ArticleThe Biochemical journal1997
Inhibition of glycerol metabolism in hepatocytes isolated from endotoxic rats.
Article in The Biochemical journal, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 14 citations in OpenAlex.
- The role of adipose and muscle tissue breakdown on interorgan energy substrate fluxes in a Pseudomonas aeruginosa induced sepsis model in female pigs.Physiological reports · 2025Article
- Time course of liver mitochondrial function and intrinsic changes in oxidative phosphorylation in a rat model of sepsis.Intensive care medicine experimental · 2018Article
- PPARalpha governs glycerol metabolism.The Journal of clinical investigation · 2004Article
- Effect of cardiopulmonary bypass on lactate metabolism.Intensive care medicine · 2003Article
- Lipopolysaccharide preconditioning attenuates metabolic alteration induced by endotoxin shock: tissue-specific monitoring by microdialysis.Intensive care medicine · 2003Article
- The mitochondrial consequences of uncoupling intact cells depend on the nature of the exogenous substrate.The Biochemical journal · 2001Article
- Manganese cell labeling of murine hepatocytes using manganese(III)-transferrin.Contrast media & molecular imagingArticle
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Sepsis or endotoxaemia inhibits gluconeogenesis from various substrates, the main effect being related to a change in the phosphoenolpyruvate carboxykinase transcription rate. In addition, sepsis has been reported to affect the oxidative phosphorylation pathway. We have studied glycerol metabolism in hepatocytes isolated from rats fasted and injected 16 h previously with lipopolysaccharide from Escherichia coli. Endotoxin inhibited glycerol metabolism and led to a very large accumulation of glycerol 3-phosphate; the cytosolic reducing state was increased. Furthermore glycerol kinase activity was increased by 33% (P<<0.01). The respiratory rate of intact cells was significantly decreased by sepsis, with glycerol or octanoate as exogenous substrates, whereas oxidative phosphorylation (ATP-to-O ratio or respirations in state 4, state 3 and the oligomycin-insensitive state as well as the uncoupled state) was unchanged in permeabilized hepatocytes. Hence the effect on energy metabolism seems to be present only in intact hepatocytes. An additional important feature was the observation of a significant increase in cellular volume in cells from endotoxic animals, which might account for the alterations induced by sepsis.
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