Ketone body metabolism ط Ketogenesis, Site and steps ط Ketolysis, sites and steps for utilization ط Regulation of ketogenesis and ketolysis ط Starvation.

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Presentation transcript:

Ketone body metabolism ط Ketogenesis, Site and steps ط Ketolysis, sites and steps for utilization ط Regulation of ketogenesis and ketolysis ط Starvation and ketosis ط Clinical correlation Ketoacidosis D

KB Synthesis (only in liver Mitoch) KB are water-soluble lipid-base energy (AcetoAcetate=> reduced => β- Hydroxybutarate) fig.9.24, ACoA + ACoA  KT-lase  AACoA AACoA + ACoA  HMGCoA S-ase (+CoA)  HMGCoA HMGCoA  HMGCoA Lyase (+CoA)  Acetoacetate + ACoA Acetoacetate => acetone + CO 2  AADH (–NADH)  d- β -Hydroxybutarate

KB Utilization KB is used by extrahepatic tissues (cardiac& skeletal muscles / CNS) Acetoacetate + SCoA  AA:SCoA T-ase  AACoA + Succinate AACoA  KetoThiolase (–CoA)  Acetate => TCA cycle Succinate => TCA cycle AACoA  AA KT  Acetoacetate

Importance of KB 1. Conserve Glu for CNS support 2. Uptake by brain for further conservation 3. In Diabetes, Hormonal control for Glu conservation (Ketosis)

Clinical Correlation of KB · Rufsum’s Disease cc.9.6 o Phytanic Acid (milk lipid, animal fat) ==X=stop ==> no α-oxid => 3 PCoA + 3 ACoA + 1 IsobutyrylCoA o Lack of a-hydroxylation enzyme lead to accumulation of Phytanic Acid causing neurological problems - Retinitis pigmentation / peripheral neurophathy / cerebellar ataxia / nerve deafness o Treat by restriction of dietary dairy & meat products · Ketoacidosis cc.9.7 o Diabetic ketoacidosis is common with NIDM o Ketosis is triggered by INS deficiency / GLG Excess + Elevated Epineph, cortisol, GH o Hyperglycemia, Ketonemia, Ketonuria (metabolic acidosis) o Decrease in INS does not restrain FA to liver leading to high plasma FA causing high hepatic ketone production o Treated with INS