A known alcoholic presents with a blood glucose level of 35 mg/dL. What best explains this result?

In individuals with chronic alcoholism, several metabolic derangements can occur that significantly affect glucose homeostasis. The presentation of hypoglycemia, particularly in a known alcoholic, suggests hepatic glycogen depletion and impaired gluconeogenesis as the most plausible explanation for the low blood glucose level.

Alcohol metabolism predominantly occurs in the liver, where alcohol is converted into acetaldehyde and subsequently to acetyl-CoA. This process not only utilizes NAD+ but also promotes the excessive production of NADH. The accumulation of NADH leads to a shift in the metabolic balance, inhibiting gluconeogenesis and glycogenolysis, which are crucial for maintaining blood glucose levels, especially during fasting states or increased energy demands.

When glycogen stores are depleted—common in malnourished alcoholics who may not be consuming adequate carbohydrates—there is a diminished capacity for gluconeogenesis due to the adverse effects of alcohol metabolism on the liver. Consequently, the body struggles to produce glucose, resulting in hypoglycemia.

Understanding this mechanism emphasizes the importance of the liver's role in glucose production and the impact that chronic alcohol consumption has on these processes, culminating in hypoglycemia as witnessed in the patient's presentation.