Questions:

1. As the time increases since ingestion of the last meal, hormonal changes occur as one leaves the fed state and enters the fasting state.  All the following changes and effects of adipose tissue are true EXCEPT
  1. Insulin increases and activates lipolysis
  2. Glucagon increases and increases lipolysis
  3. With long term fasting or exercise, epinephrine increases and activates lipolysis
  4. With long term fasting or exercise, cortisol increases and activates lipolysis
2. All of the following statements are true about free fatty acids released from adipose tissue EXCEPT
  1. Fatty acids are hydrophobic
  2. Fatty acids are not soluble in blood, the cytosol, or any other water solution
  3. Fatty acids are transported in the blood by albumin
  4. Fatty acids bind to a hydrophilic binding pocket of albumin
  5. Fatty acids are transported in the cytosol bound to proteins
3. The major pathway used to oxidize free fatty acids in humans is called

  1. The ketone body catabolic pathway
  2. The phosphatidic acid catabolic pathway
  3. Lipolysis
  4. The carnitine:palmitoyl transferase I and II pathway
  5. Β-oxidation
4. All of the following about the fatty acyl CoA synthetase reaction are true EXCEPT
  1. Almost all free fatty acids use this reaction to become activated
  2. ATP is a substrate
  3. Free fatty acids are substrates
  4. ADP is a product
  5. Fatty acyl CoA is a product
5. Free fatty acids from adipose tissue enter the cytosol, become activated, and must enter the mitochondria to be oxidized.  All of the following are part of the pathway whereby Acyl CoA in the cytosol becomes a substrate for Β-oxidation EXCEPT
  1. In the cytosol, the acyl group is transferred to carnitine by the enzyme carnitine palmitoyltransferase I
  2. Acylcarnitine enters the mitochondrion using carnitine acylcarnitine translocase
  3. In the mitochondrion, the acyl group is transferred to CoA by the enzyme carnitine palmitoyltransferase II
  4. The free CoA generated in the mitochondria travels back to the cytosol using carnitine acylcarnitine translocase
  5. The product of the carnitine palmitoyltransferase II reaction is oxidized by Β-oxidation
6. All of the following statements about Β-oxidation are true EXCEPT
  1. The pathway helps to generate energy and acetyl CoA from fatty acyl CoA
  2. The pathway produces NADH and FADH2 as products
  3. The pathway is found in all tissues that contain mitochondria
  4. The rate of the pathway is dependent upon the rate of fatty acyl CoA entering the mitochondria and the amount of NAD+ and FAD available
  5. The pathway is reversible
7. If stearyl CoA (18 carbon fatty acyl group) were oxidized by Β-oxidation, all of the following would result EXCEPT
  1. 8 acetyl CoA
  2. 8 FADH2
  3. 8 NADH
  4. 32 ATP
  5. The uptake of 8 CoAs into Acetyl CoA
8. In the normal oxidation of an odd chain fatty acid, all of the following would be part of the process EXCEPT
  1. Each odd chain fatty acyl CoA will produce one propionyl CoA
  2. Propionyl CoA enters the mitochondria using the Carnitine: palmitoyltransferase I system
  3. Propionyl CoA is converted to methylmalonyl CoA
  4. Methylmalonyl CoA is converted to succinyl CoA
  5. There is an increase in the number of 4 carbon intermediates in the TCA cycle
9. There are several factors that regulate the rate of Β-oxidation.  All of the following make sense EXCEPT
  1. In the fed state, insulin inhibits the release of free fatty acids from adipose tissue and therefor limits substrate for Β-oxidation
  2. In the fed state, insulin will cause dephosphorylation and activation of acetyl CoA carboxylase that produces malonyl CoA, an inhibitor of CPT1
  3. If the ATP/ADP ratio is low, AMP dependent protein kinase will phosphorylate and inactivate acetyl CoA carboxylase
  4. In the fasting state, the low insulin/glucagon ratio will result in the disappearance of malonyl CoA and activation of CPT1
  5. If the ATP/ADP ratio is low, then high concentrations of FADH2 and NADH will inhibit Β-oxidation
10. Concerning the pathway for ketone body synthesis, all of the following make sense EXCEPT
  1. Three acetyl CoA molecules can become 3-hydroxy-3-methyl glutaryl CoA (HMG CoA)
  2. HMG CoA is used for cholesterol and ketone body synthesis
  3. HMG CoA lyase produces acetoacetate and acetyl CoA
  4. Acetoacetate is oxidized to beta-hydroxybutyrate and acetone
  5. The rate of ketone body production is proportional to the excess acetyl CoA in the liver mitochondria
11. The production of ketone bodies is normally a way to transport excess acetyl CoA from the liver to other tissues of the body.  All of the following help to explain the process EXCEPT
