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30 Cards in this Set
- Front
- Back
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1. What is the utilization of fatty acids from energy production?
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1. Lipids (store in adipose tissue as triglycerides)
-fat mobilization from adipose tissue 2. Fatty Acids -activation -transportation (cytosol - mitochon.) -β oxidation 3. Acetyl CoA either i. TCA ii. respiratory chain iii. H2O and ATP OR i. ketone body ii. non-hepatic tissues iii. acetyl CoA iv. TCA cycle |
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2. How are free fatty acids from adipocytes transported to other tissues through the blood?
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Free fatty acids binds with albumin
Albumin is water soluble with hydrophobic domain so it can bind FFA and carry it through blood |
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3. How do they cross the cell membrane?
Do all FA need to do this? |
Bind to membrane protein
-Fatty Acid Binding Protein (FABP) Short and medium chain FA can enter cell spontaneoulsy |
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4. What triggers fat mobilization for energy utilization?
What increases? What is a key enzyme? |
Hormones and is signalled by starvation
Hormone-sensitive lipolysis increases during starvation Hormone-sensitive triglyceride lipase |
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5. How does insulin affect fat?
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Promotes fat storage
Blocks fat release in adipocytes **Antilipolytic hormone |
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6. How is insulin during fasting?
What is a result? |
Insulin is low (glucagon is high)
Fat release is enhanced |
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7. How are long chain fatty acids activated and cross the mitochondrial membrane?
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1. FA -> Acyl CoA
-Use ATP -Acyl CoA synthase -large neg G so facilitates acyl CoA crosiing outer mitochon. membrane 2. Crosses through outer membrane which has many holes 3. Reacts w/ carnitine to form a fatty acyl-carnitine -Carnitin palmitoyl transferase I 1. |
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8. How are long chain fatty acids activated and cross the mitochondrial membrane?
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4. Fatty acyl-carnitine is translocated into matrix and carnitine moves out
-carnitine acylcarnitine translocase 5. Fatty acyl group is transferred back to acyl CoA -carnitne palmitoyl-transferase II 6. Fatty acyl CoA goes on for β-oxidation |
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9. What system is involved in long chain FA activation?
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Carnitine Transport System
3 enzymes |
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10. What are the different lengths of FA chains?
Where are they activated? |
1. Short chain (2-3 C)
-cytosol or mitochondria 2. Medium chain (4-12 C) -enter mitochondria directly w/o activation -activated in mitochondria 3. Long chain (12-20 C) -ER, outer mitochondrial membrane, and peroxisomal membranes 4. Very long chain (20+ C) |
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11. How many high energy phosphate bonds are required in the activation process?
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2 for one FA molecule
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12. What inhibits carnitne acyltransferase (CPT 1)?
What does this prevent? |
Malonyl-CoA
This is an intermediate in fat synthesis Prevents futile cycle (synthesis followed by immediate degradation) **FA synthesis is active, β-oxidation is inactive |
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13. What are the four steps of β-oxidation?
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1. Fatty acyl CoA -> fatty enoyl CoA
-acyl CoA dehydrogenase -1 FADH2 2. Enoyl CoA hydratase 3. β-hydroxy acyl CoA dehydrogenase -1 NADH 4. Cleave molecule to get fatty acyl CoA (2 c shorter) and acetyl CoA |
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14. How many times does the cycle repeat?
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Even # FA: until all converted to acetyl CoA
Odd # FA: have one additional product at end (acetyl CoA + propionyl) |
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15. What can genetic deficiencies in acyl-CoA Dehydrogenase cause?
What does Jamaican vomiting sickness do? |
SIDS
Get hypoglycemia Result from irreversible inhibition of acyl-CoA dehydrogenase by hypoglycin |
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16. When palmitoyl CoA is oxidized what is formed?
What is the total ATP that can be produced from its oxidation? What is the net ATP production? |
7 FADH2
7 NADH 8 Acetyl CoA 131 ATP 129 ATP (use 2 ATP for activation) |
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17. When does ketogenesis occur?
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When there is excess acetyl CoA (rate at which it is processed through TCA cycle does not keep with rate of production)
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18. What are the three ketone bodies mainly produced?
Where are they produced? Under what conditions are ketone bodies produced? |
Acetoacetate
3-hydroxybutyrate Acetone Liver mitochondira Metabolic conditions: -starvation -depletion of carb reserve -high fat diet -insulin deficiency |
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19. What is the key regulatory enzyme for ketone body synthesis?
What are three characteristics? |
HMG CoA synthetase
1. Inducible 2. Synthesized when fats are high in blood 3. Inhibited by high level of CoA-SH |
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20. How does activation and inhibition of HMG-CoA synthetase occur?
Where is the enzyme abundant? |
FA high in liver, CoA-SH levels are reduced and HMG-CoA synthetase is activated (ketogenesis)
FA in liver decrease, CoA-SH levels accumulate and inhibit enzyme In liver (not in non-hepatic tissues) **liver doesn't utilize ketone bodies |
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21. What can acetoacetate be reduced to?
What does this depend on? |
3-hydroxbutyrate
Mitochondrial NADH/NAD+ ratio High NADH levels will reduce it |
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22. What does utilization of ketone bodies as fuel first require?
What catalyzes this reaction? Where is this enzyme present? |
Activated to CoA derivative
Acetoacetate succinyl CoA reductase (thiotransferase) Most non-hepatic tissues (absent in liver) |
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23. What does acetoacetyl CoA form?
What happens to this molecule? What is the total ATP generation? |
2 acetyl CoA
Enters TCA cycle 24 ATP (12 from each acetyl CoA) |
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24. How many acetyl CoA does acetoacetate produce? How many ATP?
When β-hydroxybutyrate is converted to acetoacetae what is produced? |
2 acetyl CoA (24 ATP)
1 NADH which produces additional 3 ATP |
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25. What is the net production of ATP though?
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23 for acetoacetate
26 for β-hydroxybutyrate **Use on high energy molecule to activate ketone body |
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26. What changes in FA and ketone bodies occur during fasting?
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1. Blood glucose (insulin) drops and glucagon levels elevate
2. High glucagon triggers fat mobilization (released into blood stream) 3. β-oxidation in liver (NADH, ATP, and acetyl CoA) *pyruvate dehydrogenase is inhibited if high acetyl CoA |
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27. What changes in FA and ketone bodies occur during fasting?
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4. Flow of C into TCA cycle is used for synthesis of glucose
5. Oxaloacetate is reduced to malate which is converted to glucose 6. Acetyl CoA accumulates since oxaloacetate levels are low 7. Acetyl CoA forms ketone bodies |
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28. In a nutshell what does fasting cause?
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Increase in fatty acid metabolism
Generate more acetyl CoA Consequentially, ketone body synthesis increases |
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29. What does pyruvate dehydrogenase do?
What happens instead? |
Convert pyruvate to acetyl CoA
Pyruvate is converted to oxaloacetate which is used to make glucose -enzyme is pyruvate carboxylase |
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30. During starvation what happens to levels of things in metabolism?
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1. Glycogen stores are depleted, glucagon levels are elevated, FFA and keton body levels increased
2. Muscle decreases utilization of ketone bodies so brain uses them as fuel 3. Brain uses less glucose and liver gluconeogensis slows 4. Body uses fat stores as primary source of energy during starvation to conserve functional protein |
