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Original Article |

Nutritional Intervention High in Vitamins, Protein, Amino Acids, and ω3 Fatty Acids Improves Protein Metabolism During the Hypermetabolic State After Thermal Injury FREE

Marc G. Jeschke, MD; David N. Herndon, MD; Christoph Ebener, MD; Robert E. Barrow, PhD; Karl-Walter Jauch, MD, PhD
[+] Author Affiliations

From the Klinik und Poliklinik f[[uuml]]r Chirurgie, Klinikum der Universit[[auml]]t Regensburg, Regensburg, Germany (Drs Jeschke, Ebener, and Jauch); and the Shriners Hospital for Children and Department of Surgery, University of Texas Medical Branch, Galveston (Drs Jeschke, Herndon, and Barrow).


Arch Surg. 2001;136(11):1301-1306. doi:10.1001/archsurg.136.11.1301.
Text Size: A A A
Published online

Hypothesis  Characteristic of the hypermetabolic response to a thermal injury is the massive protein catabolism and compromised structure and function of essential organs. Nutrition has been suggested to affect protein metabolism and clinical outcome after a severe injury but published studies show controversial data. The purpose of this study was to determine the effect of enriched nutritional support during the postburn hypermetabolic state on protein metabolism in serum, liver, muscle, and skin.

Setting  Laboratory.

Intervention  Twenty-two rats were given burns covering 60% of their total body surface area and randomized to receive either standard rat chow (control) or a diet high in vitamins, protein, amino acids, and ω3 fatty acids.

Main Outcome Measures  Five weeks after injury, body weight, serum, muscle, and hepatic protein content, insulin-like growth factor I concentration, and wound healing (reepithelization) were determined.

Results  Rats receiving the enriched diet showed a gradual improvement in body weight 1, 2, 3, 4, and 5 weeks postburn compared with controls (P<.001). Diet-fed rats demonstrated higher protein and insulin-like growth factor 1 content in serum, muscle, and liver 5 weeks after trauma (P<.001). Serum protein, albumin, and transferrin levels were significantly increased in rats receiving the diet compared with control rats (P<.001). Reepithelization was accelerated in rats receiving the enriched diet 4 (diet-fed, mean ± SD, 23% ± 1% vs controls, 17% ± 1%; P<.001) and 5 (diet-fed, 24% ± 1% vs controls, 18% ± 1%; P<.001) weeks postburn compared with control rats.

Conclusions  Nutritional intervention high in protein, vitamins, amino acids, and ω3 fatty acids improves protein net balance during the hypermetabolic response to thermal injury. Compromised organ function and structure and clinical outcome during the hypermetabolic response may be improved.

Figures in this Article

THE RESPONSE to injury, known as the hypermetabolic response, occurs after a severe thermal injury.1,2 Increases in cardiac output, oxygen consumption, nitrogen loss, lipolysis, body weight loss, and metabolic rate are directly proportional to the size of the burn.1 The pathophysiology of this state is associated with the inflammatory cascade of cytokines, glucocorticoids, and prostaglandins.3 The metabolic rate postinjury is extremely high and energy requirements are immense. Increased protein turnover, degradation, and negative nitrogen balance are characteristics of this critical state.4,5 These energy requirements are met by mobilization of carbohydrates, fat, and protein stores. However, energy stores, particularly glycogen stores, are quickly depleted and the energy needs are met by increased glycogenesis from amino acid mobilization originating from the skeletal muscle, which leads to loss of muscle tissue and malnutrition.6 Consequently, the structure and function of essential organs are compromised, such as skeletal muscle, skin, and the immune system, and cellular membrane transport functions are altered.7,8 Another important step in the hypermetabolic cascade is growth hormone resistance and decreased production and action of insulin-like growth factor I (IGF-I).9,10

