Attempts to characterize the hypoglycemia that may follow alcohol ingestion have disclosed the following: The hypoglycemia can be reproduced with pure ethanol and it occurs at blood alcohol levels which do not exceed the range of mild intoxication. It is not attended by plasma changes characteristicof liver damage or peripheral “insulin-like” actions. Circulating immunologically-reactive insulin does not increase and pancreatic responsiveness to islet cell secretogogues such as glucose and tolbutamide is preserved. The hypoglycemia cannot be terminated by glucagon. From infusion experiments, it cannot be ascribed to enhanced peripheral utilization of glucose.
In normal humans or dogs, induction of experimental alcohol hypoglycemia with alcohol requires several days of preliminary fasting; in patients with diminished gluconeogenic reserve, regardless of etiology, lesser dietary deprivation is required. Ethanol can also attenuate the prevailing hyperglycemia in fasted “juvenile” diabetics from whom insulin has been withheld to the point of early ketoacidosis.
In vitro studies have corroboratedthat at least some of the blood sugar lowering actions of alcohol may be ascribed to a direct impairment in the endogenous formation of glucose from smaller precursors. Oxidative-decarboxylation of added substrates by slices of human, rabbit or rat liver is invariably reduced in the presence of alcohol.Under appropriate conditions, a concomitant inhibition of gluconeogenesis isobserved. It has been proposed that the effects of alcohol upon gluconeogenesis by cellular preparation may be conditioned by the alternative pathways available for reoxidizing the cytoplasmic NADH2 which is generatedduring alcohol oxidation.
A pivotal role has been assigned to the prevailing intrahepatic availability and turnover of pyruvate.