Fatty Acid Metabolism and Ketogenesis in the Rat Exposed to Streptococcus pneumoniae.
Abstract
Under the dual stress of infectious illness and starvation, the septic host's reduced ability to convert fatty acids to ketone bodies may be partly responsible for the protein-wasting state that accompanies the illness. Previous studies have shown that livers from rats infected with Streptococcus pneumoniae have a decreased ketogenic capacity compared to fasted controls. This study examines possible control sites of hepatic ketogenesis, including hepatic concentrations of coenzyme A, carnitine and malonyl-coenzyme A.. These studies show that during pneumococcal sepsis, the decreased ketogenic capacity of the liver is accompanied by increased hepatic carnitine concentrations, especially acetylcarnitine, and decreased hepatic coenzyme A (CoA). Infection had no effect on muscle carnitine concentrations or hepatic malonyl-CoA content. These data demonstrate that the decreased rate of ketone body production during infection is not due to a carnitine deficiency. In contrast to malonyl-CoA's regulatory role in the fed and fasted state, the concentration of malonyl-CoA does not appear to be of major importance in determining the rate of ketogenesis during infection. The liver of the fasted-infected rat appears to be shuttling acetyl groups to carnitine, and fatty acyl-CoA away from oxidative pathways toward esterification.
Document Details
- Document Type
- Technical Report
- Publication Date
- Apr 30, 1980
- Accession Number
- ADA084718
Entities
People
- Francis A. Beall
- Harold A. Neufeld
- Judith G. Pace
- Robert W. Wannemacher Jr.
Organizations
- United States Army Medical Research Institute of Infectious Diseases