Lipid Metabolism and Mitochondrial Biogenesis in Septic Liver – A Mini Review Focused on PGC-1α Expression

Decreased fatty acid (FA) oxidation and oxidative phosphorylation are observed in many tissues and organs during sepsis.The suppression of catabolism appears to lead to an insufficient supply of energy and is associated with multiple organ failure.In septic models that utilize endotoxemia or live bacteria, FA oxidation is generally suppressed.Furthermore, peroxisome proliferator-activated receptor gamma-coactivator 1 alpha (PGC-1α), which induces mitochondrial biogenesis and promotes FA oxidation, is typically downregulated.However, despite similar experimental settings, increased mRNA expression of PGC-1α has been found in some studies, implying the restoration of mitochondrial functions.Such finding might indicate that PGC-1α gene expression can be rapidly controlled by subtle differences in the dose and time course of septic insult.In this review, we aimed to discuss liver and hepatocyte studies that assessed PGC-1α expression.Although the cause-and-effect relationship between decreased mitochondrial function and multi-organ failure is still debatable, recent evidence favors the view that the overexpression of PGC-1α can promote the restoration of the mitochondria following sepsis-induced damage.