Some unexplained features of hepatic ethanol oxidation.
Ethanol is an excellent substrate for the liver, competing effectively for oxidation with other substrates such as fatty acids. Using isolated liver cells from fed and starved rats, we have found that ethanol strongly inhibits Krebs cycle oxidations, so that the combustion through the cycle of acetyl CoA, derived from fatty acids, is reduced more than 50%. In contrast, fatty acid beta-oxidation to acetyl CoA is inhibited only 20% in fed and fasted states. Ethanol was not antiketogenic. In the fed state, octanoate but not palmitate inhibited ethanol oxidation whereas in cells from fasted rats palmitate inhibited ethanol oxidation. Gluconeogenesis from lactate was reduced 50% in hepatocytes from fasted rats but oxygen consumption was unaffected. This paradoxical maintenance of oxygen consumption in a state where the only overt need for ATP synthesis is depressed, suggests that ethanol oxidation may not be exclusively coupled to ATP synthesis but also can be linked to other energy transducing processes.
D000818:Animals; D000431:Ethanol / Q000378:metabolism* / Q000494:pharmacology; D005227:Fatty Acids / Q000378:metabolism / Q000494:pharmacology; D005943:Gluconeogenesis / Q000187:drug effects; D007773:Lactates / Q000378:metabolism; D019344:Lactic Acid; D008099:Liver / Q000378:metabolism*; D008297:Male; D010084:Oxidation-Reduction; D010101:Oxygen Consumption; D051381:Rats; D011919:Rats, Inbred Strains
D005227:Fatty Acids; D007773:Lactates; D019344:Lactic Acid; D000431:Ethanol