ArticleJPEN. Journal of parenteral and enteral nutrition2012
Thermal injury activates the eEF2K-dependent eEF2 pathway in pediatric patients.
Article in JPEN. Journal of parenteral and enteral nutrition, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed, 8 citations in OpenAlex.
- Molecular mechanisms of post-burn muscle wasting and the therapeutic potential of physical exercise.Journal of cachexia, sarcopenia and muscle · 2023Review
- Insulin and exercise improved muscle function in rats with severe burns and hindlimb unloading.Physiological reports · 2019Article
- The surgically induced stress response.JPEN. Journal of parenteral and enteral nutrition · 2013Article
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Authors and funding
8 authors at 4 institutions in 2 countries.
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Abstract
backgroundBurn 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.
methodsEight 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.
resultsBurn 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.
conclusionBurn induces prolonged activation of eEF2K and eEF2. Alterations in these mediators may contribute to profound hypermetabolism in severely burned patients.
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