Abstract
Though diet restriction has proven efficacy in protecting injured organ models, evidence is also provided that jeopardizing energetic charge may be detrimental. The liver plays a particular energetic role in regulating glycemia between meals. To this purpose, the liver produces glucose by gluconeogenesis from metabolic precursors, some of which in turn may also be oxidized by liver mitochondria. This is the case for oxaloacetate (OAA), a substrate of both gluconeogenesis and mitochondrial Krebs' cycle oxidation, and which, in a recent issue of this journal has been shown to protect rat liver and energetic charge under warm ischemia/reperfusion injury. Here we document experimental lactate‐based protection of injured ex vivo rat liver and energetic charge.
Conclusion
Injured livers may be protected by double‐edged liver metabolites, which are the substrates of both energy‐expensive gluconeogenesis and mitochondrial energy‐producing pathways. Liver protection appears to be associated with preservation/gain of energetic charge, a feature that suggests, as an energetic protective mechanism, preponderance of hepatocyte mitochondrial oxidations over gluconeogenesis in processing double‐edged metabolites, OAA and lactate. Discussion on key determinants that direct their metabolism toward energy‐producing oxidations (vs. gluconeogenesis) might point to new liver preservation/protection strategies.
