Lactate production due to ethanol intoxication is another incidence of lactate metabolism being derailed by the poor availability of NAD, or rather the excess of NADH.
NADH produces an imbalance in the equilibrium equation which governs the proportion of lactate and pyruvate.; and of course by the Law of Mass Action the NADH/NAD ratio determines the lactate/pyruvate ratio. Too much NADH, and lactate cannot be converted into pyruvate; the reverse takes place instead. Hence, when ethanol is metabolised into acetaldehyde, it creates a vast excess of NADH which drives the conversion of pyruvate into lactate (and prevents the conversion of pyruvate into glucose).
Additionally, ethanol is ultimately metabolised into acetate, which plugs straight into oxidative phosphorylation by combining with coenzyme A (making acetyl-CoA). With this much acetyl-CoA freely available, who needs pyruvate? And indeed, the increased acetyl-CoA levels inhibit pyruvate dehydrogenase, decreasing the flow of pyruvate into Krebs Cycle.
Thus, the increased NADH/NAD ratio favours the conversion of pyruvate into lactate, rather than into glucose.
Methanol, ethylene glycol and pretty much all the alcohols that get metabolised by alcohol dehydrogenase will perform in this fashion.
Is this clinically relevant? Perhaps not. At least in one review of drunks, lactate levels were never very high (less than 5mmol/L in all cases). And in all cases the lactate could be attributed to something else.
In short, just because something is biochemically possible, does not mean it has any influence on the organism.
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