What is the effect of alcohol on hepatic glucose production and hypoglycemia risk?

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Multiple Choice

What is the effect of alcohol on hepatic glucose production and hypoglycemia risk?

Explanation:
Alcohol primarily disrupts hepatic glucose production by changing the liver’s redox state during metabolism. When alcohol is being processed, the liver’s NADH/NAD+ ratio rises, which slows gluconeogenesis from substrates such as lactate, alanine, and glycerol. With gluconeogenesis impaired, hepatic glucose output drops, and in people taking insulin or a sulfonylurea, the risk of hypoglycemia increases and can be prolonged because the liver can’t compensate by making more glucose. Alcohol does not directly raise blood glucose; in fact, it can precipitate or deepen hypoglycemia in fasting or low-gucose states. So the statement that alcohol impairs gluconeogenesis, prolonging insulin- or sulfonylurea-induced hypoglycemia, best reflects its effect.

Alcohol primarily disrupts hepatic glucose production by changing the liver’s redox state during metabolism. When alcohol is being processed, the liver’s NADH/NAD+ ratio rises, which slows gluconeogenesis from substrates such as lactate, alanine, and glycerol. With gluconeogenesis impaired, hepatic glucose output drops, and in people taking insulin or a sulfonylurea, the risk of hypoglycemia increases and can be prolonged because the liver can’t compensate by making more glucose. Alcohol does not directly raise blood glucose; in fact, it can precipitate or deepen hypoglycemia in fasting or low-gucose states. So the statement that alcohol impairs gluconeogenesis, prolonging insulin- or sulfonylurea-induced hypoglycemia, best reflects its effect.

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