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ISU BBMB 405 - Ketone Bodies

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BBMB 405 1st Edition Lecture 11Outline of Last Lecture XIV. Chapter 22: Fatty Acid MetabolismC. Unsaturated and odd-chain fatty acids require additional steps for degradationOutline of Current Lecture XIV. Chapter 22: Fatty Acid MetabolismC. Unsaturated and odd-chain fatty acids require additional steps for degradation (con’t)Current LectureXIV. Chapter 22: Fatty Acid MetabolsimC. Unsaturated and odd-chain fatty acids require additional steps for degradation6. Ketone bodies are formed from acetyl CoA when fat breakdown predominatesa. What if too much FA coming into liver, excess end up as ketone bodies (KB) and dumped into blood streamb. Fatty acid (irreversible) Pyruvate  glucosec. Ac-CoA d. KB  --TCA cycle 2CO2e. Fatty acid oxidation is incomplete: ketone metabolismf. Anything that produce Ac-CoA is non glucogenicg. Handout (2/4) Major Fates of FA in liverh. FA  FA-CoA  TAG in VLDL (very low density and get out of liver)i. FA-CoA via beta-oxidation  Ac-CoA  KB (when lover overwhelmed) or 2CO2 via TCA cycleThese notes represent a detailed interpretation of the professor’s lecture. GradeBuddy is best used as a supplement to your own notes, not as a substitute.j. Ketone bodies: acetoacetate, Beta Hydroxybutyrate (not really ketone), ketone, possibly acetatek. Enzymes of ketogenesis: Thiolase, HMG-CoA synthase, HMG-CoA lyase, BHBAdehydrogenasel. (Con’t) Handout (2/4)i. Conditions associated with increased ketogenesis are all related to shortage of glucoseii. Etiology of ketosis (increase ketogenesis) leads to Ketonemia (ketone bodies in blood) and ketonuria (abnormally high amounts of ketones and ketone bodies in urine)iii. Development of fatty liver/ketosis- Glucose shortage  increase glucagon and decrease insulin increased FA in liver and Protein in muscle and liver  increase ratio of NADH to NAD+ in lver partial inhibition of TCA cycle in liver  decrease in OAA, amino acids, Methionine increase TAG in liver and KB synthesism. Formation of Ketone bodiesn. Acetoacetate is not stable and is decarboxylated to acetone and kydroxy-butyrate, released into blood stream for other tissueso. Excrete acetone through lungs or urinep. Brain cell starvationi. Extreme starvation (~ 7 days)ii. Brain adapts and burns ketone bodiesiii. Fatty acids is not used as fueliv. 50% of ATP by ketone bodiesv. Have no idea how much brain cell produces in ATPq. Utalization of acetoacetate as fuelr. CoA tranferase allows us to activate acetoacetate, enzyme is missing in liver and that is why acetoacetate is end product in livers.t. Animals cannot convert fatty acids into glucoseu.D. Fatty acids are synthesized by fatty acid synthase (FAS)1. Note: will do this section in next lecture2. Note: Lectures 1 through 11 are on exam


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