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Biochemistry · Metabolism: ethanol
Sample itemA chronic alcohol drinker is found after a binge without food, with hypoglycaemia and lactic acidosis. What best explains the hypoglycaemia?
Original practice item, not a recalled exam question. Nothing here is recorded.
The answer and the reasoning
D. High NADH/NAD+ ratio diverting pyruvate to lactate and oxaloacetate to malate, impairing gluconeogenesis
Oxidation of ethanol by alcohol and aldehyde dehydrogenase generates large amounts of NADH. The excess NADH converts pyruvate to lactate and oxaloacetate to malate, depleting substrates for gluconeogenesis when glycogen stores are low, and this causes fasting hypoglycaemia and lactic acidosis.
Option by option
A. Conversion of acetyl-CoA from fatty acid oxidation into glucose
Humans cannot convert acetyl-CoA into glucose, because pyruvate dehydrogenase is irreversible.
B. Absence of hepatic glucose-6-phosphatase
Glucose-6-phosphatase is present in the liver, and its absence causes von Gierke disease, a genetic disorder.
C. Direct stimulation of insulin release by acetaldehyde
Hypoglycaemia in alcoholics is due to impaired glucose production, not insulin excess driven by acetaldehyde.
D. High NADH/NAD+ ratio diverting pyruvate to lactate and oxaloacetate to malate, impairing gluconeogenesis (correct)
Correct. A high NADH/NAD+ ratio diverts gluconeogenic precursors and blocks glucose production.
Source note: Original NextPrep sample item — pending expert review. This item is original practice material awaiting independent expert review, so confirm important facts in a standard textbook.
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