Oxaloacetate deficiency in MCT-induced ketogenesis.
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.
D000105:Acetyl Coenzyme A / Q000378:metabolism; D000818:Animals; D001224:Aspartic Acid / Q000494:pharmacology; D005215:Fasting; D005943:Gluconeogenesis; D007657:Ketone Bodies / Q000096:biosynthesis; D007659:Ketones / Q000096:biosynthesis*; D008099:Liver / Q000378:metabolism*; D008297:Male; D010071:Oxaloacetates / Q000172:deficiency / Q000378:metabolism / Q000494:pharmacology*; D051381:Rats; D014280:Triglycerides / Q000494:pharmacology*; D014364:Tryptophan / Q000494:pharmacology
D007657:Ketone Bodies; D007659:Ketones; D010071:Oxaloacetates; D014280:Triglycerides; D001224:Aspartic Acid; D000105:Acetyl Coenzyme A; D014364:Tryptophan