  1. Blood Β-hydroxybutyrate enters the mitochondria non-liver cells where it will be catabolized
  2. Beta-hydroxybutyrate is oxidized to acetoacetate by beta-hydroxybutyrate dehydrogenase, NADH is produced
  3. Acetoacetate is activated using the enzyme acyl CoA synthetase and ATP
  4. Acetoacetyl CoA + CoA yield two acetyl CoAs which usually enter the TCA cycle and produce energy
  5. Acetoacetate is not catabolized by the liver because the liver lacks the enzyme succinyl CoA acetoacetate CoA transferase
12. Free fatty acid release from adipose tissue and an increase in the concentration of blood free fatty acids are expected in all of the following cases EXCEPT
  1. During a fast because of increased glucagon
  2. During starvation because of increased glucagon, epinephrine and cortisol
  3. During exercise because of increased epinephrine
  4. During stress because of increased glucagon, epinephrine and cortisol
  5. During a regular meal because of the increased insulin/glucagon ratio
13. All of the following would be expected during an extended fast (starvation) EXCEPT
  1. After about a day, blood glucose levels would remain constant at the low end of the normal range
  2. Blood ketone bodies would rise to very high concentrations over the first 20 days
  3. Blood fatty acids would rise during the first 3 days and very little after that time
  4. The use of blood ketone bodies by the brain would spare the use of blood glucose
  5. The catabolism of muscle protein to produce glucose would increase every day
14. Select the statement that is not true.  As a person in a resting state (no exercise) enters a fast after a mixed meal
  1. Most tissues switch from using mostly fatty acids as fuel to using mostly glucose as fuel
  2. The decrease in insulin inhibits the production of malonyl CoA and this activates CPT1 so more fatty acids can enter the mitochondria
  3. The decrease in insulin/glucagon increases blood free fatty acids
  4. The increased utilization of fatty acids causes inhibition of pyruvate dehydrogenase and hexokinase
  5. Exercise would increase both the use of blood fatty acids and blood glucose for energy production
15. All of the following help to explain the increased production of ketone bodies as a person enters a fast EXCEPT
  1. The insulin/glucagon ratio drops and release of free fatty acid from adipose tissue increases
  2. Decreased insulin results in phosphorylation of acetyl CoA carboxylase and decreased malonyl CoA
  3. Increased fatty acyl CoA enters the liver mitochondria because CPT I is not inhibited
  4. Β-oxidation produces too much NADH and FADH2 so Β-oxidation is inhibited
  5. More Acetyl CoA is produced than is needed by the TCA cycle so the excess it used to make ketone bodies
16. Otto Shape begins a 20-mile run.  All of the following are true EXCEPT
  1. The uptake of blood glucose by muscle will increase within a minute and blood glucose will be lowered
  2. Low blood glucose and increased blood epinephrine and norepinephrine will both decrease insulin release
  3. Decreased insulin release will increase glucagon release
  4. Blood cortisol, which must be synthesized before it is released, will start to increase within seconds
  5. Cortisol, glucagon, epinephrine and norepinephrine will all cause increased release of free fatty acids from adipose tissue
17. During a 20-mile run there is an increase in the rate at which acyl CoA is taken up by the mitochondria and used by Β-oxidation.  Part of the increase can be explained by the increase fatty acid entering the cell and part is explained by all of the following EXCEPT
  1. The more muscles contract, the higher the concentration of ADP and AMP
  2. AMP-dependent protein kinase causes the phosphorylation of acetyl CoA carboxylase
  3. Phosphorylation of acetyl CoA carboxylase inhibits the production of malonyl CoA
  4. The malonyl CoA concentration drops and inhibition of carnitine: palmitoyltransferase II is removed
  5. Much more acyl carnitine is available to use the carnitine-acylcarnitine translocase
18. Otto shape is in the process of running 20 miles.  As he started the race, the uptake and utilization of glucose by muscle cells increased.  All of the following help to explain why this happened EXCEPT
  1. The more muscles contract, the higher the concentration of ADP and AMP
  2. An active AMP-dependent protein kinase results in phosphorylation and activation of hexokinase
  3. The more glucose transporters in muscle cell membrane, the more glucose can enter the cell
  4. A lower ATP/ADP ratio activated phosphofructokinase-1 and increased the rate of glycolysis
  5. Even with increased Β-oxidation, there was a decrease in the inhibitors of pyruvate dehydrogenase
