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21 Cards in this Set
- Front
- Back
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what are pre-cursor molecules of oxaloacetate? |
glucose glucogenic AAs odd-chain FAs (succinylCoA --> OAA) glycerol (--> DHAP --> pyruvate) lactate (--> pyruvate) |
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in liver cells, what happens with OAA during extreme starvation |
there is no net gain of OAA
OAA is used to produce glucose (via gluconeogenesis)
OAA used in citric acid cycle --> provide energy for the liver |
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what happens to acetylCoA during extreme starvation |
there is a build-up of acetylCoA molecules because no net gain of OAA
the acetylCoA molecules are used to construct ketone bodies |
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what are 3 ketone bodies? |
1. acetone 2. acetoacetate 3. D-beta-hydroxybutyrate
"blood friendly" versions of acetyl CoA |
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acetone |
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acetoacetate |
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D-beta-hydroxybutyrate |
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acetone |
ketone body produced in smaller quantities and is exhaled |
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acetoacetate |
ketone body transported by blood to tissues other than the liver (including skeletal and heart muscle, renal cortex, and the brain) |
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D-beta-hydroxybutyrate |
ketone body transported by blood to tissues other than the liver (including skeletal and heart muscle, renal cortex, and the brain) |
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why can't the brain use free FAs for energy? |
FAs are not able to penetrate the BBB -prolonged starvation -> 75% of fuel required by the brain comes from ketone bodies |
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where are ketone bodies produced? |
liver cells mitochondrial matrix |
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acetoacetate synthesis |
1. 2 acetylCoA molecules combine to form acetoacetylCoA (reverse of last step of B-ox) via thiolase 2. acetoacetylCoA condenses with another acetylCoa to form HMG-CoA via HMG-CoA synthase -a CoA is produced in this step! 3. HMG-CoA is cleaved to form acetoacetate via HMG-CoA lyase -acetylCoA is also produced |
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acetone synthesis from acetoacetate |
decarboxylation via acetoacetate decarboxylase |
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D-beta-hydroxybutyrate synthesis from acetoacetate |
via D-beta-hydroxybutyrate dehydrogenase using 1 NADH |
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what determines whether acetoacetate or D-beta-hydroxybutyrate is made? |
the ratio of NADH/NAD+
higher [NADH], then higher [D-beta-hydroxybutyrate] |
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what happens to D-beta-hydroxybutyrate when it arrives at extrahepatic tissues? |
it is oxidized (+1 NADH) to form acetoacetate via D-beta-hydroxybutyrate dehydrogenase |
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what happens to acetoacetate when it reaches extrahepatic tissues |
after 2 enzymatic steps (beta-ketoacyl-CoA transferase and thiolase), acetoacetate is made into 2 acetylCoA molecules
the acetylCoA can enter the TCA cycle of extrahepatic tissues |
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why do liver cells express extremely low levels of beta-ketoacyl-CoA transferase? |
liver cells are the producer ketone bodies
the liver does not want to utilize the KBs for energy production - would be a futile cycle |
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where do extrahepatic tissues obtain OA during severe starvation? |
from glucose that is produced from the liver |
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ketoacidosis |
an increased concentration of ketone bodies in the blood -due to accumulation of acetylCoA if prolonged starvation or untreated diabetes
ketone bodies are acidic and can cause significant lowering of blood pH this can lead to coma and death |
