Effects of Ethanol on Gluconeogenesis

  • H. A. Krebs


It is now firmly established that ethanol can inhibit hepatic gluconeogenesis from several (though not all) precursors, and that this is a major factor responsible for the hypoglycaemia observed when alcohol is consumed in the fasting or semi-fasting state (1). The reasons why alcohol inhibits hepatic gluconeogenesis are at least partially understood: the facts agree with the assumption that the primary process is the interaction between ethanol and liver alcohol dehydrogenase, a relatively rapid reaction in the cytoplasm, which shifts the [NAD]/[NADH2] ratio in the direction of reduction, as indicated by the shift of the [lactate]/[pyruvate] ratio. The inhibition of hepatic gluconeogenesis by ethanol and the shift of the redox state of the NAD couple can be readily demonstrated on the isolated perfused rat liver(2). The shift in the redox state can also be shown in vivo in freeze-clamped liver. In contrast to hepatic gluconeogenesis renal gluconeogenesis is not affected by ethanol. This is in accordance with the fact that the activity of alcohol dehydrogenase is very weak in the kidney.


Redox State Pyruvate Carboxylase Hepatic Gluconeogenesis Mitochondrial Oxidation Hexose Phosphate 
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© Springer-Verlag Berlin · Heidelberg 1971

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  • H. A. Krebs

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