Metabolic fate of extrahepatic arginine in liver after burn injury

Chen, Chung Lin; Fei, Zhewei; Carter, Edward A.; Lu, Xiao Ming; Hu, Rey‐Heng; Young, Vernon R.; Tompkins, Ronald G.; Yu, Yong Ming

doi:10.1016/s0026-0495(03)00282-8

Cited by 13 publications

(11 citation statements)

References 32 publications

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“…Thus, in this study, we observed a more muted response than what we had previously reported, where the same burn injury model significantly up-regulated the hepatic oxygen uptake rate and fluxes through the electron transport chain, the citric acid cycle, the urea cycle, gluconeogenesis, and the metabolism of several other amino acids. On the other hand, the lack of an increase in the uptake of oxygen is consistent with other recent published data using a similar burn model and perfusion system [41]. Although we did not investigate the reasons for these discrepancies, we suspect that variations in the burn-induced response may be the result of subtle differences in animal husbandry, such as housing temperature and humidity, both of which could impact on heat and evaporative loss from the burned skin, which in turn may affect resting energy expenditure and therefore many aspects of metabolism [49].…”

Section: Discussionsupporting

confidence: 93%

Effects of Dehydroepiandrosterone Administration on Rat Hepatic Metabolism Following Thermal Injury

Banta

Yokoyama

Berthiaume

et al. 2005

Journal of Surgical Research

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Section: Discussionsupporting

confidence: 93%

Effects of Dehydroepiandrosterone Administration on Rat Hepatic Metabolism Following Thermal Injury

Banta

Yokoyama

Berthiaume

et al. 2005

Journal of Surgical Research

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“…Detailed quantitative analyses of metabolism in disease states have been performed, in many instances with the help of isotopically labeled tracers (Cabral et al, 2008; Chen et al, 2003; Yarmush et al, 1999; Zhaofan et al, 2002), typically at the whole-body level. Although metabolic probing could be made minimally invasive, thus introducing little to no perturbation to the system, it could not clearly identify the role of individual organs and tissues in the overall response.…”

Section: Introductionmentioning

confidence: 99%

In situ metabolic flux analysis to quantify the liver metabolic response to experimental burn injury

Izamis

Sharma

Uygun

et al. 2010

Biotech & Bioengineering

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Trauma such as burns induces a hypermetabolic response associated with altered central carbon and nitrogen metabolism. The liver plays a key role in these metabolic changes; however, studies to date have evaluated the metabolic state of liver using ex vivo perfusions or isotope labeling techniques targeted to specific pathways. Herein, we developed a unique mass balance approach to characterize the metabolic state of the liver in situ, and used it to quantify the metabolic changes to experimental burn injury in rats. Rats received a sham (control uninjured), 20% or 40% total body surface area (TBSA) scald burn, and were allowed to develop a hypermetabolic response. One day prior to evaluation, all animals were fasted to deplete glycogen stores. Four days post-burn, blood flow rates in major vessels of the liver were measured, and blood samples harvested. We combined measurements of metabolite concentrations and flow rates in the major vessels entering and leaving the liver with a steady-state mass balance model to generate a quantitative picture of the metabolic state of liver. The main findings were: (1) Sham-burned animals exhibited a gluconeogenic pattern, consistent with the fasted state; (2) the 20% TBSA burn inhibited gluconeogenesis and exhibited glycolytic-like features with very few other significant changes; (3) the 40% TBSA burn, by contrast, further enhanced gluconeogenesis and also increased amino acid extraction, urea cycle reactions, and several reactions involved in oxidative phosphorylation. These results suggest that increasing the severity of injury does not lead to a simple dose-dependent metabolic response, but rather leads to qualitatively different responses.

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“…The 20% burn injury model used in this study induces a significant, nonlethal injury response in rats that is different from more severe burn injury models (i.e., 40% TBSA burn injury or burn injury followed by infection). The 20% TBSA model has been extensively used to characterize burn-injury-induced insulin resistance as well as hypermetabolism [7,26,27]. This being a nonlethal model, the changes in expression observed in this study reflect dynamics of the normal and successful systemic response to burn injury where there is virtually no mortality.…”

Section: Discussionmentioning

confidence: 97%

“…The latter studies involve perfusing the organ after burn injury for determining net rates of production or uptake of various metabolites [7,9]. This approach has been used to describe changes in metabolic processes and establish a biochemical basis for the liver response to burn injury [7,10,11]. However, few studies have established the gene expression basis for these changes [12,13].…”

Section: Introductionmentioning

confidence: 99%

Gene Expression Profiling of Long-Term Changes in Rat Liver Following Burn Injury

Jayaraman

Maguire

Vemula

et al. 2009

Journal of Surgical Research

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The inflammatory response initiated upon burn injury is also associated with extensive metabolic adjustments. While there is a significant body of literature on the characterization of these changes at the metabolite level, little is known on the mechanisms of induction, especially with respect to the role of gene expression. We have comprehensively analyzed changes in gene expression in rat livers during the first 7 d after 20% total body surface area burn injury using Affymetrix microarrays. A total of 740 genes were significantly altered in expression at 1, 2, 4, and 7 d after burn injury compared to sham-burn controls. Functional classification based on gene ontology terms indicated that metabolism, transport, signaling, and defense/inflammation response accounted for more than 70% of the significantly altered genes. Fisher least-significant difference post-hoc testing of the 740 differentially expressed genes indicated that over 60% of the genes demonstrated significant changes in expression either on d 1 or on d 7 postburn. The gene expression trends were corroborated by biochemical measurements of triglycerides and fatty acids 24 h postburn but not at later time points. This suggests that fatty acids are used, at least in part, in the liver as energy substrates for the first 4 d after injury. Our data also suggest that long-term regulation of energy substrate utilization in the liver following burn injury is primarily at the posttranscriptional level. Last, relevance networks of significantly expressed genes indicate the involvement of key small molecules in the hepatic response to 20% total body surface area burn injury.

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Metabolic fate of extrahepatic arginine in liver after burn injury

Cited by 13 publications

References 32 publications

Effects of Dehydroepiandrosterone Administration on Rat Hepatic Metabolism Following Thermal Injury

Effects of Dehydroepiandrosterone Administration on Rat Hepatic Metabolism Following Thermal Injury

In situ metabolic flux analysis to quantify the liver metabolic response to experimental burn injury

Gene Expression Profiling of Long-Term Changes in Rat Liver Following Burn Injury

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