Karlsson N, Fellenius E, Kiessling K H
Acta Physiol Scand. 1977 Jan;99(1):113-22. doi: 10.1111/j.1748-1716.1977.tb10360.x.
The effect of acetate, at concentrations normally found during ethanol combustion in intact animals and man in vivo, on the uptake and oxidation of beta-hydroxybutyrate by the perfused rat hind-quarter was studied. The addition of acetate did not significantly affect the total uptake of beta-hydroxybutyrate, but caused a 40% decrease in the oxidation of beta-hydroxybutyrate to CO2. The oxidation of 14C-beta-hydroxybutyrate to 14CO2 accounted for about 10% of the total oxygen consumption by the perfused muscle in the absence of acetate. In the presence of acetate this figure was reduced to about 5%. The addition of beta-hydroxybutyrate did not significantly affect the metabolic fate of 14C-acetate. It is concluded that acetate is preferred as oxidative substrate to beta-hydroxybutyrate. The inhibited oxidation of beta-hydroxybutyrate by acetate did not affect the concentration ratio between beta-hydroxybutyrate and acetoacetate in the medium at the end of the perfusion, indicating that the ability of the muscle tissue to restore an increased redoxlevel, "exported" from the liver during ethanol combustion to extrahepatic tissues, was not impaired by acetate.
