 [272 mL/(kg·d) TPN, 52 mL/(kg·d) lipid] and Experiment 2 [480 mL/(kg·d)] were adjusted so that energy and nitrogen intakes were identical for all piglets. The base amino acid profile of the TPN consisted of (mg/g total L-amino acids): alanine, 92; arginine, 61; aspartic acid, 61; cysteine, 15; glutamic acid, 105; glycine, 33; histidine, 31; isoleucine, 46; leucine, 104; lysine, 56; methionine, 19; phenylalanine, 32; proline, 83; serine, 56; taurine, 5; threonine, 53; tryptophan, 21; tyrosine, 27 (supplied as the soluble dipeptide glycyl-L-tyrosine); and valine, 53. The amino acid profile was based on human milk protein (Vaminolact: Pharmacia-Upjohn) with phenylalanine and tyrosine provided at their estimated safe levels of intake (House et al. 1997a and 1997b).
). Immediately after the infusion, piglets were killed by infusion of 750 mg of sodium pentobarbital into the venous sampling catheter.
).
). SRA for plasma phenylalanine and tyrosine for each time point during the infusion study were plotted. Plateau values were calculated as the mean of the plasma SRA at the time points within the plateau. Plateaux were verified by determining through regression analysis that the slope was not different from zero.
, Seber 1977). Regression variables included the level of amino acid intake as the independent variable, and phenylalanine oxidation [µmol/(kg·h) and percentage of dose] or phenylalanine balance as the dependent variable. The upper limit of the 95% confidence interval (CI) of the breakpoint was estimated to determine a safe level of intake.
RESULTS
Abstract
Introduction
Methods
Results
Discussion
References
View this table:
Table 1.
Experiment 1: plateau values for 14CO2 production and phenylalanine (Phe) and tyrosine (Tyr) specific radioactivity (SRA) in plasma of piglets receiving total nutrition parenterally with graded intakes of threonine1
View this table:
Table 2.
Experiment 1: phenylalanine kinetics of piglets receiving total nutrition parenterally with graded intakes of threonine1
).
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Fig 1.
Experiment 1: rate of L-[1-14C]phenylalanine oxidation in piglets receiving total nutrition parenterally with graded intakes of threonine. Pooled SD: 4 µmol/(kg·h).
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[in a new window]
Fig 2.
Experiment 1: oxidation of L-[1-14C]phenylalanine as a percentage of dose in piglets receiving total nutrition parenterally with graded intakes of threonine. Pooled SD: 0.5%.
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Fig 3.
Experiment 1: apparent phenylalanine balance in piglets receiving total nutrition parenterally with graded intakes of threonine. Pooled SD: 4 µmol/(kg·h).
View this table:
Table 3.
Experiment 2: plateau values for 14CO2 production and phenylalanine (Phe) and tyrosine (Tyr) specific radioactivity (SRA) in plasma in piglets receiving total nutrition intragastrically with graded intakes of threonine1
View this table:
Table 4.
Experiment 2: phenylalanine kinetics of piglets receiving total nutrition intragastrically with graded intakes of threonine1
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[in a new window]
Fig 4.
Experiment 2: rate of L-[1-14C]phenylalanine oxidation in piglets receiving total nutrition intragastrically with graded intakes of threonine. Pooled SD: 12 µmol/(kg·h).
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[in a new window]
Fig 5.
Experiment 2: oxidation of L-[1-14C]phenylalanine as a percentage of dose in piglets receiving total nutrition intragastrically with graded intakes of threonine. Pooled SD: 2.1%.
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[in a new window]
Fig 6.
Experiment 2: apparent phenylalanine balance in piglets receiving total nutrition intragastrically with graded intakes of threonine. Pooled SD: 12 µmol/(kg·h).
DISCUSSION
Abstract
Introduction
Methods
Results
Discussion
References
). Because threonine has a complicated metabolic pathway, the direct oxidation technique is inappropriate; if threonine oxidation had been measured by the production of labeled 14CO2 from 14C-threonine, a major underestimate would have been introduced by the sequestration of carbons 1 and 2 of threonine into glycine (Ballevre et al. 1990). Thus, the use of the indicator amino acid oxidation technique is a more suitable method to estimate threonine requirements.
). However, NRC requirements cannot be used for direct comparison because they are extrapolated from data that are expressed as a percentage of a corn-soybean meal diet (Kim et al. 1983). Furthermore, within the experiments used to determine the requirements, the protein intakes and digestibilities varied widely. Therefore, to provide a direct comparison for the parenteral threonine requirement, we determined the oral threonine requirement in similar piglets continuously fed identical diets via intragastric catheters. The data for the oral requirement study indicated that the mean oral threonine requirement was 0.46 g/(kg·d) [upper 95% CI: 0.61 g/(kg·d)] when based on either phenylalanine oxidation rate or balance, and 0.42 g/(kg·d) [upper 95% CI: 0.51 g/(kg·d)] when based on phenylalanine oxidation as a percentage of dose. As in the parenteral requirement study, the data set for phenylalanine oxidation as a percentage of dose was the least variable; therefore, an oral threonine intake of 0.51 g/(kg·d) (34 mg/g amino acids) is proposed as a safe intake level for intragastrically fed piglets.
