Questions:

1. Concerning the storage of glucose in the liver, all of the following are true EXCEPT
  1. Regulated by glucose concentration and insulin concentration
  2. Occurring when both glycogen synthase and glycogen phosphorylase are both phosphorylated
  3. Not part of a futile cycle because when glycogen synthase is activated, glycogen phosphorylase is inactivated
  4. Inhibited by glucagon and epinephrine which both activate the cAMP cascade
  5. Limited to times when glucose concentration is high because the Km (S0.5) of glucokinase is about 7 mM
2. When more carbohydrate is consumed than can be used for present energy needs and glycogen storage, the carbohydrate is converted to fatty acid in the liver.  All of the following statements about the first part of this pathway are true EXCEPT
  1. Carbohydrate is converted to pyruvate using glycolysis
  2. Activated by dephosphorylation of phosphofructokinase-2/fructose-2,6-bisphosphatase
  3. The allosteric activator fructose-2,6-bisphosphate is required
  4. The dephosphorylation of pyruvate kinase is required
  5. The inhibition of protein phosphatases by insulin is required
3. When carbohydrate is converted to fatty acid in the liver.  All of the following statements are true EXCEPT

  1. Some pyruvate is converted to acetyl CoA by pyruvate dehydrogenase
  2. Some pyruvate is converted to oxaloacetate by pyruvate carboxylase in the presence of high concentrations of acetyl CoA
  3. Acetyl CoA and oxaloacetate form citrate and the citrate leaves the mitochondria
  4. In the cytosol, citrate synthase produces ATP, oxaloacetate and acetyl CoA from citrate and ADP
  5. The oxaloacetate is converted back to pyruvate in the cytosol
4. The fatty acid synthase requires reducing a reducing agent.  This reducing agent is made by
  1. Pumping protons from the mitochondria
  2. Reduced coenzyme Q in the electron transport chain
  3. The pentose phosphate pathway and malic enzyme
  4. FADH2 and NADH produced in the mitochondria by the TCA cycle
  5. NADH produced by anaerobic glycolysis
5. The control enzyme for fatty acid synthesis
  1. Is activated by glucagon, epinephrine, and AMP
  2. Is inhibited by insulin and protein phosphatase
  3. Produces malonyl CoA and ATP
  4. Requires biotin as a cofactor
  5. Is found only in the endoplasmic reticulum
6. All of the following are true during fatty acid synthesis in the liver EXCEPT
  1. The concentration of insulin and glucose are both high
  2. The mobilization of free fatty acids from adipose is inhibited
  3. Acetyl CoA carboxylase and pyruvate carboxylase are both activated
  4. The concentration of malonyl CoA in the cytosol is very low
  5. Carnitine: palmitoyltransferase-1 is inhibited
7. All of the following are true statements about the fate of the product of the fatty acid synthase complex in the fed state EXCEPT
  1. Palmitate is activated to palmitoyl CoA
  2. Much of the palmitoyl CoA is elongated and desaturated in the endoplasmic reticulum
  3. Fatty acyl CoA combines with diacylglycerol phosphate to form phosphatidic acid
  4. Phosphatidic acid is dephosphorylated to diacylglycerol, which combines with acyl CoA to form triacylglycerol
  5. Triacylglycerol combines with Apo B-100, cholesterol, cholesterol esters, and glycerophospholipids to form a VLDL
8. Assume that a lot of VLDL and chylomicrons are produced during and immediately following the meal and that the concentration of VLDL decreases to between the Km for adipose and muscle lipoprotein lipase by 8 hours after the meal.  All of the following statements about lipoprotein lipase are true EXCEPT.