Malnutrition in thermally injured patients has been suggested to be subverted to some extent by exogenous nutritional support11 and several modifications of the nutrient composition have undergone basic and clinical investigations. The results are somewhat contrary. An arginine-supplemented diet has been suggested to decrease proinflammatory cytokines and to improve survival in burned rats,12 while the administration of an ω3 fatty acid–enriched diet has been found to enhance the immune system.13 However, there have been studies that have found no beneficial effects of arginine or ω3 fatty acids.14 The effect of high-protein supplementation has also been described with controversy. Nelson et al15 found that a high-protein diet is associated with increased bacterial translocation in septic guinea pigs, while Saffle et al14 reported improved survival of burned rats receiving a high-protein diet. Demling and colleagues16 studied the effect of a high-calorie, high-protein diet on weight gain and muscle function in the recovery phase after severe burns and found that increased protein intake by adding a protein hydrolysate increases the rate of restoration of body weight and muscle function.

The purpose of our study was to determine whether early enteral administration of a diet high in protein, vitamins, ω3 fatty acids, and amino acids improves protein metabolism and the hepatic acute-phase response during the posttrauma hypermetabolic state. Protein metabolism was evaluated by measuring hepatic protein synthesis, hepatic, serum, and muscle protein levels; IGF-I concentration; and dermal wound healing in the form of reepithelization.

Twenty-two adult male Sprague-Dawley rats (350-375 g) were placed in wire-bottomed cages housed in a temperature-controlled room with a 12-hour light-dark cycle. Rats were acclimatized to their environment for 7 days before the study. All rats received water ad libitum throughout the study. Four days before the injury, rats were randomized into 2 groups: rats fed standard rat chow (control, n = 11) or rats fed a diet rich in vitamins, ω3 fatty acids, protein, and carbohydrates (enriched diet, n = 11).

Each rat received a 60% total body surface area full-thickness scald burn under general anesthesia (pentobarbital 50 mg/kg of body weight) and analgesia (buprenorphine, 1 mg/kg body weight) following a modified procedure as previously described.17 Rats were anesthetized, shaved, and scalded with 99° water over 60% of their total body surface area (10 seconds of contact to the back and 1.5 seconds to the belly). This model ensures that both groups are similar in metabolic rates. After the thermal injury, rats were immediately resuscitated by intraperitoneal injection of Ringer's lactate (50 mL/kg of body weight).

The study period lasted 5 weeks after the injury. Animals were euthanized by decapitation. Blood was collected into serum and plasma separators, spun at 1000g for 15 minutes, and the supernatant and pellet were separated and stored at −73°C. Samples of liver, muscle, and skin from the back were harvested, snap-frozen in liquid nitrogen, and stored at −73°C for analysis.

NUTRITION

Rat chow was composed of 64% carbohydrates, 5% fat, and 14% protein (Harlan Teklad 2014; Harlan, Madison, Wis). The mean ± SD food intake of rats receiving chow was 26 ± 3 g/d. The liquid diet (Sustacal; Mead Johnson Nutritionals, Evansville, Ind), rich in vitamins, protein, and carbohydrates, had a caloric distribution of 24% protein, 21% fat, and 55% carbohydrates, resulting in an energy intake of 1.01 cal/mL. The diet had a renal solute load of 510 mOsm/L, an osmolality of 650 mOsm/kg of water, and was lactose free. The nutrient values for Sustacal and chow are presented in Table 1. Nutrient compositions were provided by the manufacturers.

Table Graphic Jump LocationTable 1. Nutrition Information for Sustacal and Rat Chow*

Both groups of rats were pair-fed according to the caloric intake. The feeding protocol was as follows: 25 calories on the day of the burn, 51 calories on the first day postburn, 76 calories on the second, and 101 calories from the third day on. Nutritional intake was the same in all groups.

Serum total protein, albumin, and transferrin as constitutive hepatic proteins were determined to be nutritional markers. Protein levels were determined by a Behring nephelometer (Behring, Deerfield, Ill). Liver and muscle protein concentrations were determined by protein assay. Wet-dry ratios were determined in liver and muscle using the formula:

in which w indicates wet weight; and d, dry weight.

