First, a lack of oral intake results in a depletion of glycogen stores. Second, volume depletion may induce these counter-regulatory hormones, increasing glucagon levels while suppressing insulin. Third, the oxidation of ethanol produces acetaldehyde, which is oxidized to acetate. This reduces hepatic gluconeogenesis, further reducing glucose levels. Hence, insulin levels remain suppressed, and serum glucagon levels remain elevated.
Several mechanisms act to facilitate ketone production.
Decreased insulin favors lipolysis and fatty acid mobilization. Increased glucagon indirectly stimulates mitochondrial carnitine acyltransferase, which transports fatty acids into the mitochondria for beta-oxidation. Fatty acids therefore are shunted into the beta-oxidation pathway. Morbidity more often is due to other alcohol-associated conditions. No specific distribution of this disorder based on race or ethnicity has been identified.