| 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 |
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