19. Otto Shape is engaged in a 20 mile run.  When compared to the resting state, you would expect the exercise to cause all of the following EXCEPT

  1. Increased ADP concentration
  2. Increased ATP synthase activity as a result of increased ADP concentration
  3. Increased pumping of protons into the mitochondria by the electron transport chain
  4. Increased NADH and FADH2 utilization by the electron transport chain
  5. Increased NAD+ and FAD available as substrates for Β-oxidation
20. Your patient suffers from medium chain acyl CoA (MCAD) deficiency.  Compared to a normal person, you would expect all of the following EXCEPT
  1. An increase in the rate at which liver glycogen stores are depleted and decrease time of onset of hypoglycemia following a mixed meal
  2. An increase in blood glucose utilization in the fasting state because the cells cannot get enough energy form Β-oxidation
  3. An increase in ketone body synthesis because of inhibition of the TCA cycle
  4. A decrease in gluconeogenesis in the liver because gluconeogenesis depends upon energy supplied by Β-oxidation
  5. Symptoms to appear anytime the patient does not eat regularly
21. Your patient suffers from type-1 diabetes.  If she missed her regular insulin injection, you would expect all of the following EXCEPT
  1. Decreased insulin and increased stress hormones (glucagon, epinephrine, norepinephrine, cortisol, and others)
  2. Increased mobilization of fatty acids from adipose tissue and increased entrance of fatty acids into all cells of the body except brain
  3. Low insulin and high glucagon to both result in the inhibition of acetyl CoA carboxylase and decreased concentrations of malonyl CoA
  4. Low malonyl CoA would result in faster entrance of acyl CoA into the mitochondria, more Β-oxidation, and more acetyl CoA
  5. Increased ketone body synthesis will result in an increase in blood pH
22. In the pathway for the conversion of propionyl CoA to a TCA cycle intermediate, all of the following are true EXCEPT?
  1. Acetyl CoA is the product
  2. Methylmalonyl CoA is an intermediate
  3. ATP is used
  4. CO2 is added to propionyl CoA in a reaction that requires biotin
  5. Coenzyme B12 is used
23. Which of the following statements are FALSE? There are several factors that regulate the rate of Β-oxidation: The rate of mobilization of fatty acids, the concentration of malonyl CoA and the concentration of NADH and FAD(2H). Acetyl CoA Carboxylase is
  1. Active in the fed state because insulin activates phosphatases that dephosphorylate the enzyme
  2. Inactive in the fasting state because Protein kinase A phosphorylates and inactivates the enzyme
  3. Inactive if the fasting state if epinephrine has activated the cAMP cascade
  4. Inactive if cellular concentrations of AMP are high because AMP-activated protein kinase will phosphorylate and inactivate the enzyme
  5. Inactive if cellular concentrations of citrate are high because citrate is an allosteric inhibitor of the enzyme
24. The rate of beta oxidation is decreased by all of the following except?
  1. High concentrations of oxygen
  2. High concentrations of NADH
  3. High concentrations of FAD (2H)
  4. High concentrations of malonyl CoA
  5. High concentrations of insulin
25. Compared to a 24 hour fast, all of the following would be true for after five days of starvation EXCEPT
  1. Brain cells use less glucose and more ketone bodies to synthesize ATP
  2. The brain takes up less Glucose
  3. Less glucose is made in the liver to maintain blood glucose levels
  4. Less amino acids are used for gluconeogenesis
  5. More protein is catabolized to supply substrate for gluconeogenesis
26. During starvation, when the brain uses more ketone bodies, all of the following are true EXCEPT
  1. Total energy usage by the brain is about the same as the fed state
  2. Ketone bodies supply much more energy than they normally do
  3. Less glucose needs to be used to maintain normal levels of ATP
  4. Less glucose is removed from blood by brain cells
  5. Less gluconeogenesis occurs in muscle cells
27.Five hours following a mixed meal, your patient begins vigorous exercise. All of the following would occur in striated muscle cells EXCEPT
  1. The AMP concentration would rise dramatically
  2. Increased AMP-Protein Kinase would inhibit acetyl CoA carboxylase
  3. Increased Malonyl CoA would inhibit Carnitine palmitoyl transferase
  4. More fatty acids would be used for energy
  5. More glucose would be used for energy
28. Your patient suffers from medium chain acyl CoA (MCAD) deficiency. In the fasting state and compared to a normal person’s muscle cell, all of the following would be true EXCEPT?
