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.
Protein digestion & amino acid absorption
Free amino acids inside the enterocyte
Made from Free amino acids by SLC transporters — SECONDARY ACTIVE, Na⁺-coupled (apical)
SLC transporters — SECONDARY ACTIVE, Na⁺-coupled (apical) — Protein digestion & amino acid absorption
Deficiency: CYSTINURIA — defective COAL transporter (Cystine, Ornithine, Arginine, Lysine). The most common inherited disorder of amino acid transport (~1 in 7,000). All four spill into urine but only cystine is insoluble, so it precipitates into stones — HEXAGONAL crystals on urinalysis. Treat with hydration, urinary alkalinisation, penicillamine
Separate carriers for different amino acid classes, which is why a defect can be selective.
Condition cards:Cystinuria →
Made from Di- and tripeptides by PepT1 — H⁺-coupled peptide transporter, then hydrolysed INSIDE the cell
PepT1 — H⁺-coupled peptide transporter, then hydrolysed INSIDE the cell — Protein digestion & amino acid absorption
More efficient than free amino acid uptake: one transport event moves three residues. It is also a redundancy route when an individual amino acid carrier is broken — which is why peptide-based formulas sometimes outperform elemental (free amino acid) formulas in malabsorption.
Becomes Portal blood → liver via Sodium-INDEPENDENT transporters (basolateral)
Sodium-INDEPENDENT transporters (basolateral) — Protein digestion & amino acid absorption
Free amino acids leave into the portal circulation; the liver sees them first.