Intermediary hepatic metabolism of rat after oral medium chain triglyceride load.
Hepatic ketogenesis was studied in rats given medium chain triglycerides (MCT). Acetyl-CoA accumulated in the liver, indicating a very rapid beta-oxidation of medium chain fatty acids. Citrate level increases. Ketogenesis is strongly enhanced. Cytoplasm and particularly mitochondria are more reduced after MCT. This may explain the very high increase in hepatic malate. Under our experimental conditions, there appears to be a significant linear relationship between the hepatic acetyl-Coa level and those of total ketone bodies and malade respectively.
D000090:Acetoacetates / Q000378:metabolism; D000105:Acetyl Coenzyme A / Q000378:metabolism; D000818:Animals; D002951:Citrates / Q000378:metabolism; D004041:Dietary Fats; D005947:Glucose / Q000378:metabolism; D006885:Hydroxybutyrates / Q000378:metabolism; D007657:Ketone Bodies / Q000378:metabolism; D007773:Lactates / Q000378:metabolism; D008099:Liver / Q000187:drug effects / Q000378:metabolism*; D008112:Liver Glycogen / Q000378:metabolism; D008293:Malates / Q000378:metabolism; D008297:Male; D011773:Pyruvates / Q000378:metabolism; D051381:Rats; D014280:Triglycerides / Q000378:metabolism / Q000494:pharmacology*
D000090:Acetoacetates; D002951:Citrates; D004041:Dietary Fats; D006885:Hydroxybutyrates; D007657:Ketone Bodies; D007773:Lactates; D008112:Liver Glycogen; D008293:Malates; D011773:Pyruvates; D014280:Triglycerides; D000105:Acetyl Coenzyme A; D005947:Glucose