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Thermal injury activates the eEF2K-dependent eEF2 pathway in pediatric patients
Juquan Song1, Celeste C Finnerty, David N Herndon
1Department of Surgery, University of Texas Health Science Center at San Antonio, San Antonio, Texas, USA.
JPEN. Journal of Parenteral and Enteral Nutrition
|January 25, 2012
Summary
Severe burns cause hypermetabolism by altering protein synthesis. This study found prolonged activation of eukaryotic elongation factor 2 (eEF2) and eEF2 kinase (eEF2K) in burned children, potentially contributing to metabolic changes.
Area of Science:
- Biochemistry
- Physiology
- Pediatric Medicine
Background:
- Burns trigger a hypermetabolic state impacting protein metabolism, increasing morbidity and mortality.
- Eukaryotic elongation factor 2 (eEF2) regulates protein synthesis, but its role in burn hypermetabolism is unknown.
- eEF2 kinase (eEF2K) inactivates eEF2.
Purpose of the Study:
- To investigate the expression of eEF2 and eEF2K in pediatric patients with severe burns.
- To understand the role of eEF2 and eEF2K in burn-induced hypermetabolism and protein catabolism.
Main Methods:
- Muscle and skin biopsies from 8 severely burned children and 3 controls were analyzed at different time points post-burn.
- Measured resting energy expenditure (REE), body composition, and muscle protein fractional synthesis rate (FSR).
- Utilized Western blotting and microarray analysis to examine eEF2K and eEF2 expression and phosphorylation.
Main Results:
- Burned patients showed increased REE and loss of lean body mass, indicating a catabolic state.
- Phosphorylation of eEF2 was downregulated in muscle early and mid-postburn.
- eEF2K and eEF2 levels showed similar changes in skin early postburn, while total protein amounts remained unaltered.
Conclusions:
- Severe burns lead to prolonged activation of eEF2K and eEF2.
- These alterations in eEF2K and eEF2 may contribute to the hypermetabolic state observed in severely burned pediatric patients.
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