  1. Less inhibition of Pyruvate dehydrogenase by acetyl CoA
  2. More pyruvate converted to acetyl CoA
  3. More glucose converted into pyruvate
  4. More inhibition of Phosphofructokinase-1 by ATP
  5. Less production of ATP and NADH via B-oxidation
29. Your patient has type-1 diabetes. If she missed her regular inulin injection, you would expect all of the following EXCEPT
  1. A low insulin would contribute to the low activity of acetyl CoA carboxylase
  2. A high epinephrine would contribute to the low activity of acetyl CoA carboxylase in muscle cells
  3. A high glucagon would contribute to the low activity of acetyl CoA carboxylase in liver cells
  4. High malonyl CoA would increase the influx of acyl carnitine into the mitochondria
  5. High acetyl CoA would increase the production of ketone bodies in the liver
30. During the activation of fatty acids by fatty acid synthetase, pyrophosphate (PPI) is produced.  Which of the following statements is NOT true?
  1. PPi is hydrolyzed to 2 Pi by inorganic pyrophosphatase
  2. PPi does not contain a high energy bond
  3. The hydrolysis of PPi provides the driving force for the activation of fatty acids
  4. Without the hydrolysis of PPi, the fatty acid synthetase reaction would be reversible
  5. In vivo, hydrolysis of PPi causes the fatty acid synthetase reaction to be irreversible

Answers:

1. Answer: A. Chapter 23 , Objective 1: Between meals, lipolysis is activated in adipose tissue as a result of changes in hormone concentrations. Which responsible hormones are increased or decreased? Back to question 1.
2. Answer: D. Chapter 23 , Objective 2: How are free fatty acids transported from adipose tissue to muscle or liver cells? Back to question 2.
3. Answer: E. Chapter 23 , Objective 3: Name the major pathway used to oxidize fatty acids into acetyl CoA. Back to question 3.
4. Answer: D. Chapter 23 , Objective 4: What are the reactants and products of the fatty acyl CoA synthetase reaction? Back to question 4.
5. Answer: D. Chapter 23 , Objective 5: Describe the pathway for transport of fatty acyl CoA in the cytosol to fatty acyl CoA in the mitochondria. Use the terms carnitinepalmitoyltransferase I and II, carnitine, CoA, inner mitochondrial membrane, and carnitine acylcarnitine translocase, CoA in your explanation. Back to question 5.
6. Answer: E. Chapter 23 , Objective 6: Use the criteria for understanding and describing all pathways to describe Β-oxidation: Names: Functions: Substrates: Product: Control Enzymes: Regulation: Compartment(s): Tissues of interest Back to question 6.
7. Answer: A. Chapter 23 , Objective 7: Given a saturated, straight chain fatty acid, be able to calculate the number of molecules of Acetyl-CoA, FADH2, and NADH produced by Β-oxidation. How much ATP would this be equivalent to? Back to question 7.
8. Answer: B. Chapter 23 , Objective 8: Be able to name the three metabolites and two important cofactors in the conversion of part of an odd chain fatty acid to a TCA cycle intermediate. (Skip the epimerase) reaction.) Back to question 8.
9. Answer: E. Chapter 23 , Objective 9: What are the major factors that control the synthesis of acetyl-CoA by Β-oxidation muscle and/or liver? Back to question 9.
10. Answer: D. Chapter 23 , Objective 10: Describe the pathway for the synthesis of ketone bodies by naming substrates, the first ketone body made in the pathway, the next two ketone bodies made in the pathway, the intermediate in the pathway that can be used either for ketone body synthesis or cholesterol synthesis, and the enzyme that actually produces the first ketone body as a product. Control? Where does this pathway reside? Back to question 10.
11. Answer: C. Chapter 23 , Objective 11: Name a few tissues that oxidize ketone bodies. Why not the liver? What happens to blood ketone bodies? Name the intermediates in the pathway from B-Hydroxybutyrate to acetyl CoA. What does the enzyme succinyl CoA:acetoacetate CoA transferase do? Back to question 11.
12. Answer: E. Chapter 23 , Objective 12: What is the effect of insulin, glucagon, or epinephrine upon lipolysis in adipose tissue? Back to question 12.
13. Answer: E. Chapter 23 , Objective 13: What happens to the blood levels of fatty acids, glucose, and ketone bodies during an extended fast? Explain how the use of ketone bodies by the brain spares muscle protein. Back to question 13.
14. Answer: A. Chapter 23 , Objective 14: If a person eats a balanced meal, does not exercise, and then begins a 10 hour fast. What happens to the rate of carbohydrate and fatty acid oxidation in muscle? Assume that the person dose not exercise. What would happen if they began to exercise vigorously after 5 hours? Back to question 14.
15. Answer: D. Chapter 23 , Objective 15: How can a decrease in the insulin/glucagon ratio explain the increased production of ketone bodies during a fast? Back to question 15.
