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Leucine metabolism in preterm infants receiving parenteral nutrition with medium-chain compared with long-chain triacylglycerol emulsions^1,2,3

	ABSTRACT

TOP ABSTRACT INTRODUCTION SUBJECTS AND METHODS RESULTS DISCUSSION REFERENCES

 
Background: Although medium-chain triacylglycerols (MCTs) may be utilized more efficiently than long-chain triacylglycerols (LCTs), their effect on protein metabolism remains controversial.

Objective: The aim of the study was to compare the effects of mixed MCT-LCT and pure LCT emulsions on leucine metabolism in preterm infants.

Design: Fourteen preterm [gestational age: 30 ± 1 wk; birth weight: 1409 ± 78 g ( ± SE)] neonates were randomly assigned to receive, from the first day of life, either a 50:50 MCT-LCT (mixed MCT group; n = 7) or an LCT (LCT group; n = 7) lipid emulsion as part of an isonitrogenous, isoenergetic total parenteral nutrition program. On the fourth day, infants received intravenous feeding providing 3 g lipid, 15 g glucose, and 3 g amino acidskg^-1d^-1 and underwent 1) indirect calorimetry and 2) a primed, 2-h infusion of H¹³CO₃Na to assess the recovery of ¹³C in breath, immediately followed by 3) a 3-h infusion of L-[1-¹³C]leucine.

Results: The respiratory quotient tended to be slightly but not significantly higher in the mixed MCT than in the LCT group (0.96 ± 0.06 compared with 0.93 ± 0.03). We did not detect a significant difference between the mixed MCT and LCT groups with regard to release of leucine from protein breakdown (B; 309 ± 40 compared with 257 ± 46 µmolkg^-1h^-1) and nonoxidative leucine disposal (NOLD; 296 ± 36 compared with 285 ± 49 µmolkg^-1h^-1). In contrast, leucine oxidation was greater in the mixed MCT than in the LCT group (113 ± 10 compared with 67 ± 10 µmolkg^-1h^-1; P = 0.007). Net leucine balance (NOLD - B) was less positive in the mixed MCT than in the LCT group (-14 ± 9 compared with 28 ± 10 µmolkg^-1h^-1; P = 0.011).

Conclusion: Mixed MCTs may not be as effective as LCT-containing emulsions in promoting protein accretion in parenterally fed preterm neonates.

Key Words: Parenteral nutrition • protein metabolism • preterm infants • [¹³C]leucine • [¹³C]bicarbonate • lipid emulsions • stable isotopes • energy substrates • medium-chain triacylglycerols • long-chain triacylglycerols

	INTRODUCTION

TOP ABSTRACT INTRODUCTION SUBJECTS AND METHODS RESULTS DISCUSSION REFERENCES

 
Over the first few weeks of life, preterm infants are faced with the challenging task of doubling their body weight (1), at a time when they have a high risk of developing sepsis as well as other severe diseases associated with protein wasting. In that context of accelerated growth and intense stress, accretion of body protein is a major goal of nutrition. Because the gastrointestinal system of prteterm infants is immature, the bulk of nutrients must be supplied intravenously, at least for the first several weeks.

Because lipid emulsions are more energy dense and potentially as effective as glucose for protein accretion (2), intravenous lipid emulsions are increasingly used in preterm infants receiving total parenteral nutrition (TPN). Compared with the conventional long-chain triacylglycerols (LCTs), medium-chain triacylglycerols (MCTs) have potential benefits (3) because they may 1) be more rapidly cleared from plasma, 2) enter liver mitochondria without the need for carnitine-mediated transport, and 3) preserve immune function better than do LCTs (4).

Studies performed in animals (5) and healthy adult humans (6), however, suggest that MCT emulsions may not be as effective as LCT emulsions in promoting protein deposition. The aim of this study was therefore to determine whether, when administered as part of an isonitrogenous, isoenergetic TPN regimen, MCTs have the same protein-sparing effect as LCT-containing emulsions in preterm neonates.

