The effects of ethanol concentration on glycero‐3‐phosphate accumulation in the perfused rat liver

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Abstract
The dose‐dependent effect of ethanol on the hepatic metabolism of the perfused rat liver has been investigated by (a) 31P‐NMR spectroscopy for the follow‐up of intracellular phosphorylated metabolites and (b) HPLC for compounds released in the effluents. Perfusion of livers from fed rats with ethanol induced an increase in the level of sn‐glycerol 3‐phosphate and net accumulations of 3.30 ± 0.33 and 0.69 ± 0.15 μmol × g−1 wet liver were reached after 20 min, for 70 mM and 0.5 mM ethanol, respectively. sn‐Glycerol‐3‐phosphate accumulation was fully detected by 31P NMR as indicated by comparing quantitations based on NMR and biochemical assays. Ethanol administration up to a concentration of 10 mM induced a dose‐dependent decrease in the release of lactate + pyruvate by the liver. Lactate release decreased from 1129 ± 39 to 674 ± 84 nmol × min−1× g−1, while pyruvate decreased from 230 ± 9 to 6.2 ± 0.4 nmol × min−1× g−1, after 20 min of perfusion with 10 mM ethanol. Nevertheless, the flux through 6‐phosphofructo‐1‐kinase, as measured by both the accumulation of sn‐glycerol 3‐phosphate and release of lactate + pyruvate, was not affected in the early phase of ethanol oxidation. Finally, data obtained from oxygen consumption, the release of acetate and the accumulation of sn‐glycerol 3‐phosphate do not support the involvement of the microsomal ethanol‐oxidizing system in the catalysis of ethanol oxidation, even at high doses of alcohol.