Gastric intubation of female Sprague-Dawley rats with 5 g of ethanol/kg body wt. nearly doubled oxygen uptake by the isolated perfused rat liver maximally after only 2.5 h of treatment (Swift Increase in Alcohol Metabolism). Inhibition of enhanced oxygen uptake by KCN (2mM) and 4-methylpyrazole (0.8 mM) suggested the involvement of the mitochondrial respiratory chain and alcohol dehydrogenase in this phenomenon. Glycolysis was depressed after ethanol treatment. Diminished ATP generation via glycolysis accounts for a portion (23-50%) of the increased oxygen uptake, assuming that other rates of biosynthesis remain constant. Injection of adrenaline (2 mg/kg) 1 h before perfusion mimicked partially the action of ethanol on hepatic oxygen uptake. The increases produced by ethanol and adrenaline were not additive, suggesting that adrenaline is involved in the action of ethanol. Moreover, the increase in hepatic oxygen uptake produced by 2.5 h of ethanol treatment could be blocked by either alpha-(phenoxybenzamine; 40 mg/kg) or beta-(propranolol; 40 mg/kg) adrenergic blocking agents. Blood glucose increased after ethanol treatment, supporting the involvement of glycogenolytic hormones in this effect. These data indicate that at least part of the stimulated oxygen uptake after treatment with ethanol is a result of lower rates of glycolytic ATP generation resulting from hormone (e.g. adrenaline etc.) action. The ADP not phosphorylated in the cytosol enters the mitochondria, where it stimulates oxygen uptake.

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Abstract-Biochemical mechanisms underlying the development of alcoholic fatty liver were investigated.Acute ethanol (EtOH) administration for 3 days by an inhalation method, and continuous EtOH treatments by feeding with liquid diet or drinking water containing EtOH induced a significant increase of hepatic triglycerides (TG). A small but significant increase of TG was also observed in the blood serum.Although hepatic acetyl CoA carboxylase activity, measured in the presence and absence of citrate, was not altered by either acute or chronic EtOH administrations, fatty acid synthetase and malic enzyme activities in the liver were increased by continuous EtOH administration, but not in the acutely EtOH-treated animals.