Learn / Metabolism
Metabolic pathways
Every FMK pathway as a clickable map. Pick one pathway to hammer it — next step, enzyme, regulator, cofactor, and the facts that get tested (NADPH and who needs it, rate-limiting steps, deficiencies) — or set it to all pathways for a mixed drill. Every answer says which enzyme and which pathway.
Nitrogen transport to the liver — Cahill cycle & the glutamine shuttle
Glutamate (muscle) — the collection point
Made from BCAA catabolism + muscle protein turnover by Transamination — ALT / AST
Transamination — ALT / AST — Nitrogen transport to the liver — Cahill cycle & the glutamine shuttle
Cofactors: PLP (vitamin B₆)
Deficiency: Vitamin B₆ deficiency — isoniazid is a classic cause; transamination and the whole nitrogen-collection system suffer
Transamination does NOT eliminate nitrogen — it concentrates the amino groups of dozens of different amino acids onto ONE carrier, glutamate. It is a collection step, not a disposal step (s8). Every aminotransferase needs pyridoxal phosphate.
Becomes GLUTAMINE — carries TWO nitrogens via GLUTAMINE SYNTHETASE (+ free NH₄⁺)
GLUTAMINE SYNTHETASE (+ free NH₄⁺) — Nitrogen transport to the liver — Cahill cycle & the glutamine shuttle
Cofactors: ATP → ADP
Adds a second nitrogen to glutamate, so glutamine carries TWO per molecule — an efficient two-for-one shuttle, and the reason glutamine is the most abundant free amino acid in blood. The BRAIN has no urea cycle, so this is its ONLY way to clear ammonia; the glutamine that accumulates is osmotically active and swells astrocytes, which is the mechanism of cerebral oedema in acute hyperammonemia (s17).
Becomes ALANINE — one nitrogen + a carbon skeleton via ALANINE AMINOTRANSFERASE (ALT) — amino group onto pyruvate
ALANINE AMINOTRANSFERASE (ALT) — amino group onto pyruvate — Nitrogen transport to the liver — Cahill cycle & the glutamine shuttle
Cofactors: PLP (vitamin B₆)
The muscle end of the Cahill cycle.