Malonyl-CoA inhibits carnitine palmitoyltransferase I (CPT-I). What is the physiological significance of this in the post-prandial (fed) state in liver?
- A It prevents futile cycling by blocking fatty acid entry into mitochondria when fatty acid synthesis is active ✓
- B It stimulates ketogenesis by diverting acetyl-CoA to ketone bodies
- C It activates peroxisomal fatty acid oxidation as an alternative route
- D It promotes cholesterol synthesis by diverting malonyl-CoA to the mevalonate pathway
Correct answer: A. It prevents futile cycling by blocking fatty acid entry into mitochondria when fatty acid synthesis is active
Explanation
Malonyl-CoA is the first committed intermediate in cytosolic fatty acid synthesis (formed by acetyl-CoA carboxylase in the fed/insulin state). By inhibiting CPT-I — the rate-limiting step for long-chain fatty acid entry into mitochondria — malonyl-CoA prevents the newly synthesised fatty acids from being immediately re-oxidised. This avoids a thermodynamically wasteful futile cycle and ensures net lipogenesis in the fed state.
Reference: Harper's Illustrated Biochemistry, 32nd ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
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