SERUM, HEPATIC, AND MUSCLE IGF-I CONCENTRATIONS

Insulin-like growth factor I protein concentrations were measured by rat radioimmunoassay in serum, liver, and muscle, taken 35 days postburn. Proteins in tissues were extracted by pulverizing approximately 40 mg of tissue in liquid nitrogen, adding an extraction buffer (phosphate-buffered isotonic sodium chloride solution, 0.25 mL of PMSF, 50 mg of leupeptin, 100 mg of aprotinin, and 50 mg of antipain) in a 1:7 mixture (7 mL buffer per gram of tissue), and homogenizing the mixture. To allow proteins to recover, samples were frozen overnight at −80°C. After thawing, 50 µL of the homogenate was added to 150 µL of the extraction solution and centrifuged at 13 500 rpm for 5 minutes. One hundred microliters of supernatant was added to 400 µL of neutralization solution and the rat IGF-I radioimmunoassay was performed as described in the kit guidelines (Diagnostic System Laboratories, Webster, Tex).

WOUND HEALING

Wound healing, defined here as reepithelization, was determined as follows: The wound eschar was left intact for the first 28 days and then removed by gentle traction, caution being taken not to disturb or destroy the healing edge along the periphery. After removing the eschar, the animals were placed on a standard surface and the wound area was traced onto acetate sheets along the well-demarcated reepithelized and nonburned interface and the leading edge of the neoepithelium. The areas of these tracings were calculated by computerized planimetry. The area of reepithelization was calculated by the following formula:

in which o indicates outer area 4 or 5 weeks postburn; i, inner area 4 or 5 weeks postburn; and b, original area at the time of the burn.

Values in Figure 1 are expressed as percent reepithelization from the original burn wound.

Place holder to copy figure label and caption
Figure 1.

Wound healing measured as reepithelization 4 and 5 weeks after the thermal injury. Rats fed the enriched diet demonstrated accelerated reepithelization by almost 10% at 4 and 5 weeks after burn compared with rats fed chow (P<.05).

Graphic Jump Location
ETHICS AND STATISTICS

These studies were reviewed and approved by the Animal Care and Use Committee of the University of Texas Medical Branch, Galveston, assuring that all animals received humane care according to the criteria of the National Institutes of Health. Statistical comparisons were made by analysis of variance and the t test with a Bonferroni correction. Data are expressed as mean ± SEM. Significance was accepted at P<.05.

BODY WEIGHT

Both groups of rats lost body weight after the burn. Rats that received the enriched diet demonstrated progressive improvement in body weight 1 through 5 weeks postinjury compared with rats fed standard chow (P<.05). Rats receiving the enriched diet had a 0.5% increase in body weight (compared with the body weight preburn) 5 weeks after the burn, whereas rats receiving normal chow lost approximately 10% of their preburn weight (P<.05) (Figure 2).

Place holder to copy figure label and caption
Figure 2.

Changes in body weight during the 5-week study period. Thermally injured rats receiving the enriched diet demonstrated improvement in body weight 1, 2, 3, 4, and 5 weeks after the injury. These rats even gained weight 5 weeks after the injury in addition to the preinjury weight, whereas animals receiving regular chow lost almost 10% of their preburn body weight. Asterisks indicate significant difference between diet and chow at the same time point, P<.05.

Graphic Jump Location
SERUM, HEPATIC, AND MUSCLE PROTEIN CONCENTRATION

Rats that were fed the standard chow had significantly lower total serum protein concentrations (P<.001), lower serum albumin concentrations (P<.001), and lower serum transferrin concentrations (P<.003) 5 weeks after the thermal injury than rats that received the diet (Table 2).

