Sources of energy for the brain and physical dependence on ethanol.
This paper describes a proposed biochemical mechanism to account for physical dependence on ethanol. Long-term exposure to a continuous and plentiful supply of ethanol-derived hydrogens in NADH and ethanol-derived acetyl-CoA (AcCoA) may lead to a decreased rate of production of endogenous hydrogens in NADH and endogenous AcCoA in compensation. It is proposed that physical dependence on ethanol occurs when ketolytic- and glycolytic-based NADH and AcCoA synthetic rates fall below the rate of utilization by the brain; the brain then "depends" on alcohol-derived NADH and AcCoA for normal function.
D000105:Acetyl Coenzyme A / Q000378:metabolism; D000818:Animals; D001921:Brain / Q000378:metabolism*; D004734:Energy Metabolism; D000431:Ethanol / Q000378:metabolism; D006019:Glycolysis; D006801:Humans; D007659:Ketones / Q000378:metabolism; D008099:Liver / Q000378:metabolism; D009243:NAD / Q000378:metabolism; D013375:Substance Withdrawal Syndrome; D019966:Substance-Related Disorders / Q000378:metabolism*
D007659:Ketones; D009243:NAD; D000431:Ethanol; D000105:Acetyl Coenzyme A