). The "broken-line" regression model analysis produced a mean threonine requirement of 6.0 g/kg diet [~0.58 g/(kg body weight·d)]. Using the same technique, the mean lysine requirement was estimated at 12 g/kg diet, resulting in a threonine/lysine ratio of 1:2 (Kim et al. 1983). According to the NRC (1998), the estimated mean requirement for 3-kg piglets fed a corn-soybean meal diet (growing at 141 g/d) is 8.7 g available threonine/kg diet[~0.68 g/(kg body weight·d)] compared with the mean lysine requirement of 14.0 g/kg diet; thus, the NRC (1998) recommends a ratio of 1:1.61 for 3-kg piglets. In 10-kg piglets, Chung and Baker (1992) proposed an ideal threonine/lysine ratio of 1:1.54. Hence, according to these experiments in orally fed animals, the threonine requirement for young piglets is ~50-65% of the lysine requirement.
). A lower estimate of amino acid requirement for TPN-fed piglets compared with that of orally fed piglets might be expected because first-pass metabolism by the splanchnic organs is bypassed during parenteral feeding and the gastrointestinal tract atrophies. Indeed, in the lysine requirement study, a reduced demand (72% of oral requirement) for lysine during parenteral feeding was found [0.79 and 1.09 g/(kg·d) for TPN and oral feeding, respectively, for same age piglets] (House et al. 1998). However, the predicted threonine requirement for TPN-fed piglets of 0.4-0.5 g/(kg·d) was more than twice the mean requirement of 0.19 g/(kg·d) determined in this study. Possible explanations to be considered for this difference are as follows: TPN delivers nutrients intravenously that might affect protein and amino acid metabolism; threonine demand is reduced during TPN because threonine is a critical amino acid for the synthesis of glycoproteins at the surface of the small intestine, which is atrophied.
). In another study, the kinetics of glycine, leucine and phenylalanine, which represent different catabolic sites in the body, have been investigated during both TPN and enteral feeding in human infants (Wykes et al. 1992). That study demonstrated that kinetics of the individual amino acids were influenced by the interaction of several factors, including amino acid intake, route of feeding and route of tracer administration. The effect of the feeding regimen was specific to each amino acid such that glycine flux was lower during parenteral feeding compared with oral feeding, leucine flux was unaffected and phenylalanine flux was higher. Similar to phenylalanine, threonine is catabolized primarily in the liver; because parenteral threonine does not undergo first-pass metabolism by the gut and liver, threonine metabolism might be similarly affected during TPN.
). In a recent study in piglets, Stoll et al. (1998) showed that the gastrointestinal tract metabolizes ~35% of dietary leucine, lysine and phenylalanine on first pass, compared with 61% for dietary threonine. Furthermore, they showed that nearly 90% of this metabolized threonine was either secreted as mucosal proteins or catabolized. In humans, gastrointestinal losses of most indispensable amino acids accounted for 14-33% of daily maintenance requirement, but for threonine the contribution was up to 61% (Fuller et al. 1994). These studies suggest that threonine is in high demand by the gastrointestinal tract and that a significant proportion of the whole-body threonine requirement is accounted for by the gastrointestinal tract during oral feeding. The route of nutrient delivery has a dramatic effect on mucosal morphology and function. TPN feeding in piglets leads to a rapid reduction in small intestinal weight, villous height, mucosal depth, disaccharidase activity and the RNA/DNA ratio in spite of the maintenance of normal energy and protein intakes (Goldstein et al. 1985, Shulman 1988). Furthermore, by using piglets and protocol identical to those used in this study, those fed intravenously for 8 d had total mucosal mass that was reduced by 40% compared with piglets fed identical TPN solutions intragastrically (Bertolo et al. 1996). Reduced mucosal mass and function resulting from TPN feeding may account for a large part of the reduced whole-body requirement of threonine.
). Goblet cells throughout the length of the small and large intestine are responsible for the production and maintenance of the protective mucous coating by synthesizing and secreting mucin (Specian and Oliver 1991). Absence of enteral nutrition leads not only to atrophy of mucosal epithelial cells, but also to atrophy of the goblet cells, resulting in a deficient mucous protection layer (Bengmark and Jeppson 1995). Goblet cell atrophy during TPN feeding would reduce mucin production and hence reduce threonine requirements.
). Decreased antral and serum gastrin in TPN-maintained animals suggests that this hormone might be involved in maintenance of gut mass (Rossi 1986). In addition, growth factors in mammalian breast milk play an important role in the growth and development of the gastrointestinal tract and are missing from TPN solutions and milk formulas (Odle et al. 1996). In a recent study in which threonine was supplied to infants at an identical level via breast milk or formula, a lower plasma threonine concentration and higher threonine oxidation rates were observed in the breast milk-fed infants (Darling et al. 1995). These differences were attributed to the presence of hormones and growth factors in the breast milk. Parenteral nutrition has neither the gastrointestinal nutrients required to trigger hormone release (i.e., gastrin and CCK) nor the dietary trophic factors (i.e., IGF and EGF), that may influence threonine metabolism.
, NRC 1998), whereas the mean threonine requirement during TPN [0.19 g/(kg·d)] is 45% of the oral requirement [0.42 g/(kg·d)].
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FOOTNOTES |
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Manuscript received 3 November 1997. Initial reviews completed 5 January 1998. Revision accepted 2 June 1998.
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LITERATURE CITED |
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Abstract
Introduction
Methods
Results
Discussion
References
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