In the urea cycle, N-acetylglutamate (NAG) is the essential allosteric activator of carbamoyl phosphate synthetase I (CPS-I). NAG synthesis increases after a protein-rich meal because:
- A Arginine activates NAG synthase, signalling high amino acid load ✓
- B Glutamate directly activates CPS-I without NAG as intermediary
- C Ornithine inhibits NAG synthase feedback
- D Citrulline allosterically activates CPS-I
Explanation
N-acetylglutamate is synthesised from glutamate + acetyl-CoA by NAG synthase, which is allosterically activated by arginine. After a protein-rich meal, arginine availability rises, stimulating NAG synthesis and thereby activating CPS-I — the rate-limiting enzyme of the urea cycle. This elegant feed-forward mechanism couples dietary protein load to urea cycle capacity. NAG deficiency (NAG synthase deficiency) presents with hyperammonemia and responds dramatically to N-carbamylglutamate (a stable NAG analogue) treatment.
Reference: Harper's Illustrated Biochemistry, 32nd ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
Written and medically reviewed by the StethoPrep medical team.