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WVSOM -- Biochem
Oxidation of Ketone Bodies
| Question | Answer |
|---|---|
| Ketone Bodies are produced in the ________ | Liver |
| Is ketone body production a fed state or a fasted state event? | Fasted State |
| Are ketones toxic? | Not as long as they can be used. |
| Why is ketone body production and use in a fasted state? | Liver Beta oxidizes esxcess fatty acids mobilized from adipocytes in teh fasted state. Acetyl-CoA produced by B oxidation is the "excess" carbon for hepatic ketone body synthesis |
| What produces Acetyl CoA for ketone production? | B-Oxidation and ketogenic amino acid catabolism |
| Why can't the liver use all the acetyl CoA it produces in the fasted state? | B-oxidation produces more Aceytl CoA than can be used |
| Why can't the liver use all of the acetyl CoA it produces in the Fasted Stated | The liver must devote significant oxaloacetate to gluconeogenesis so this limites the TCA cycle activity. |
| What does teh liver obtain from its B-oxidation of excess fatty acids? | FADH2 AND NADH are used by the liver without involvement of teh TCA cycle. Can go straight to oxidative phosphorylation |
| NADH may provide "___________" for mitochondrial malate dehydrogenase’s production of malate from oxaloacetate. | reducing power |
| What does the body do with excess acetyl CoA carbons the liver cannot catabolize? | The liver converts it to ketone bodies. |
| What organs import ketone bodies? | heart, kidney and skeletal muscle |
| Why can high energy demand organs catabolize ketone bodies? | they do not have the limit on their TCA cycle activity that hepatocytes do |
| Can the liver use ketone bodies? | no |
| Can acetoacetyl CoA cross the plasma membrane? | No |
| What CoA is at a branch point of the ketone body synthesis pathway? | HMG CoA |
| Acetoacetate is reduced to | B-hydroxybutyrate |
| What reduces acetaoacetate to b-hydroxybutyrate | β-hydroxybutyrate dehydrogenase |
| What happens to acetoacetate when it remains in the blood stream? | it is converted non-enzymatically to acetone |
| How is the acetone removed from the body? | exhaled |
| Two ketone bodies increases the rate of ______________ | export from the liver and their solubility in the blood stream |
| Ketone Bodies are known as | a-b-hydroxybutyrate |
| Ketone body catabolism | b-hydroxybutyrate is converted to acetoacetate |
| What catalyzes ketone body catabolism | b-hydroxybutyrate dehydrogenase |
| Starting Materials of Ketone production | Acetyl CoA |
| Source of ketone starting material | b-oxidation |
| Products of Ketone Body Production | Acetoacetate (produced first) β-Hydroxybutyrate (produced by oxidizing acetoacetate) |
| Intermediate at the branch point of cholesterol | HMG-CoA |
| Can the brain catabolize ketone bodies? | Yes, but only after a complete fast of several days |
| Can red blood cells ever catabolize ketone bodies? | No, they do not have mitochondria |
| Can red blood cells ever catabolize ketone bodies? | No |
| What cells besides RBC cannot use ketones? | None, almost all other types of cells can catabolize ketone bodies, just in a much lesser extent |
| When does catabolism of ketone bodies increase? | As ketone body levels in the blood stream rise with increased duration of a fast. |
| When does the brain use ketone bodies? | only after a complete fast of 3-4 days |
| Is the presence of ketone bodies in the blood stream always a pathological event? | no |
| When is the presence of ketone bodies in teh blood stream a pathological event? | When hepatic ketone body production exceeds extrahepatic cell ketone body use |
| How does the body attempt to limit ketoacidosis? | Kidneys begin to excrete ketone bodies. Acetoacetate is nonenzymatically converted to acetone and exhaled. |
| What exacerbates ketoacidosis? | presence of high serum levels of lactate and/or uric acid |
| Is ketoacidosis necessarily associated with diabtes? | No |
| Causes of Ketoacidosis | Occurs in unregulated diabetic when lack of insulin mimics the fasted state. Occurs in longer fasts/starvation states in nondiabetics |