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Biological Sciences

KETOGENESIS B-OH-Butyrate reduced to Acetoacetate (AcAc) ratio determined by NADH/NAD in liver mito **only in liver mito (where B-oxidation occurs** some acetate decarbed to acetone conditions: high fat (ketogenic) diet fasting/starvation prolonged exercise diabetes (I) fasting does not affect amt of glucose in blood possible b/c alternate fuel utilization (80-fold inc in BHB) changes during starvation - brain shifts to ketone utilization to spare muscle glucose still used, but not fully oxidized (to save it) - LESS muscle breakdown “sparing effect” due to ketogenesis ACAC SYNTH: HMG-CoA CYCLE 1) THIOLASE: 2 X AcetylCoA  AcAcCoA + CoA (Thiolase INHIBITOR) 2) HMG-COA SYNTHASE: AcAc-CoA + acetyl-CoA  HMG-CoA (4C) (2C) (6C) SH-CoA is lost from Acetyl CoA and INHIBITS SYNTHASE 2) HMG COA LYASE: HMG-CoA  AcAc + AcetylCoA (used in step 2) REGULATION B-Oxidiation  inc. Acetyl CoA  inc. rate (FREE CoA is a competitive inhibitor for thiolase and synthase) SEQUENCE OF EVENTS 1) fasting  dec. glucose  inc glucagon/epi 2) inc [cAMP] in adipocyte  HS Lipase activation 3) FFA release by adipocyte 4) dec FFA synth  dec. malonyl CoA  FFA from adipocyte enters mito 5) B-OXIDATION  inc ACETYL COA  might enter TCA, but ALSO inc NADH  inc OAA reduction 6) [OAA] < Km (CS) 7) Acetyl CoA from B-Oxidation “STUCK” but can enter HMG-CoA cycle KETONE METABOLISM – ketone use depends only on how much is ava
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