	SUBJECTS AND METHODS

TOP ABSTRACT INTRODUCTION SUBJECTS AND METHODS RESULTS DISCUSSION REFERENCES

 
Materials
Purchased lots of L-[1-¹³C]leucine and H¹³CO₃Na (both 99% ¹³C; from Tracer Technologies, Somerville, MA, and Cambridge Isotope Laboratories, Woburn, MA, respectively) were tested for chemical, isotopic, and optical purity by gas chromatography–mass spectrometry (GC-MS) or GC–isotope ratio MS (GC-IRMS). Tracer solutions were prepared in sterile, 0.45%-saline solution under a laminar flow hood and verified to be sterile (plate culture) and pyrogen free (Limulus lysate assay). Infusates were passed through a 0.22-µm Millipore filter (Bedford, MA) and stored in sterile containers at 4°C for <24 h until used.

Subjects
Written, informed consent was obtained from the parents of 14 neonates before enrollment and after the purpose and potential risks of the study had been fully explained to them, according to procedures approved by the Ethical Committee of the University Hospital of Nantes, France (CCPPRB no. 2, Région des Pays-de-Loire). Subjects were recruited from the neonatal intensive care unit at Hôpital Mère-Enfant, Nantes. Patients were excluded if they had major surgery, were considered to be near death, required an inspired air oxygen fraction (FiO₂) >50% or had an elevated C-reactive protein concentration or other evidence of infection, a decreased platelet count, or bilirubin concentration >150 mg/L.

Nutritional regimen
In both groups, parenteral nutrition was started on the first day of life. Glucose was started at 5 mgkg^-1min^-1 (7 gkg^-1d^-1), and rapidly increased as tolerated up to 15 gkg^-1d^-1. Parenteral amino acids (Primène-10%; Baxter/Clintec, Maurepas, France) were started on day 1 (1 gkg^-1d^-1) and increased by 1 gkg^-1d^-1 to reach 3 gkg^-1d^-1 by day 3. Parenteral lipids were started on day 2 at 1 gkg^-1d^-1. In a double-blind fashion, patients were randomly assigned to receive either an LCT emulsion (LCT group: Ivelip-20%; Baxter/Clintec) or a 50:50 MCT-LCT emulsion (mixed MCT group: Médialipide-20%; Braun, Boulogne, France). Lipids were increased at a rate of 1 gkg^-1d^-1 to reach 3 gkg^-1d^-1 by day 3. None of the infants received any enteral nutrition until after completion of the isotope infusion study on day 4 of life.

Protocol for isotope infusion
The isotopic study was performed on day 4 of life in a total of 13 infants in the fed state (6 in the mixed MCT group, 7 in the LCT group) while infants were receiving continuous intravenous nutrition through a central venous catheter. Amino acids and glucose were administered as a mixture through a single syringe pump, whereas the lipid solution was administered through a separate pump. Because some of the babies studied had received ventilatory assistance, they had an arterial line in place as well. In the babies who did not have an arterial line in place at the time of the study, a butterfly needle was inserted in a hand vein to sample arterialized venous blood.

At 0800 on the isotope study day, measurement of respiratory gas exchanges was started and continued throughout the study until 1600 by using an indirect calorimeter as described previously (7, 8). At 1030 a baseline arterial blood sample (0.5 mL) was obtained for measurement of background isotopic enrichment in plasma -ketoisocaproate (KIC). Three 1-min collections of expired air were obtained for determination of background ¹³CO₂. For babies who were receiving ventilatory assistance, expired air was collected from the exhaust of the ventilator into a 10-L Douglas bag. For babies who were breathing spontaneously under a hood, expired air was collected from the outlet of the ventilated canopy. Triplicate aliquots of expired air from each sampling time point were then immediately transferred with a syringe into evacuated tubes for later analysis.

