Malonyl-CoA inhibits CPT-I (carnitine palmitoyltransferase I), serving as a key regulatory link between fatty acid synthesis and oxidation. Malonyl-CoA levels are HIGH in the:
- A Fed state after carbohydrate intake, when ACC is active and fatty acid synthesis is proceeding ✓
- B Fasted state, promoting ketogenesis
- C Exercise state, when AMPK is active
- D Diabetic ketoacidosis state, when glucagon is elevated
Explanation
In the fed/postprandial state, insulin activates ACC (acetyl-CoA carboxylase) via dephosphorylation to produce malonyl-CoA; high malonyl-CoA inhibits CPT-I, preventing fatty acid entry into mitochondria for oxidation, thereby preventing futile cycling between synthesis and oxidation while directing fatty acids for esterification. In fasting, exercise, and DKA, glucagon/catecholamines activate AMPK, which phosphorylates and inhibits ACC, reducing malonyl-CoA and relieving CPT-I inhibition.
Reference: Harper's Illustrated Biochemistry, 32nd ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
Written and medically reviewed by the StethoPrep medical team.