Table Graphic Jump LocationTable 2. Serum Total Protein, Albumin, and Transferrin Concentrations 5 Weeks Postburn in Rats Receiving a Diet High in Vitamins, Protein, ω-3 Fatty Acids, and Amino Acids Compared With Rats Receiving Standard Rat Chow

Rats receiving Sustacal had an increased muscle wet-dry ratio (P<.01) and total protein content in the muscle compared with rats receiving chow (P<.02). Similarly, the Sustacal group had increased hepatic protein content as shown by increased hepatic wet-dry ratio (P<.001) and total hepatic protein content (P<.02) compared with the chow group (Table 2).

SERUM, HEPATIC, AND MUSCLE IGF-I CONCENTRATION

Animals fed Sustacal had higher serum, hepatic, and muscle IGF-I concentrations (Table 3) compared with animals fed standard chow (P<.05).

Table Graphic Jump LocationTable 3. Serum and Liver IGF-I Concentration 5 Weeks Postburn in Rats Receiving a Diet High in Vitamins, Protein, ω-3 Fatty Acids, and Amino Acids Compared With Rats Receiving Standard Rat Chow*
WOUND HEALING

Reepithelization was determined 28 and 33 days after the burn. Rats fed chow had a reepithelization of 17.3% ± 0.7% 28 days postburn and 18.4% ± 0.5% 33 days postburn, respectively. Rats fed the diet had a reepithelization of 23.3% ± 0.8% 28 days postburn and 24.0% ± 0.9% 33 days postburn (Figure 2). Therefore, rats fed Sustacal had a significantly more accelerated wound reepithelization compared with rats fed regular chow (P<.001).

The hypermetabolism and negative nitrogen balance associated with thermal injury were recognized by Cuthbertson and Zagreb.18 Since that time there has been a lot of progress in therapeutic strategies to improve the hypermetabolic response and therefore, mortality, of severely burned patients, such as maintaining patients in a warm environment (approximately 30°C), providing pain control, early wound excision, grafting using biological and synthetic wound dressings, and the prevention of sepsis.

The characteristics of critically injured patients are increased protein turnover and negative nitrogen balance.4,5 The specific pathophysiology has been recently described.7 After trauma in skeletal muscle, the rates of proteolysis and synthesis are accelerated. However, despite the increased protein synthesis rate, proteolysis dominates, leading to a negative protein net balance. Intramuscular glutamine concentration is decreased because of increased efflux and decreased de novo synthesis. As a consequence, tissues and organs characterized by rapidly replicating cells, such as the gut with its enterocytes, the skin with its granulation tissues consisting of fibroblasts and keratinocytes, the skeletal muscle, and the immune system, exhibit early decreased protein synthesis. Protein depletion results in the need for prolonged respiratory support, delayed mobilization of the patient, delayed wound healing, and compromised immune function.8

Several therapeutic approaches have been undertaken to lessen the massive protein waste, one of which is adequate nutritional support. The aims of nutritional support are to maintain and improve organ function, prevent calorie malnutrition, and improve morbidity and mortality. The change from total parenteral nutrition to early enteral feeding has been shown to decrease the incidence of sepsis and improve the hypermetabolic state.11 An arginine-supplemented diet has been found to decrease proinflammatory cytokines and improve survival rates in burned rats12 and administration of ω3 fatty acids has been reported to improve the immune system functions.14

The hepatic acute-phase response is a cascade of events initiated to prevent tissue damage and to activate repair processes. The acute-phase response is initiated by activated phagocytic cells, fibroblasts, and endothelial cells, which release proinflammatory cytokines, leading to the systemic phase of the acute-phase response. A crucial step in this cascade of reactions involves the interaction between the site of injury and the liver, which is the principal organ responsible for producing acute-phase proteins and modulating the systemic inflammatory response. After major trauma such as a severe burn, hepatic protein synthesis shifts from hepatic constitutive proteins, such as albumin, prealbumin, transferrin, and retinol-binding proteins to acute-phase proteins.1921 After a thermal injury, albumin and transferrin decrease by 50% to 70% below normal levels.2022 Albumin and transferrin, however, have important physiologic functions since they serve as transporter proteins and contribute to osmotic pressure and plasma pH.23 In the postinjury state their synthesis has been used as a predictor of mortality, nutritional status, severity of stress, and as an indicator of recovery.2224 Several other studies hypothesized that an exaggerated increase in the hepatic acute-phase response can be detrimental.2527 In our study we showed that nutritional intervention high in protein, vitamins, ω3 fatty acids, and amino acids improves the hypermetabolic and hepatic acute-phase response by increasing constitutive hepatic protein synthesis of albumin, transferrin, and total protein 33 days after a severe thermal injury. In addition, hepatic protein concentration and wet-dry weight were significantly increased in rats receiving the intervention, indicating a reduction in organ protein catabolism.

