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.

Pathway

Fatty acid synthesis · Cytosol — liver, adipose, lactating mammary gland (fed state, insulin). Enzymes sit beside the arrows, ★ = rate-limiting, ⊕/⊖ = activators/inhibitors (toggle), −ATP +NADH = what the step spends and makes (toggle ⚡), dashed = allosteric signal, shaded bands = compartment. Drag to pan.

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Fatty acid synthesis

Malonyl-CoA

Made from Acetyl-CoA (cytosol) by Acetyl-CoA carboxylase (ACC) ★

Acetyl-CoA carboxylase (ACC) ★ rate-limiting · irreversible — Fatty acid synthesis

Cofactors: Biotin (B₇), ATP, CO₂ (HCO₃⁻)

Activated by: Insulin (dephosphorylation); Citrate (polymerises the enzyme)

Inhibited by: Glucagon & epinephrine (PKA/AMPK phosphorylation); Palmitoyl-CoA (product)

Rate-limiting, committed step. AMPK (low energy) phosphorylates and inactivates it — the same 'stop anabolism' switch used on HMG-CoA reductase.

Becomes Palmitate (C16) via Fatty acid synthase (FAS)

Fatty acid synthase (FAS) — Fatty acid synthesis

Cofactors: 2 NADPH per 2-carbon addition, Pantothenate (ACP arm, B₅)

7 malonyl-CoA + 1 acetyl-CoA + 14 NADPH → palmitate (C16). Elongation/desaturation in the ER afterwards. NADPH comes from the HMP shunt and malic enzyme.

Becomes CPT I inhibited via Allosteric inhibition of CPT I

Allosteric inhibition of CPT I — Fatty acid synthesis

Malonyl-CoA's second identity: it blocks fatty acyl entry into mitochondria so newly made fat isn't immediately oxidised.