Two stable-isotope infusions were carried out consecutively on the same day in each infant. First, a primed, continuous 2-h infusion (7.5 µmol/kg and 5 µmolkg^-1h^-1) of H¹³CO₃Na was performed from 1100 to 1300, ie, from time 0 to 120 min. The purpose of the first isotope infusion was to estimate the rate of total carbon dioxide production and the rate of recovery of ¹³C in breath from the appearance of ¹³C in expired air carbon dioxide. The labeled bicarbonate infusion was immediately followed by a primed, continuous 3-h infusion (15 µmol/kg and 15 µmolkg^-1d^-1) of L-[1-¹³C]leucine from 1300 to 1600 (ie, from 120 min to 300 min), designed to assess leucine kinetics.

Blood samples (0.5 mL) were drawn from the arterial catheter to determine plasma concentrations and enrichments of KIC at 1500, 1530, and 1600, ie, at 240, 270, and 300 min. The total volume of blood sampled was therefore 2 mL, which is <5% of blood volume in a 1000-g infant. Expired air samples were obtained at 15-min intervals between 1200 and 1300 and between 1500 and 1600, ie, during the last hour of labeled bicarbonate and labeled leucine infusion, respectively.

Analytic methods
Known amounts of -ketocaproate were added to each 100-µL aliquot of plasma to serve as an internal standard for measurement of KIC concentration by reverse isotope dilution. KIC was isolated from 100 µL plasma by passing the acidified plasma sample over an AG50 cation exchange column (Bio-Rad; Richmond, CA). To each KIC-containing fraction, 3 drops of 10 mol NaOH/L and 200 µL 0.36 mol hydroxylamine HCl/L were then added and samples were incubated at 60°C for 30 min to produce an oxime derivative. Samples were then cooled immediately on ice, acidified with 2 mol HCl/L, and mixed with 1 mL supersaturated ammonium sulfate. KIC was extracted twice by shaking after adding 8 mL ethylacetate. The supernate was then dried under nitrogen gas. Fifty microliters N-methyl-N-(t-butyldimethylsilyl)-trifluoroacetamide was added to each dry sample and incubated for 24–36 h at room temperature to obtain an oxime-t-butyldimethylsilyl (oxime-TBDMS) KIC derivative. This modified method enhanced the sensitivity of the KIC assay, allowing us to use smaller volumes of plasma than for the previously described TBDMS derivative (9).

Isotopic enrichments in plasma KIC were determined by selected ion monitoring GC-MS (MSD 5970; Hewlett-Packard, Palo Alto, CA). Ions at mass-to-charge ratios of 316 and 317, representing the prominent ions of natural KIC and [¹³C]KIC, respectively, were selectively monitored.

Expired air ¹³CO₂ enrichment was measured by GC-IRMS using a PoraPLOT-Q capillary column (Chrompack, Middelburg, Netherlands) in a Hewlett-Packard (model 5890) gas chromatograph connected online to a Finnigan Delta-S (Finnigan-MAT, Bremen, Germany) isotope ratio mass spectrometer.

Calculations
The fractional recovery of bicarbonate in breath (FRCO₂) was calculated on the basis of the excretion of ¹³CO₂ in expired air over the course of the intravenous infusion of H¹³CO₃Na as follows:

(1)

where CO₂ (µmolkg^-1h^-1) is the total rate of carbon dioxide production (measured by indirect calorimetry), E_bicarbCO₂ is the steady state enrichment in expired air of ¹³CO₂ during the last hour (1000–1100) of the H¹³CO₃Na infusion and i_bicarb (µmolkg^-1h^-1) is the rate of H¹³CO₃Na infusion. The concentration of labeled bicarbonate (i_bicarb) in the infusate was determined in a fresh aliquot of the infusate by reverse isotope dilution with GC-IRMS using unlabeled sodium carbonate as an internal standard, as described previously (10).

