During prolonged fasting, the liver produces large quantities of acetoacetate and beta-hydroxybutyrate yet cannot itself use these ketone bodies as fuel. The enzymatic basis for this hepatic inability is:

• A Absence of mitochondrial HMG-CoA synthase
• B Absence of beta-hydroxybutyrate dehydrogenase
• C Absence of succinyl-CoA:acetoacetate CoA transferase (SCOT, thiophorase) ✓
• D Inhibition of acetoacetyl-CoA thiolase by high NADH

Explanation

Extrahepatic tissues activate acetoacetate to acetoacetyl-CoA using SCOT (thiophorase), which transfers CoA from succinyl-CoA. Hepatocytes lack this enzyme, ensuring ketones are exported rather than consumed locally, even though the liver contains all enzymes of ketogenesis including mitochondrial HMG-CoA synthase and beta-hydroxybutyrate dehydrogenase. This spares hepatic ketone utilization and makes option C the defining feature of the liver's role as a ketone supplier.

Reference: Harper's Illustrated Biochemistry, 32nd ed.

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