Thermal injury activates the eEF2K-dependent eEF2 pathway in pediatric patients

Juquan Song, Celeste Finnerty, David Herndon, Robert Kraft, Darren Boehning, Natasha C. Brooks, Ronald G. Tompkins, Marc G. Jeschke

Research output: Contribution to journalArticle

2 Citations (Scopus)

Abstract

Background: Burn induces a hypermetabolic state characterized by alterations in protein metabolism, which is associated with increased morbidity and mortality. Eukaryotic elongation factor 2 (eEF2) plays a crucial role in regulating protein synthesis in many diseases, but whether it participates in burn-induced hypermetabolism is unclear. The aim of this study was to determine the expression of eEF2 and the upstream eEF2-inactivating kinase, eEF2K, in severely burned pediatric patients. Methods: Eight pediatric patients (> 40% total body surface area) and 3 nonburned pediatric volunteers were enrolled. Muscle and skin biopsies were collected at early (0-10 days postburn [dpb]), middle (11-49 dpb), and late (50-365 dpb) time points. Resting energy expenditure (REE), body composition, and muscle protein fractional synthesis rate (FSR) were measured. Proteins were extracted and analyzed by Western blotting. To further investigate the protein synthesis pathway, microarray data from muscle and skin were examined from 22 nonburned and 20 burned children. Results: Burn patients exhibited a profound hypermetabolic response, as seen by a significant increase in REE (P < .05) and loss of lean body mass without altered muscle FSR, indicating a shift to catabolism after thermal injury. In muscle, the phosphorylation of eEF2K-dependent eEF2 was down regulated early and middle postburn. Similar changes in eEF2K and eEF2 levels occurred in skin at the early time point. Total amounts of eEF2 and eEF2K were not altered. Conclusion: Burn induces prolonged activation of eEF2K and eEF2. Alterations in these mediators may contribute to profound hypermetabolism in severely burned patients. (JPEN J Parenter Enteral Nutr. 2012;36:596-602).

Original languageEnglish (US)
Pages (from-to)596-602
Number of pages7
JournalJournal of Parenteral and Enteral Nutrition
Volume36
Issue number5
DOIs
StatePublished - Sep 2012

Fingerprint

Peptide Elongation Factor 2
Hot Temperature
Pediatrics
Wounds and Injuries
Muscles
Skin
Energy Metabolism
Elongation Factor 2 Kinase
Proteins
Muscle Proteins
Body Surface Area
Body Composition
Burns
Small Intestine
Volunteers
Western Blotting
Phosphorylation
Morbidity
Biopsy
Mortality

Keywords

  • burn
  • hypermeta-bolism
  • muscle
  • protein synthesis
  • skin

ASJC Scopus subject areas

  • Medicine (miscellaneous)
  • Nutrition and Dietetics

Cite this

Thermal injury activates the eEF2K-dependent eEF2 pathway in pediatric patients. / Song, Juquan; Finnerty, Celeste; Herndon, David; Kraft, Robert; Boehning, Darren; Brooks, Natasha C.; Tompkins, Ronald G.; Jeschke, Marc G.

In: Journal of Parenteral and Enteral Nutrition, Vol. 36, No. 5, 09.2012, p. 596-602.

Research output: Contribution to journalArticle

Song, Juquan ; Finnerty, Celeste ; Herndon, David ; Kraft, Robert ; Boehning, Darren ; Brooks, Natasha C. ; Tompkins, Ronald G. ; Jeschke, Marc G. / Thermal injury activates the eEF2K-dependent eEF2 pathway in pediatric patients. In: Journal of Parenteral and Enteral Nutrition. 2012 ; Vol. 36, No. 5. pp. 596-602.
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abstract = "Background: Burn induces a hypermetabolic state characterized by alterations in protein metabolism, which is associated with increased morbidity and mortality. Eukaryotic elongation factor 2 (eEF2) plays a crucial role in regulating protein synthesis in many diseases, but whether it participates in burn-induced hypermetabolism is unclear. The aim of this study was to determine the expression of eEF2 and the upstream eEF2-inactivating kinase, eEF2K, in severely burned pediatric patients. Methods: Eight pediatric patients (> 40{\%} total body surface area) and 3 nonburned pediatric volunteers were enrolled. Muscle and skin biopsies were collected at early (0-10 days postburn [dpb]), middle (11-49 dpb), and late (50-365 dpb) time points. Resting energy expenditure (REE), body composition, and muscle protein fractional synthesis rate (FSR) were measured. Proteins were extracted and analyzed by Western blotting. To further investigate the protein synthesis pathway, microarray data from muscle and skin were examined from 22 nonburned and 20 burned children. Results: Burn patients exhibited a profound hypermetabolic response, as seen by a significant increase in REE (P < .05) and loss of lean body mass without altered muscle FSR, indicating a shift to catabolism after thermal injury. In muscle, the phosphorylation of eEF2K-dependent eEF2 was down regulated early and middle postburn. Similar changes in eEF2K and eEF2 levels occurred in skin at the early time point. Total amounts of eEF2 and eEF2K were not altered. Conclusion: Burn induces prolonged activation of eEF2K and eEF2. Alterations in these mediators may contribute to profound hypermetabolism in severely burned patients. (JPEN J Parenter Enteral Nutr. 2012;36:596-602).",
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AU - Finnerty, Celeste

AU - Herndon, David

AU - Kraft, Robert

AU - Boehning, Darren

AU - Brooks, Natasha C.

AU - Tompkins, Ronald G.

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AB - Background: Burn induces a hypermetabolic state characterized by alterations in protein metabolism, which is associated with increased morbidity and mortality. Eukaryotic elongation factor 2 (eEF2) plays a crucial role in regulating protein synthesis in many diseases, but whether it participates in burn-induced hypermetabolism is unclear. The aim of this study was to determine the expression of eEF2 and the upstream eEF2-inactivating kinase, eEF2K, in severely burned pediatric patients. Methods: Eight pediatric patients (> 40% total body surface area) and 3 nonburned pediatric volunteers were enrolled. Muscle and skin biopsies were collected at early (0-10 days postburn [dpb]), middle (11-49 dpb), and late (50-365 dpb) time points. Resting energy expenditure (REE), body composition, and muscle protein fractional synthesis rate (FSR) were measured. Proteins were extracted and analyzed by Western blotting. To further investigate the protein synthesis pathway, microarray data from muscle and skin were examined from 22 nonburned and 20 burned children. Results: Burn patients exhibited a profound hypermetabolic response, as seen by a significant increase in REE (P < .05) and loss of lean body mass without altered muscle FSR, indicating a shift to catabolism after thermal injury. In muscle, the phosphorylation of eEF2K-dependent eEF2 was down regulated early and middle postburn. Similar changes in eEF2K and eEF2 levels occurred in skin at the early time point. Total amounts of eEF2 and eEF2K were not altered. Conclusion: Burn induces prolonged activation of eEF2K and eEF2. Alterations in these mediators may contribute to profound hypermetabolism in severely burned patients. (JPEN J Parenter Enteral Nutr. 2012;36:596-602).

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