STUDIES ON THE MECHANISM OF ETHANOL-INDUCED HYPOGLYCEMIA*

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Abstract
Hypoglycemia was consistently produced in humans by the ingestion of 35 to 50 ml of ethanol after a 2-day fast. Similar amounts of ethanol were ineffective after an overnight-fast and did not interfere with the hyperglycemic response to glucagon. The failure of glucagon to increase blood glucose during ethanol-induced hypoglycemia would be consistent with an absence of liver glycogen. Hypoglycemia was associated with a rise in plasma free fatty acids, suggesting that it was not insulin-mediated. During hypoglycemia, intravenously administered fructose was normally converted to glucose, but there was some inhibition of its conversion to glycogen. Studies using perfused rat livers and liver slices from ethanol-treated rabbits also demonstrated decreased glycogen synthesis. Besides inhibiting glycogen synthesis, ethanol also interfered with glucose and urea formation in the isolated, perfused rat liver, but not with amino acid mobilization, suggesting a block in oxidative deamination of amino acids. Inhibition of gluconeogenesis is probably primarily responsible for hypoglycemia, in conjunction with depletion of liver glycogen.