Muscle protein concentration and wet-dry weight ratios in muscles were increased in rats receiving the diet compared with rats receiving standard rat chow. The reduction of protein loss was further reflected in the pattern of loss of body weight. Rats fed Sustacal showed an improvement in body weight compared with rats receiving chow. A possible mechanism of improved protein metabolism in our burn model could be the dermal regeneration growth hormone (GH)–IGF-I axis. Thermally injured skin is a major source of proinflammatory cytokines early after the injury occurs, such as tumor necrosis factor α or interleukin 1, which are systemically released.28 Tumor necrosis factor α and interleukin 1 enhance and support the protein catabolism and decrease the anabolic hormones GH and IGF-I.29 Growth hormone and IGF-I are anabolic agents that accelerate protein synthesis rates.30 During the hypermetabolic state, catabolism is enhanced because of GH resistance and decreased production and action of IGF-I.9,10 This leads to the hypothesis that 2 augmenting factors decrease GH and IGF-I–GH resistance and the release of proinflammatory cytokines from the burn wound. Accelerated wound healing would therefore lead to decreased release of proinflammatory cytokines, which is followed by a decreased hypermetabolic response, a negative nitrogen balance, and increased GH and IGF-I concentrations. We found that animals receiving Sustacal had an accelerated dermal regeneration compared with animals receiving regular chow and increased IGF-I concentrations in serum, liver, and muscle. It is, however, unclear whether IGF-I was increased because of accelerated wound healing or whether the diet increased IGF-I, leading to improved protein synthesis and accelerated wound healing. Furthermore, it has been shown that dietary supplements of antioxidant vitamins A, C, and E, which serve as radical scavengers, are associated with improved resistance to oxidative stress and enhanced and accelerated wound regeneration.31

We showed that nutritional intervention that is high in protein, vitamins, amino acids, and ω3 fatty acids improves protein metabolism during the hypermetabolic response to a thermal injury. Thermally injured rats receiving the diet had an improvement in body weight, increased protein concentrations in serum, liver, and muscle, and increased IGF-I levels compared with animals fed standard rat chow. Rats receiving the diet had accelerated wound healing in terms of reepithelization. Because the diet used in our study was varied in overall composition, it is difficult to determine the specific factor causing the positive effects. However, diets that are used clinically are often composed of a variety of elements. Another concern is the bioavailability of the different diets we used. We have no data on the bioavailability but speculate that resorption and utilization of the 2 diets are similar.

This study was supported by grants 8010 from the Shriners Hospital for Children, and DFG Je 233/1-2 from the Deutsche Forschungsgemeinschaft, Bonn, Germany.

Corresponding author: Marc G. Jeschke, MD, Klinik und Poliklinik für Chirurgie, Klinikum der Universität Regensburg, Franz-Joseph-Strauss Allee 11, 93053 Regensburg, Germany (e-mail: mcjeschke@hotmail.com).

