During prolonged starvation, the liver produces large amounts of acetoacetate and beta-hydroxybutyrate, yet the liver itself cannot consume them as fuel. The reason is:
- A Liver lacks thiophorase (succinyl-CoA:acetoacetate CoA transferase) ✓
- B Hepatic cells lack the transporter for monocarboxylates
- C Acetoacetate is toxic to hepatocyte mitochondria
- D Hepatic NAD+ levels are too low to oxidize beta-hydroxybutyrate
Correct answer: A. Liver lacks thiophorase (succinyl-CoA:acetoacetate CoA transferase)
Explanation
Extrahepatic tissues activate acetoacetate to acetoacetyl-CoA using thiophorase (SCOT). The liver deliberately lacks this enzyme, ensuring that ketones produced by the liver are exported for use by brain, heart and muscle rather than consumed locally, which preserves glucose during fasting. Monocarboxylate transporters are present in hepatocytes, and hepatic NAD+ availability is not limiting. This absence of thiophorase in liver is a classic examined distinction.
Reference: Lippincott's Illustrated Reviews: Biochemistry, 8th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
Written and medically reviewed by the StethoPrep medical team.