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

Cholesterol synthesis · Cytosol / smooth ER — mainly liver. 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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Cholesterol synthesis

Mevalonate

Made from HMG-CoA (cytosolic) by HMG-CoA reductase ★

HMG-CoA reductase ★ rate-limiting · irreversible — Cholesterol synthesis

Cofactors: 2 NADPH → 2 NADP⁺

Activated by: Insulin; Thyroid hormone; Low sterol → SREBP-2/SCAP to Golgi → ↑ transcription of reductase and LDL receptor

Inhibited by: Statins (competitive); AMPK phosphorylation (low energy); Glucagon, epinephrine, glucocorticoids; High sterol → INSIG retains SREBP-2 in ER and tags reductase for degradation

The PFK-1 of cholesterol synthesis. Statins lower intracellular cholesterol → SREBP-2 → more LDL receptors — that is the actual LDL-lowering mechanism.

Condition cards:Statins (HMG-CoA reductase inhibition) →

Becomes Isoprenoid units (IPP) via Mevalonate kinases / decarboxylase

Mevalonate kinases / decarboxylase — Cholesterol synthesis

Cofactors: 3 ATP

Isopentenyl pyrophosphate — also the source of dolichol, ubiquinone (CoQ) and prenyl groups (why statins can cause myopathy).