Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2017 Oct;1863(10 Pt B):2633-2644.
doi: 10.1016/j.bbadis.2017.02.019. Epub 2017 Feb 20.

The biochemical alterations underlying post-burn hypermetabolism

Christopher Auger  1 , Osai Samadi  1 , Marc G Jeschke  2
Affiliations
Review

The biochemical alterations underlying post-burn hypermetabolism

Christopher Auger et al. Biochim Biophys Acta Mol Basis Dis. 2017 Oct.

Abstract

A severe burn can trigger a hypermetabolic state which lasts for years following the injury, to the detriment of the patient. The drastic increase in metabolic demands during this phase renders it difficult to meet the body's nutritional requirements, thus increasing muscle, bone and adipose catabolism and predisposing the patient to a host of disorders such as multi-organ dysfunction and sepsis, or even death. Despite advances in burn care over the last 50 years, due to the multifactorial nature of the hypermetabolic phenomenon it is difficult if not impossible to precisely identify and pharmacologically modulate the biological mediators contributing to this substantial metabolic derangement. Here, we discuss biomarkers and molecules which play a role in the induction and mediation of the hypercatabolic condition post-thermal injury. Furthermore, this thorough review covers the development of the factors released after burns, how they induce cellular and metabolic dysfunction, and how these factors can be targeted for therapeutic interventions to restore a more physiological metabolic phenotype after severe thermal injuries. This article is part of a Special Issue entitled: Immune and Metabolic Alterations in Trauma and Sepsis edited by Dr. Raghavan Raju.

Keywords: Burns; Catabolism; Hypermetabolism; Insulin resistance; Mitochondria; Trauma.

PubMed Disclaimer

Figures

Figure 1
Figure 1
The hypermetabolic response post-burn is characterized by an increase in resting energy expenditure (REE) and loss of lean body mass driven by stress hormones and pro-inflammatory cytokines.
Figure 2
Figure 2
Following a severe burn, white adipose tissue (WAT) adopts the characteristics of brown adipose tissue (BAT).
Figure 3
Figure 3
Factors which induce ER stress subsequently increase the cellular resistance to insulin signalling via JNK.
Figure 4
Figure 4
Glucose control, beta-blockade and anabolic agents can be used to counter the systemic derangements initiated by the hypermetabolic response.
See this image and copyright information in PMC

References

    1. World Health Organization. The injury chartbook: a graphical overview of the global burden of injuries. Geneva: 2002.
    1. Jeschke MG, Gauglitz GG, Kulp GA, Finnerty CC, Williams FN, Kraft R, Herndon DN. Long-term persistance of the pathophysiologic response to severe burn injury. PloS one. 2011;6(7):e21245. - PMC - PubMed
    1. Wolfe RR. Review: acute versus chronic response to burn injury. Circulatory shock. 1980;8(1):105–115. - PubMed
    1. Jeschke MG, Chinkes DL, Finnerty CC, Kulp G, Suman OE, Norbury WB, Herndon DN. The pathophysiologic response to severe burn injury. Annals of surgery. 2008;248(3):387. - PMC - PubMed
    1. Jeschke MG, Mlcak RP, Finnerty CC, Norbury WB, Gauglitz GG, Kulp GA, Herndon DN. Burn size determines the inflammatory and hypermetabolic response. Critical care. 2007;11(4):1. - PMC - PubMed

Publication types