Herndon  DNCurrerei  PW Metabolic response to thermal injury and its nutritional support. Cutis. 1978;22501- 506
Pierre  EHerndon  DNBarrow  RE Growth hormone therapy in the treatment of burns. Torosian  MHed.Growth Hormone in Critical Illness: Research and Clinical Studies. Austin, Tex R.G. Landes Co1996;105- 116
Wilmore  D Hypermetabolic response to burn injury. J Trauma. 1990;30S4- S6
Arnold  JCampbell  ITSamuels  TA Increased whole body protein breakdown predominates over increased whole body protein synthesis in multiple organ failure. Clin Sci (Colch). 1993;84655- 661
Rennie  MJ Muscle protein turnover and wasting due to injury and disease. Br Med Bull. 1985;41257- 264
Chiolero  RRevelly  JPTappy  L Energy metabolism in sepsis and injury. Nutrition. 1997;13 (9 suppl) 45S- 51S
Biolo  GToigo  GCiocchi  B  et al.  Metabolic response to injury and sepsis: changes in protein metabolism. Nutrition. 1997;13 (9 suppl) 52S- 57S
Takala  LERuokonen  NRWebster  MS  et al.  Increased mortality associated with growth hormone treatment in critically ill patients. N Engl J Med. 1999;341785- 792
van den Berghe  Gde Zeghe  FVeldhuis  JD The somatotropic axis in critical illness: effect of continuous growth hormone (GH)-releasing hormone and GH-releasing peptide-2 infusion. J Clin Endocrinol Metab. 1997;82590- 599
Timmins  ACCotterill  AMHughes  SC Critical illness is associated with low circulating concentrations of insulin-like growth factors-I and –II, alterations in insulin like growth factors binding proteins, and induction of an insulin-like growth factor binding protein 3 protease. Crit Care Med. 1996;241460- 1466
Wolf  SEHerndon  DN Burn Care.  Austin, Tex Landes Bioscience1999;66- 71
Cui  XLIwasa  MIwasa  YOgoshi  S Arginine-supplemented diet decreases expression of inflammatory cytokines and improves survival in burned rats. JPEN J Parenter Enteral Nutr. 2000;2489- 96
Beale  RJBryg  DJBihari  DJ Immunonutrition in the crtitically ill: a systemic review of clinical outcome. Crit Care Med. 1999;272799- 2805
Saffle  JRWiebke  GJennings  KMorris  SEBarton  RG Randomized trial of immune enhancing enteral nutrition in burn patients. J Trauma. 1997;42793- 800
Nelson  JLAlexander  JWGianotti  LChalk  CLPyles  T High protein diets are associated with increased bacterial translocation in septic guinea pigs. Nutrition. 1996;12195- 199
Demling  RHDe Santi  L Increased protein intake during the recovery phase after severe burns increases body weight gain and muscle function. J Burn Care Rehabil. 1998;19161- 168
Herndon  DNWilmore  DUMason  AD  Jr Development and analysis of a small animal model stimulating human postburn hypermetabolic response. J Surg Res. 1978;25394- 403
Cuthbertson  DPZagreb  HC The metabolic response to injury and its nutritional implications: retrospect and prospect. JPEN J Parenter Enteral Nutr. 1979;3108- 129
Baumann  HGauldie  J The acute phase response. Immunol Today. 1994;1574- 80
Jeschke  MGBarrow  REHerndon  DN IGF-I/IGFBP-3 attenuates the pro-inflammatory acute phase response in severely burned children. Ann Surg. 2000;231246- 252
Moshage  H Cytokines and the hepatic acute phase response. J Pathol. 1997;181257- 266
Barnum-Huckins  KMMartinez  AORivera  EV A comparison of the suppression of human transferrin synthesis by lead and lipopolysaccharide. Toxicology. 1997;11811- 22
Brown  ROBradley  JEBekemeyer  WBLuther  RW Effect of albumin supplementation during parenteral nutrition on hospital mortality. Crit Care Med. 1988;161177- 1183
Smith  DJRoberts  D Effects of high volume and/or intense exercise on selected blood chemistry parameters. Clin Biochem. 1994;27435- 440
Livingston  DHMosenthal  ACDeitch  EA Sepsis and multiple organ dysfunction syndrome: a clinical-mechanistic overview. New Horizons. 1995;3276- 287
de Maio  Ade Mooney  MLMatesic  LEPaidas  CNReeves  RH Genetic component in the inflammatory response induced by bacterial lipopolysaccharide. Shock. 1998;10319- 323
Selzman  CHShames  BDMiller  SA  et al.  Therapeutic implications of interleukin-10 in surgical disease. Shock. 1998;10309- 318
Rodriguez  JLMiller  CGGarner  WL Correlation of the local and systemic cytokine response with clinical outcome following thermal injury. J Trauma. 1993;34684- 694
Frost  RALang  CHGelato  MC Transient exposure of human myoblasts to tumor necrosis factor-α inhibits serum and insulin-like growth factor-I stimulated protein synthesis. Endocrinology. 1997;1384153- 4159
Bondy  CAUnderwood  LEClemmons  DRGuler  HPBach  MASkarulis  M Clinical uses of insulin-like growth factor I. Ann Intern Med. 1994;120593- 601
Preiser  JCGossum  ABerre  JVincent  JLCarpentier  Y Enteral feeding with a solution enriched with antioxidant vitamins A, C, and E enhances the resistance to oxidative stress. Crit Care Med. 2000;283828- 3832

