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.