¹³C-Labeled bicarbonate infusion can be used to estimate CO₂ by isotope dilution as well. The appearance rate of carbon dioxide (R_aCO₂) was calculated as follows:

(2)

as shown by us (10) and others (3), and

(3)

where FRCO₂ is the fractional recovery of 13CO₂ in breath. When labeled bicarbonate is infused, the recovery of ¹³C in expired air is usually <100%. R_aCO₂ therefore usually exceeds CO₂ determined by indirect calorimetry.

Leucine appearance
R_a (µmolkg^-1h^-1) into the plasma compartment was calculated as

(4)

where i_Leu is the rate of [¹³C]leucine infusion (µmolkg^-1h^-1) and E_i and E_p are the ¹³C enrichments (mol % excess) in the infusate leucine and in plasma KIC, respectively.

Because leucine kinetics was measured under fed conditions, both exogenous (leucine from parenteral nutrition; PN_Leu) and endogenous leucine contributed to leucine R_a (flux). Because leucine is an essential amino acid, release from protein breakdown (B) is the only endogenous source of leucine; it was therefore calculated by subtracting PN_Leu intake from total leucine R_a: B = R_a - PN_Leu. Leucine oxidation (Ox, µmolkg^-1h^-1 ) was calculated as

(5)

where E_LeuCO₂ is ¹³CO₂ enrichment in expired air over the last hour of L-[1-¹³C]leucine infusion (1500–1600).

Nonoxidative leucine disposal (NOLD), an index of whole-body protein synthesis, was calculated as NOLD = R_a - Ox. Finally, net leucine balance, an index of the net protein leucine gain, was calculated as NOLD - B.

Statistics
Results are expressed as means ± SEs. Comparisons between groups were performed by using two-tailed, unpaired Student's t tests (11).

	RESULTS

TOP ABSTRACT INTRODUCTION SUBJECTS AND METHODS RESULTS DISCUSSION REFERENCES

 
Selected relevant clinical variables for the population studied, as well as the babies' nutritional intake on day 4, ie, on the day of the isotopic study, are given in Table 1. We detected no significant differences between the groups for birth weight or gestational age.

Neither O₂ (9.1 ± 1.9 compared with 9.0 ± 2.4 mLkg^-1min^-1 in the mixed MCT compared with the LCT group; P = 0.85) nor CO₂ (8.5 ± 2.0 compared with 8.4 ± 1.8 mLkg^-1min^-1; P = 0.92) differed significantly between the groups. Respiratory quotient was not significantly different in mixed MCT compared with LCT group (0.96 ± 0.14 compared with 0.93 ± 0.09; P = 0.64).

Near steady state (as defined by a CV <10% over the sampling period) was achieved in breath ¹³CO₂ and plasma [¹³C]KIC over the last hour of labeled bicarbonate infusion and [¹³C]leucine infusion (Figure 1): the equations for steady state described in the methods section were therefore used to quantitate carbon dioxide recovery and leucine kinetics.

View larger version (17K): [in this window] [in a new window]   FIGURE 1. Time course of plasma -ketoisocaproate (KIC) concentration (bottom panel), plasma [13C]KIC enrichment (middle panel), and breath 13CO2 enrichment (top panel) over the last 60 min of L-[1-13C]infusion in preterm infants receiving parenteral nutrition with medium-chain (mixed MCT group) or long-chain (LCT group) triacylglycerol emulsions. Each point represents the mean ± SD of measurements performed in 6–7 infants.

The values of R_aCO₂, as determined by using isotope dilution of labeled bicarbonate, and CO₂, determined by using indirect calorimetry, are listed in Table 2. As expected, because the fractional recovery of ¹³C in breath is always <1, R_aCO₂ exceeded CO₂. When a mean recovery of 83.9% was used to "correct" the measured R_aCO₂, however, the values obtained were not significantly different from those measured using indirect calorimetry (Table 2).