Figures

Place holder to copy figure label and caption
Figure 1.

Wound healing measured as reepithelization 4 and 5 weeks after the thermal injury. Rats fed the enriched diet demonstrated accelerated reepithelization by almost 10% at 4 and 5 weeks after burn compared with rats fed chow (P<.05).

Graphic Jump Location
Place holder to copy figure label and caption
Figure 2.

Changes in body weight during the 5-week study period. Thermally injured rats receiving the enriched diet demonstrated improvement in body weight 1, 2, 3, 4, and 5 weeks after the injury. These rats even gained weight 5 weeks after the injury in addition to the preinjury weight, whereas animals receiving regular chow lost almost 10% of their preburn body weight. Asterisks indicate significant difference between diet and chow at the same time point, P<.05.

Graphic Jump Location

Tables

Table Graphic Jump LocationTable 1. Nutrition Information for Sustacal and Rat Chow*
Table Graphic Jump LocationTable 2. Serum Total Protein, Albumin, and Transferrin Concentrations 5 Weeks Postburn in Rats Receiving a Diet High in Vitamins, Protein, ω-3 Fatty Acids, and Amino Acids Compared With Rats Receiving Standard Rat Chow
Table Graphic Jump LocationTable 3. Serum and Liver IGF-I Concentration 5 Weeks Postburn in Rats Receiving a Diet High in Vitamins, Protein, ω-3 Fatty Acids, and Amino Acids Compared With Rats Receiving Standard Rat Chow*

