The Effect of Streptococcus pneumoniae Infection on the Concentrations of Carnitine and Its Derivatives in Liver, Muscle and Plasma of the Rat.

Abstract

Bacterial infections diminish "starvation-induced" ketosis via an undefined metabolic lesion (53). There is no change in the oxidation of palmitylcarnitine by rat liver mitochondria suggesting that the processes of 13-oxidation and the tricarboxylic acid cycle (TCA) are intact in infected rats. However, liver perfusion studies show a decrease in ketone body production from oleic acid but not from octanoic acid in infected rats compared to starved controls, which suggests a defect in long-chain fatty acid transport. Carnitine concentration correlates directly with increased hepatic ketogenic capacity in starvation or diabetes (51). Therefore, this relationship was investigated at various stages of Streptococcus pneumoniae infection using a modified radioisotopic assay for carnitine. Free and total carnitine increased to the same extent in starved and infected rats. However, carnitine derivatives were significantly altered in infected rats; short-chain acylcarnitines increased in liver and plasma, long-chain acylcarnitines decreased in liver and muscle. Liver short-chain acylcarnitines were inversely proportional to plasma P,-hydroxybutrate in fed, starved and infected rats. Despite elevated free and total carnitine, an infected rat has a low ketogenic capacity. Rather, it appears that hepatic ketone body production during infection may well be altered, at least in part, by the relative proportions of short- and long-chain acylcarnitines which differ from those measured in starved controls.