  1. The Km for adipose lipoprotein lipase is much higher than the Km of muscle lipoprotein lipase
  2. Eight hours following a meal, the concentration of VLDL will still be above the Km for muscle lipoprotein lipase
  3. Eight hours following a meal, the velocity of muscle lipoprotein lipase reaction will be between ½ Vmax and Vmax
  4. During a meal, insulin will increase the synthesis and secretion of adipose lipoprotein lipase
  5. During and for a few hours following a meal, the concentrations of blood VLDL and chylomicrons will be below 0.1 Km for adipose lipoprotein lipase
9. In the fed state, insulin affects the delivery and storage of free fatty acids to adipose tissue in all of the following ways EXCEPT
  1. Insulin will increase the synthesis and secretion of the isoenzyme of lipoprotein lipase found in adipose tissue
  2. Insulin will increase the Glut4 in the adipose membrane so glucose can enter the cells faster
  3. Insulin will activate glycolysis so that dihydroxyacetone phosphate can be made faster
  4. Insulin will inhibit glycerol-3-phosphate dehydrogenase and prevent the loss of dihydroxyacetone phosphate
  5. Insulin inhibits the cAMP cascade in adipose so that triacylglycerol is not hydrolyzed
10. When triacylglycerol is synthesized in adipose tissue, all of the following are true EXCEPT
  1. The insulin to glucagon ratio is high
  2. Glycerol phosphate is synthesized from glucose by glycolysis
  3. Fatty acids from chylomicrons or VLDL are activated to form acyl CoAs
  4. Phosphatidic acid is not an intermediate
  5. Diacylglycerol is an intermediate
11. Concerning the products of the lipoprotein lipase reaction in the blood vessels of adipose tissue, all of the following are true EXCEPT
  1. The lipoprotein lipase reaction in adipose is usually activated in the fed state
  2. The products of the reaction are 3 fatty acids and one glycerol molecule
  3. The fatty acids enter the adipose cell and are activated by fatty acyl CoA synthetase
  4. The glycerol enters the liver and is phosphorylated by glycerol-3-phosphate dehydrogenase
  5. The glycerol could be used by the liver to synthesize another molecule of triacylglycerol
12. During fasting, the blood glucose is maintained by the liver.  Because of  low insulin to glucagon ratios, all of the following contribute to this process EXCEPT
  1. The cAMP cascade is active so phosphorylase b is converted to phosphorylase a
  2. Glycerol is available for gluconeogenesis
  3. Phosphofructokinase-1 and phosphofructokinase-2 are both active
  4. Β-oxidation and the TCA cycle are providing energy for gluconeogenesis
  5. High acetyl CoA concentrations activating pyruvate carboxylase and inhibiting pyruvate dehydrogenase
13. During the fasting state, the insulin to glucagon ratio is low.  In the liver, all of the following result EXCEPT
  1. The cyclic-AMP cascade is active and cAMP phosphodiesterase is inhibited
  2. cAMP combines with the regulatory subunits of protein kinase A
  3. Protein kinase A is activated and this inhibits glycolysis and glycogen synthesis
  4. Protein kinase A is activated and this activates gluconeogenesis and glycogenolysis
  5. Protein kinase A causes dephosphorylation of glycogen synthase, which changes its conformation and activity
14. As one enters the fasting state, liver glycolysis is inhibited while gluconeogenesis is activated.  All of the following are important in this process EXCEPT
  1. Protein kinase A activates phosphofructokinase-2 and the concentration of fructose-2,6-bisphosphate rises
  2. In the absence of fructose-2,6-bisphosphate, fructose-1,6-bisphosphatase is active
  3. Protein kinase A phosphorylates pyruvate kinase so that phosphoenolpyruvate must become 2-phosphoglycerate and eventually glucose
  4. Energy is provided by free fatty acids that are mobilized, enter the mitochondria, and are oxidized by b-oxidation
  5. The increased Acetyl CoA activates pyruvate carboxylase so that pyruvate can be used as a substrate
15. All of the following statements about the regulation of fatty acid mobilization (release from adipose) are true EXCEPT
  1. The control enzyme is called hormone sensitive lipase
  2. Insulin activates a protein phosphatase that removes a phosphate from hormone sensitive lipase
  3. Cortisol inhibits hormone sensitive lipase using the cAMP cascade
  4. Epinephrine activates hormone sensitive lipase using the cAMP cascade
  5. Glucagon activates hormone sensitive lipase using the cAMP cascade
16. All of the following help to explain why ketone bodies are produced during a fast EXCEPT
  1. Low insulin to glucagon ratio ensures the activation of hormone sensitive lipase and mobilization of fatty acids
  2. Low insulin to glucagon ratio ensures the entrance of activated fatty acids into the mitochondria
  3. If more acetyl CoA is made than is needed by the TCA cycle, then hydroxymethylglutaryl CoA will be made
  4. The liver has an active enzyme, hydroxymethylglutaryl CoA lyase that produces acetoacetate and acetyl CoA
  5. The liver has an active enzyme beta-hydroxybutyrate dehydrogenase that converts acetoacetate into acetone
17. As a fast is prolonged, glycogenolysis becomes less important and gluconeogenesis becomes more important.  All of the following are important for gluconeogenesis EXCEPT
  1. Pyruvate must not be converted to acetyl CoA
  2. Beta-oxidation produces high concentrations of acetyl CoA which activate pyruvate carboxylase
  3. Phosphoenolpyruvate must not be converted to 2-phosphoglycerate
  4. β-oxidation produces high concentrations of acetyl CoA which inhibit pyruvate dehydrogenase
  5. Beta-oxidation and The TCA cycle produce NADH and FADH2, which, in turn, produces ATP
