BCM 475 Chapter Notes - Chapter 17: Isocitrate Dehydrogenase, Pyruvate Dehydrogenase, Acetyl-Coa
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Pyruvate dehydrogenase complex strictly controlled; entry point for oxidative metabolism. High concentrations of rxn products: energy needs are met or enough fatty acids are degraded to produce acetyl coa and nadh: acetyl coa inhibits e2 binds directly, nadh inhibits e3, atp inhibits pdh complex. Spares glu(cid:272)ose; does(cid:374)"t use pyru(cid:448)ate (cid:894)deri(cid:448)ed fro(cid:373) glu(cid:272)ose (cid:271)y gly(cid:272)olysis(cid:895) Stimulated by ca2: rise in cytoplasmic ca2+ increases mitochondrial ca2, rise activates phosphatase. Hormones: liver: epinephrine initiates phosphatidylinositol pathway, increases [ca2+] Binds to alpha-adrenergic receptors: liver/adipose tissue: insulin stimulates phosphatase (increases pyruvate acetyl coa) Phosphorylation switches off activity of pdh: pyruvate dehydrogenase kinase i (pdk) phosphorylates e1. Deactivation is reversed by dephosphorylation = on: pyruvate dehydrogenase phosphatase (pdp) Phosphatase deficiency = always inactive pdh complex: glucose lactate (instead of acetyl coa) causing lactic acidosis (high lactic acid levels) Does not convert pyruvate acetyl-coa deactivation) Active pyruvate dehydrogenase converts pyruvate to acetyl-coa enters citric-acid cycle. Primary control points = the first 2 enzymes to generate high-energy e-
