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.
Gluconeogenesis
Oxaloacetate (mito)
Made from Acetyl-CoA (from β-oxidation) by Allosteric activation of pyruvate carboxylase
Allosteric activation of pyruvate carboxylase — Gluconeogenesis
Not a carbon flow: acetyl-CoA from β-oxidation is the signal that tells the liver to make glucose instead of burning it.
Made from Pyruvate by Pyruvate carboxylase
Pyruvate carboxylase · irreversible — Gluconeogenesis
Cofactors: Biotin (B₇), ATP
Activated by: Acetyl-CoA
Deficiency: Pyruvate carboxylase deficiency — lactic acidosis, hypoglycemia, neurologic impairment (also seen with biotin deficiency)
Bypass 1 (mitochondrial). Deficiency: pyruvate can't become OAA → lactic acidosis, hypoglycemia, poor TCA anaplerosis.
Condition cards:Pyruvate carboxylase deficiency →
Becomes Malate (shuttle) via Malate dehydrogenase (mito)
Malate dehydrogenase (mito) — Gluconeogenesis
Cofactors: NADH → NAD⁺
OAA can't cross the inner membrane; it leaves as malate (or aspartate).