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Ethanol effects of substrate utilization by the human brain

A Juhlin-Dannfelt

    Scandinavian Journal of Clinical and Laboratory Investigation
    |September 1, 1977
    PubMed
    Summary

    Ethanol consumption impacts brain metabolism, reducing glucose uptake and abolishing lactate release. The brain can utilize acetate, potentially contributing to energy needs.

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    Area of Science:

    • Neuroscience
    • Metabolic Research
    • Pharmacology

    Background:

    • Ethanol (alcohol) is widely consumed and affects various physiological processes.
    • Understanding ethanol's metabolic impact on the human brain is crucial for public health.
    • Previous studies suggest complex interactions between ethanol and brain substrate metabolism.

    Purpose of the Study:

    • To investigate the effects of ethanol infusion on cerebral substrate exchange in healthy males.
    • To quantify changes in arterial and arterio-jugular vein differences for key metabolites.
    • To determine the brain's metabolic response to acute ethanol administration.

    Main Methods:

    • Seven healthy male volunteers underwent ethanol infusion to achieve a blood alcohol concentration of approximately 12 mmol/l.
    • Arterial and jugular venous blood samples were collected to measure concentrations of ethanol, acetate, glucose, lactate, pyruvate, glycerol, free fatty acids, and ketone bodies.
    • Arterio-jugular vein (A-JV) oxygen differences were monitored throughout the study.

    Main Results:

    • Ethanol administration led to a significant decrease in blood glucose concentration and a reduced A-JV glucose difference, indicating attenuated brain glucose uptake.
    • Arterial acetate levels increased, and a positive arterio-venous difference for acetate was observed, suggesting brain acetate uptake.
    • Ethanol doubled arterial lactate concentration and abolished the normal net release of lactate from the brain.

    Conclusions:

    • The brain can take up acetate, which, if fully oxidized, could supply approximately 6% of the brain's oxygen consumption.
    • Ethanol attenuates cerebral glucose uptake, as evidenced by the decreased A-JV glucose difference.
    • The abolition of brain lactate net release is likely due to elevated systemic arterial lactate concentrations caused by ethanol.

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