Oxaloacetate Deficiency in Mct-Induced Ketogenesis

Abstract

This study was an attempt to discover whether a deficiency in hepatic oxaloacetate can explain the acceleration of ketogenesis observed after the ingestion of medium-chain triglycerides (MCT, constituent fatty acids from C₈ to C₁₂).

The method of investigation used consisted in supplying oxaloacetate (by intraperitoneal injection of oxaloacetate, aspartate, or L-tryptophan) to rats that had ingested MCT.

The indirectly given oxaloacetate caused a decrease in ketone body levels in the liver. The stimulation of ketogenesis induced by an exogenous supply of MCT is therefore at least partly due to a deficiency of oxaloacetate. The results show that this can be explained both by a leakage of this metabolite into the pathway of gluconeogenesis and by its reduction into malate. Since the acetyl-CoA derived from oxidized medium-chain fatty acids cannot enter into the Krebs cycle, it is diverted to the production of ketone bodies.