16. Answer: D. Chapter 23 , Objective 16: Concerning Otto shape, what hormonal changes occur during the long distance run and how do they affect the release of free fatty acids from adipose tissue? Back to question 16.
17. Answer: D. Chapter 23 , Objective 17: Concerning Otto shape, during his long distance run the change in the concentration of AMP ensures the increased uptake of fatty acyl CoA into his muscle mitochondria. Explain this using the terms: muscle contraction, ATP, AMP, AMP-dependent protein kinase, acetyl CoA carboxylase, malonyl CoA, inhibition, carnitine:palmitoyltransferase I, and carnitine-acylcarnitine translocase Back to question 17.
18. Answer: B. Chapter 23 , Objective 18: Concerning Otto shape, during his long distance run the change in the concentration of AMP ensures the increased uptake of glucose into muscle tissue. How does this happen? Use the terms muscle contraction, ATP, AMP, AMP-dependent protein kinase, glucose transporters, and membrane. Back to question 18.
19. Answer: C. Chapter 23 , Objective 19: Concerning Otto shape, during his long distance run the change in the concentration of ADP causes increased Β-oxidation. Explain this using the terms muscle contraction, ADP, ATP synthase, proton gradient, electron transport chain, NADH oxidation, FAD(2H) oxidation, and Β-oxidation. Back to question 19.
20. Answer: C. Chapter 23 , Objectives 20: Concerning Lofata Burne: Explain why medium chain acyl CoA (MCAD) deficiency would cause a decrease in ketone body synthesis during a fast. Also, from an energy point of view, explain why MCAD deficiency would increase the utilization of blood glucose by most tissues of the body and why gluconeogenesis in the liver is less than expected. Back to question 20.
21. Answer: E. Chapter 23 , Objectives 21: Concerning Di Abietes, who suffers from Type I diabetes, what is the cause of her disease? What effect does this have upon blood concentrations of glucagon, catecholamines, and cortisol? What effect do these hormones have upon fatty acid mobilization from adipose tissue? What effect does low insulin and high glucagon have upon fatty acyl CoA entrance into liver mitochondria? What is the effect upon Β-oxidation? What effect does this have upon ketone body synthesis? What effect does this have upon blood pH? Back to question 21.
22. Answer: A. Chapter 23, Objectives 8:Be able to name the three metabolites and two important cofactors in the conversion of part of an odd chain fatty acid to a TCA cycle intermediate. (Skip the epimerase reaction.) Back to question 22.
23. Answer: E. Chapter 23, Objectives 9:What are the major factors that control the synthesis of acetyl-CoA by B-oxidation muscle and/or liver? Back to question 23.
24. Answer: A. Chapter 23, Objectives 9:What are the major factors that control the synthesis of acetyl-CoA by B-oxidation muscle and/or liver? Back to question 24.
25. Answer: E. Chapter 23, Objectives 13:What happens to the blood levels of fatty acids, glucose, and ketone bodies during an extended fast? Explain how the use of ketone bodies by the brain spares muscle protein Back to question 25.
26. Answer: E. Chapter 23, Objectives 13: What happens to the blood levels of fatty acids, glucose, and ketone bodies during an extended fast? Explain how the use of ketone bodies by the brain spares muscle protein. Back to question 26.
27. Answer: C. Chapter 23, Objectives 14: If a person eats a balanced meal, does not exercise, and then begins a 10 hour fast. What happens to the rate of carbohydrate and fatty acid oxidation in muscle? Assume that the person dose not exercise. What would happen if they began to exercise vigorously after 5 hours? Back to question 27.
28. Answer: D. Chapter 23, Objectives 20: Concerning Lofata Burne: Explain why medium chain acyl CoA (MCAD) deficiency would cause a decrease in ketone body synthesis during a fast. Also, from an energy point of view, explain why MCAD deficiency would increase the utilization of blood glucose by most tissues of the body and why gluconeogenesis in the liver is less than expected. Back to question 28.
29. Answer: D. Chapter 23, Objectives 21: Concerning Di Abietes, who suffers from Type I diabetes, what is the cause of her disease? What effect does this have upon blood concentrations of glucagon, catecholamines, and cortisol? What effect do these hormones have upon fatty acid mobilization from adipose tissue? What effect does low insulin and high glucagon have upon fatty acyl CoA entrance into liver mitochondria? What is the effect upon B-oxidation? What effect does this have upon ketone body synthesis? What effect does this have upon blood pH? Back to question 29.
30. Answer: B. Chapter 23, Objectives 4: What are the reactants and products of the fatty acyl CoA synthetase reaction? Back to question 30.