Acute effect of ethanol on metabolite concentrations of dog pancreas in vivo.

Sections of dog pancreas were freeze-clamped before and 1 hr after oral administration of 1 g/kg of ethanol in anesthetized, respirated, 24-hr-fasted animals, and multiple metabolites were determined in the perchloric acid extract of the frozen tissue. In spite of the fact that the pancreas contained little or no alcohol dehydrogenase activity (less than 0.01 IU/g of tissue), significant metabolite changes did occur. Although arterial oxygenation was constant and adequate (pO2 = 100 +/- 7 mM Hg) there was a significant 1.7-fold rise in L-lactate and fall in the cytoplasmic free [NAD+]/[NADH] ratio from 719 +/- 87 to 453 +/- 88 after ethanol. Except for a tendency for L-malate and L-alpha-glycerolphosphate to parallel the rise in L-lactate, there was little consistent disturbance in the remainder of the glycolytic metabolites (glucose, glucose 6-phosphate, pyruvate, 2-ketoglutarate, citrate, 3-phosphoglycerate, etc.) or in high energy intermediates and related compounds (ATP, creatine phosphate, ADP, Pi, creatine). There was, however, an unexpected and significant fall in the levels of the major transaminating amino acids, L-glutamate, L-aspartate, and L-alanine. The results can be only partially explained by an influence of blood-borne metabolites and imply significant effects of ethanol on the metabolism of the pancreas in vivo not directly mediated through alcohol dehydrogenase. Evidence is presented suggesting that both L-alanine and L-aspartate aminotransferases are functioning near equilibrium in the pancreas in vivo.