Rat liver peroxisomal and mitochondrial fatty acid oxidation in sepsis.
Time course changes in hepatic mitochondrial and peroxisomal fatty acid oxidative capacities, as well as changes in the related enzyme activities, were investigated in rats with sepsis induced by cecal ligation and puncture. Palmitoyl-L-carnitine oxidation was not altered, but carnitine palmitoyl-transferase (CPT) dependent palmitoyl-CoA (plus L-carnitine) oxidation was slightly increased in the liver mitochondria of the septic rats. Hepatic CPT activity, being the rate-limiting step of mitochondrial beta-oxidation, was also enhanced by sepsis. In contrast, cyanide-insensitive peroxisomal beta-oxidation and the carnitine acetyltransferase and catalase activities associated with the peroxisomal-enriched fraction were markedly reduced by abdominal sepsis. Cyanide-insensitive beta-oxidation in control livers showed optimal specificity for lauroyl- and myristoyl-CoA and this pattern remained unchanged by sepsis. However, oxidation rates were reduced for all acyl-CoA esters tested, being more pronounced with longer carbon chain length acyl-CoA substrates. These results indicate that in early sepsis, hepatic mitochondrial fatty acid oxidative capacity was increased, probably due to enhanced CPT activity, whereas peroxisomal beta-oxidation was seriously disturbed along with reduced catalase activity.
Yamamoto
T
T
Department of Emergency and Critical Care Medicine, Kansai Medical University, Osaka, Japan.
D000818:Animals; D004195:Disease Models, Animal; D005227:Fatty Acids / Q000378:metabolism*; D007239:Infections / Q000378:metabolism*; D008099:Liver / Q000201:enzymology / Q000378:metabolism*; D008297:Male; D008830:Microbodies / Q000378:metabolism*; D008930:Mitochondria, Liver / Q000378:metabolism*; D010084:Oxidation-Reduction; D010085:Oxidative Phosphorylation; D051381:Rats; D017208:Rats, Wistar
D005227:Fatty Acids