ArticleBiotechnology and bioengineering2007
Contribution of gene expression to metabolic fluxes in hypermetabolic livers induced through burn injury and cecal ligation and puncture in rats.
Article in Biotechnology and bioengineering, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed.
- Sodium acetate increases the productivity of HEK293 cells expressing the ECD-Her1 protein in batch cultures: experimental results and metabolic flux analysis.Frontiers in bioengineering and biotechnology · 2024Article
- Mechanistic identification of biofluid metabolite changes as markers of acetaminophen-induced liver toxicity in rats.Toxicology and applied pharmacology · 2019Article
- MiR-21-3p Plays a Crucial Role in Metabolism Alteration of Renal Tubular Epithelial Cells during Sepsis Associated Acute Kidney Injury via AKT/CDK2-FOXO1 Pathway.BioMed research international · 2019Article
- Metabolic network-based predictions of toxicant-induced metabolite changes in the laboratory rat.Scientific reports · 2018Article
- Integration of Metabolic Modeling with Gene Co-expression Reveals Transcriptionally Programmed Reactions Explaining Robustness in Mycobacterium tuberculosis.Scientific reports · 2016Article
- Metabolic Flux Distribution during Defatting of Steatotic Human Hepatoma (HepG2) Cells.Metabolites · 2016Article
- Burn trauma disrupts circadian rhythms in rat liver.International journal of burns and trauma · 2016Article
- Article
- Dynamics of short-term gene expression profiling in liver following thermal injury.The Journal of surgical research · 2012Article
- Development of Metabolic Indicators of Burn Injury: Very Low Density Lipoprotein (VLDL) and Acetoacetate Are Highly Correlated to Severity of Burn Injury in Rats.Metabolites · 2012Article
- Dynamic epistasis for different alleles of the same gene.Proceedings of the National Academy of Sciences of the United States of America · 2012Article
- Long-term dynamic profiling of inflammatory mediators in double-hit burn and sepsis animal models.Cytokine · 2012Article
- Stoichiometry based steady-state hepatic flux analysis: computational and experimental aspects.Metabolites · 2012Article
- Metabolic response of perfused livers to various oxygenation conditions.Biotechnology and bioengineering · 2011Article
- The dynamics of the early inflammatory response in double-hit burn and sepsis animal models.Cytokine · 2011Article
- Comparison of the cytokine and chemokine dynamics of the early inflammatory response in models of burn injury and infection.Cytokine · 2011Article
- In situ metabolic flux analysis to quantify the liver metabolic response to experimental burn injury.Biotechnology and bioengineering · 2011Article
- Pathway analysis of liver metabolism under stressed condition.Journal of theoretical biology · 2011Article
- Advanced stoichiometric analysis of metabolic networks of mammalian systems.Critical reviews in biomedical engineering · 2011Review
- Effects of burn injury on markers of hypermetabolism in rats.Journal of burn care & research : official publication of the American Burn AssociationArticle
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6 authors.
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Abstract
Severe injury activates many stress-related and inflammatory pathways that can lead to a systemic hypermetabolic state. Prior studies using perfused hypermetabolic rat livers have identified intrinsic metabolic flux changes that were not dependent upon the continual presence of elevated stress hormones and substrate loads. We investigated the hypothesis that such changes may be due to persistent alterations in gene expression. A systemic hypermetabolic response was induced in rats by applying a moderate burn injury followed 2 days later by cecum ligation and puncture (CLP) to produce sepsis. Control animals received a sham-burn followed by CLP, or a sham-burn followed by sham-CLP. Two days after CLP, livers were analyzed for gene expression changes using DNA microarrays and for metabolism alterations by ex vivo perfusion coupled with Metabolic Flux Analysis. Burn injury prior to CLP increased fluxes while decreases in gene expression levels were observed. Conversely, CLP alone significantly increased metabolic gene expression, but decreased many of the corresponding metabolic fluxes. Burn injury combined with CLP led to the most dramatic changes, where concurrent changes in fluxes and gene expression levels occurred in about 1/3 of the reactions. The data are consistent with the notion that in this model, burn injury prior to CLP increased fluxes through post-translational mechanisms with little contribution of gene expression, while CLP treatment up-regulated the metabolic machinery by transcriptional mechanisms. Overall, these data show that mRNA changes measured at a single time point by DNA microarray analysis do not reliably predict metabolic flux changes in perfused livers.
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