Hypoglycemic Convulsions in Children after Alcohol Ingestion

Tolis, Apostolos

doi:10.1016/s0031-3955(16)31713-8

Cited by 17 publications

(2 citation statements)

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“…Since both dog and man are sensitive to low concentrations of alcohol, it seems reasonable to assume that DNPH mediated inhibition of gluconeogenesis is the most statisfactory explanation of the phenomenon in these species. However, the observations that hypoglycemia may not occur in susceptible individuals until alcohol concentrations reach 100 mg. per cent (20 mM) or higher, 22 that the tendency for it may persist despite realimentation and presumably correction of gluconeogenic substrate deficiency, 22 and that it occurs in well nourished children, 23 suggests that in some situations its effect on gluconeogenesis depends primarily on inhibition of substrate uptake by the liver and, ultimately, a deficiency of 3 carbon hydrogen acceptors. A recent article has emphasized the multiplicity of defects in carbohydrate metabolism associated with alcohol hypoglycemia.…”

Section: Discussionmentioning

confidence: 99%

Effect of Alcohol on Glucose Production and Lactate, Pyruvate and Ketone Body Metabolism by the Isolated Perfused Rat Liver

Kreisberg

1967

Diabetes

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The purpose of these experiments was to determine whether the effect of ethanol on glucose production could be dissociated from its effect on the cytoplasmic DPN/DPNH ratio in the presence of adequate substrate. Isolated rat livers were perfused with a Krebs bicarbonate Ringer buffer containing 4 per cent albumin and 10 mM alanine in the presence of increasing concentrations of ethanol. Lactate, pyruvate, B-hydroxybutyrate and acetoacetate were used to reflect the cellular redox state. Despite producing maximum changes in lactate, pyruvate and ketone body metabolism, 10 mM ethanol did not inhibit glucose production. Ethanol concentrations of 20 and 40 mM produced no further change in the production of lactate and pyruvate but significantly inhibited ketone body and glucose production by the isolated perfused rat liver. These results are compatible with the proposal that increased entry and intramitochondrial oxidation of DPNH which results from alcohol metabolism inhibits oxidation of fatty acids, acetyl CoA generation and subsequently gluconeogenesis. DIABETES 16: 784-90, November, 1967. Alcohol is currently believed to inhibit gluconeogenesis as a result of its effect on cellular redox state. 1 In the absence t?f adequate supplies of cytoplasmic hydrogen acceptors necessary for substrate reoxidation of the DPNH resulting from alcohol metabolism, 2 gluconeogenesis is inhibited. This mechanism, however, has been derived primarily from studies with rat liver slices under experimental conditions which have no in vivo counterpart. Inhibition of gluconeogenesis has been demonstrated consistently only when liver slices have been obtained from fed and fasted animals and incubated in Krebs-Ringer phosphate buffer, a medium in which basal gluconeogenesis is already limited, or when tissue was obtained from fasted animals and incubated in Krebs-Ringer bicarbonate buffer in the absence of substrate. 2 Because recent studies have demonstrated that From the Medical College of Alabama, Birmingham, Alabama. maintenance of glucose production by rat liver is dependent upon an adequate extrahepatic supply of substrate, 3 the question is raised whether or not there are other mechanisms by which alcohol inhibits gluconeogenesis in the rat and perhaps other animals. Since the use of the liver slice as a means for studying gluconeogenesis has been questioned, 4 the effects of alcohol on glucose production were investigated with use of an in vitro preparation which allows closer simulation of conditions known to exist in vivo.In the studies to be described, the effects of increasing concentrations of alcohol on glucose production and cellular redox state were investigated in an attempt to dissociate the abilities of alcohol to alter redox state and inhibit gluconeogenesis. The rationale for this approach was that alterations in gluconeogenesis would be independent of the cellular redox state once sufficient alcohol was present to saturate the metabolic pathways for alcohol degradation and assure its constant metabolism. METHODSLiv...

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Section: Discussionmentioning

confidence: 99%

Effect of Alcohol on Glucose Production and Lactate, Pyruvate and Ketone Body Metabolism by the Isolated Perfused Rat Liver

Kreisberg

1967

Diabetes

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“…Ethyl alcohol is fatal in doses of 6 ml/kg of 100% alcohol if ingested in one hour's time 11 . Since alcohol is rarely of high concentration in any medicinal product it is not considered a significant hazard 3 .…”

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confidence: 99%