References

Herndon  DNCurrerei  PW Metabolic response to thermal injury and its nutritional support. Cutis. 1978;22501- 506
Pierre  EHerndon  DNBarrow  RE Growth hormone therapy in the treatment of burns. Torosian  MHed.Growth Hormone in Critical Illness: Research and Clinical Studies. Austin, Tex R.G. Landes Co1996;105- 116
Wilmore  D Hypermetabolic response to burn injury. J Trauma. 1990;30S4- S6
Arnold  JCampbell  ITSamuels  TA Increased whole body protein breakdown predominates over increased whole body protein synthesis in multiple organ failure. Clin Sci (Colch). 1993;84655- 661
Rennie  MJ Muscle protein turnover and wasting due to injury and disease. Br Med Bull. 1985;41257- 264
Chiolero  RRevelly  JPTappy  L Energy metabolism in sepsis and injury. Nutrition. 1997;13 (9 suppl) 45S- 51S
Biolo  GToigo  GCiocchi  B  et al.  Metabolic response to injury and sepsis: changes in protein metabolism. Nutrition. 1997;13 (9 suppl) 52S- 57S
Takala  LERuokonen  NRWebster  MS  et al.  Increased mortality associated with growth hormone treatment in critically ill patients. N Engl J Med. 1999;341785- 792
van den Berghe  Gde Zeghe  FVeldhuis  JD The somatotropic axis in critical illness: effect of continuous growth hormone (GH)-releasing hormone and GH-releasing peptide-2 infusion. J Clin Endocrinol Metab. 1997;82590- 599
Timmins  ACCotterill  AMHughes  SC Critical illness is associated with low circulating concentrations of insulin-like growth factors-I and –II, alterations in insulin like growth factors binding proteins, and induction of an insulin-like growth factor binding protein 3 protease. Crit Care Med. 1996;241460- 1466
Wolf  SEHerndon  DN Burn Care.  Austin, Tex Landes Bioscience1999;66- 71
Cui  XLIwasa  MIwasa  YOgoshi  S Arginine-supplemented diet decreases expression of inflammatory cytokines and improves survival in burned rats. JPEN J Parenter Enteral Nutr. 2000;2489- 96
Beale  RJBryg  DJBihari  DJ Immunonutrition in the crtitically ill: a systemic review of clinical outcome. Crit Care Med. 1999;272799- 2805
Saffle  JRWiebke  GJennings  KMorris  SEBarton  RG Randomized trial of immune enhancing enteral nutrition in burn patients. J Trauma. 1997;42793- 800
Nelson  JLAlexander  JWGianotti  LChalk  CLPyles  T High protein diets are associated with increased bacterial translocation in septic guinea pigs. Nutrition. 1996;12195- 199
Demling  RHDe Santi  L Increased protein intake during the recovery phase after severe burns increases body weight gain and muscle function. J Burn Care Rehabil. 1998;19161- 168
Herndon  DNWilmore  DUMason  AD  Jr Development and analysis of a small animal model stimulating human postburn hypermetabolic response. J Surg Res. 1978;25394- 403
Cuthbertson  DPZagreb  HC The metabolic response to injury and its nutritional implications: retrospect and prospect. JPEN J Parenter Enteral Nutr. 1979;3108- 129
Baumann  HGauldie  J The acute phase response. Immunol Today. 1994;1574- 80
Jeschke  MGBarrow  REHerndon  DN IGF-I/IGFBP-3 attenuates the pro-inflammatory acute phase response in severely burned children. Ann Surg. 2000;231246- 252
Moshage  H Cytokines and the hepatic acute phase response. J Pathol. 1997;181257- 266
Barnum-Huckins  KMMartinez  AORivera  EV A comparison of the suppression of human transferrin synthesis by lead and lipopolysaccharide. Toxicology. 1997;11811- 22
Brown  ROBradley  JEBekemeyer  WBLuther  RW Effect of albumin supplementation during parenteral nutrition on hospital mortality. Crit Care Med. 1988;161177- 1183
Smith  DJRoberts  D Effects of high volume and/or intense exercise on selected blood chemistry parameters. Clin Biochem. 1994;27435- 440
Livingston  DHMosenthal  ACDeitch  EA Sepsis and multiple organ dysfunction syndrome: a clinical-mechanistic overview. New Horizons. 1995;3276- 287
de Maio  Ade Mooney  MLMatesic  LEPaidas  CNReeves  RH Genetic component in the inflammatory response induced by bacterial lipopolysaccharide. Shock. 1998;10319- 323
Selzman  CHShames  BDMiller  SA  et al.  Therapeutic implications of interleukin-10 in surgical disease. Shock. 1998;10309- 318
Rodriguez  JLMiller  CGGarner  WL Correlation of the local and systemic cytokine response with clinical outcome following thermal injury. J Trauma. 1993;34684- 694
Frost  RALang  CHGelato  MC Transient exposure of human myoblasts to tumor necrosis factor-α inhibits serum and insulin-like growth factor-I stimulated protein synthesis. Endocrinology. 1997;1384153- 4159
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