	DISCUSSION

TOP ABSTRACT INTRODUCTION SUBJECTS AND METHODS RESULTS DISCUSSION REFERENCES

In addition, the calculation of leucine oxidation assumes that the recovery of labeled carbon dioxide in breath is known. The latter is known to rise in the transition from the fasting to the fed state (14), to correlate with rates of energy expenditure (15), and to depend on the route of tracer delivery (14). Carbon dioxide recovery is unlikely to be consistent from one patient to the next in preterm neonates who experience rapid growth and various degrees of stress. Therefore, in the current study we used an approach initially proposed by Van Goudeover et al (16, 17) to quantitate the recovery of labeled carbon dioxide in each individual neonate on the same day that [¹³C]leucine kinetics was determined. We therefore believe that the difference in leucine oxidation between the groups cannot be accounted for by methodologic errors.

In vitro studies consistently show inhibition of branched-chain ketoacid dehydrogenase (3-methyl-2-oxobutanoate dehydrogenase; EC: 1.2.4.4), the key enzyme for leucine oxidation, by palmitate, a long-chain fatty acid. In contrast, octanoate, a medium-chain fatty acid, may activate the decarboxylation of branched-chain keto acids under specific conditions in rat or human muscle (18–20). It is tempting to speculate that the same mechanism may operate in vivo in TPN-fed preterm neonates.

Conflicting data have appeared in the literature with regard to the compared effects of MCTs and LCTs on the preservation of body protein. Nitrogen balance was less negative when critically ill adults admitted to an intensive care unit received for 6 d TPN containing MCTs compared with LCT emulsions (21). Similarly, there was a trend toward an improved nitrogen balance in adult patients undergoing major elective surgery of the gastrointestinal tract (22) who received 10 d of MCT-containing TPN, compared with LCTs. However, no difference was observed in rates of urea production and protein breakdown between MCT- and LCT-based emulsions within 12 h of initiation of TPN in critically ill patients (23). Finally, the lesser anabolic effect of MCT in the current study is consistent with earlier studies carried out in dogs (5) and healthy adult humans (6). Both of these studies, which involved the determination of leucine metabolism by tracer methods, documented a higher rate of leucine oxidation during short-term infusion of MCT compared with LCT emulsions. To our knowledge, the current study is the first to compare the protein anabolic effects of MCTs and LCTs in a population of premature neonates. NOLD - B, the difference between leucine released from protein breakdown and leucine utilization for protein synthesis, was positive in the LCT group, whereas it was not in the mixed MCT group. Extrapolation from the current data must, however, be done with caution. Because leucine metabolism was assessed on a single occasion on the fourth day of life, it cannot be ascertained from the data whether differences in leucine kinetics would persist after longer exposure to the same doses or to different doses of MCTs. In summary, the higher rate of leucine oxidation and less positive leucine balance observed with MCTs than with LCTs suggest that intravenous MCTs may not be as effective as LCTs in promoting protein deposition in preterm infants receiving TPN in the first few days of life.

	ACKNOWLEDGMENTS

 
We thank the nursing staff of the Neonatology Unit at Hôpital Mère-Enfant for their superb care of the infants, Odile Desfontaines and Isabelle Grit for their excellent technical assistance, Philippe Mauran for dispensing the fat emulsions, and Alain Mouzard and Michel Krempf for their support and advice in performing these demanding studies.

	FOOTNOTES

 
¹ From the Division of Neonatology, Hôpital Mère-Enfant, CHU de Nantes, and Centre de Recherche en Nutrition Humaine, Nantes, France.

² Supported in part by grants from Baxter/Clintec; the Fondation pour la Recherche Médicale, Paris; the Conseil Général de Loire-Atlantique; the City of Nantes; and the Région des Pays-de-la-Loire.

³ Address reprint requests to D Darmaun, Centre de Recherche en Nutrition Humaine, Hotel-Dieu Hospital, 44093 Nantes cedex 1, France. E-mail: ddarmaun{at}nantes.inserm.fr.

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