18. In a sedentary fasting state, skeletal muscle spares blood glucose.  All of the following are important in this process EXCEPT
  1. By using mostly fatty acid, muscle needs less glucose for energy production
  2. At low insulin levels, fatty acid mobilization is increased
  3. At low insulin levels, acetyl CoA carboxylase is activated
  4. The more energy produced from fatty acids, the less glucose needs to be oxidized
  5. In a sedentary fasting state, most of the glut4 transporters have been removed from the muscle cell membrane
19. When sedentary fasting person begins to exercise, all of the follow occur EXCEPT
  1. Exercise activates AMP-protein kinase and results in more glut4 moving to the cell membrane
  2. AMP and epinephrine both activate phosphorylase so that glycogenolysis occurs
  3. AMP and epinephrine both cause activation of phosphofructokinase-1 in muscle
  4. AMP-protein kinase inhibits malonyl CoA production and activates carnitine: palmitoyltransferase-1
  5. Since more ATP is made from fatty acids and muscle glycogen, less blood glucose is used
20. Di Beatty, who has type I diabetes and has developed ketoacidosis.  Her blood contains less insulin than it should and more stress hormones that it should.  These hormone levels explain all of the following EXCEPT
  1. Some of the excess fatty acids released for adipose are converted to VLDL so the liver releases more VLDL than normal 
  2. The lipoprotein lipase of adipose is not as active as it should be so VLDL and chylomicrons are not catabolized at a normal rate
  3. Glucose enters muscle and adipose tissue at a faster rate but is not utilized as it should so blood glucose rises
  4. Gluconeogenesis is more activated and muscle protein is being catabolized which also causes blood glucose to rise
  5. More acetyl CoA is being produced than can be used so it is converted to ketone bodies
21. Ann Sulin who has type II diabetes.  Since her insulin to glucagon is always lower than it should be for the level of blood glucose and because she has insulin resistance, all of the following are true EXCEPT
  1. She releases more free fatty acids than normal from adipose and some are converted to VLDL and released by the liver
  2. Since her adipose tissue is insulin resistant, her adipose lipoprotein lipase is not as active and she does not catabolize VLDL or chylomicrons at a normal rate
  3. Since she mobilizes too much free fatty acids, she is prone to develop ketoacidosis
  4. In addition to insulin resistance, in the fed state, she releases less insulin and at a slower rate so glucose is not removed from blood in a normal manner
  5. In the fasting state, gluconeogenesis produces an abnormal amount of glucose
22. Concerning the synthesis of triacylglycerol in adipose tissue and in the fed state, all of the following are true EXCEPT
  1. Glycerol kinase is activated by phosphatases
  2. Lipoprotein Lipase is activated by insulin
  3. Glut4 in the membrane is increased by insulin
  4. Glycolysis is activated by insulin to produce energy and dihydroxyacetone phosphate
  5. Hormone sensitive lipase is inhibited by insulin
23.In the fasting state, much less glucose is used in skeletal muscle than in the fed state. All of the following help to explain this EXCEPT
  1. Increased mobilization of free fatty acids
  2. Increased malonyl CoA
  3. Increased ATP produced by β-oxidation
  4. Low insulin and low AMP results in low phosphofructokinase-1 activity
  5. Hexokinase is inhibited by high concentrations of glucose-6-phosphate

Answers:

1. Answer: B. Chapter 36, Objective 1: Describe the pathway for the storage of glucose in the liver in the fed state? How is this pathway regulated.? Are there any possible futile cycles prevented? Back to question 1.
2. Answer: E. Chapter 36, Objective 2: What pathway provides for the production of pyruvate to be used for fatty acid synthesis in the fed state? How is this pathway regulated? Back to question 2.
3. Answer: D. Chapter 36, Objective 3: During the conversion of glucose to fatty acid, how is pyruvate, produced from glycolysis, converted to citrate in the cytosol? In which compartment does each reaction take place? Back to question 3.
4. Answer: C. Chapter 36, Objective 4: What are the sources of the reducing agent used for the reductive biosynthesis of fatty acids? Back to question 4.
5. Answer: D. Chapter 36, Objective 5: Which enzyme controls the pathway for the synthesis of fatty acids from acetyl CoA in the cytosol? How is this pathway regulated? (ignore citrate) Back to question 5.
6. Answer: D. Chapter 36, Objective 6: What keeps newly formed free fatty acid from entering the mitochondria in the fed state? Back to question 6.
7. Answer: C. Chapter 36, Objective 7: What happens to the product of the fatty acid synthase complex before it is found in the blood? Back to question 7.
8. Answer: E. Chapter 36, Objective 8: Compare the Km for lipoprotein lipase in heart and adipose tissue. What implications dose this have for the usage of blood triacylglycerol in the fed and fasting state? Back to question 8.
9. Answer: D. Chapter 36, Objective 9: How does insulin affect the delivery of free fatty acid into adipose cells in the fed state? Back to question 9.
10. Answer: D. Chapter 36, Objective 10: What are the pathways for the synthesis of triacylglycerol in adipose from glucose and free fatty acids? How is the production of glycerol phosphate regulated? Back to question 10.
11. Answer: D. Chapter 36, Objective 11: What happens to the glycerol released in the lipoprotein lipase reaction in the fed state? Back to question 11.
12. Answer: C. Chapter 36, Objective 12: What pathways provide blood glucose during fasting? Why are these pathways active? Back to question 12.
13. Answer: E. Chapter 36, Objective 13: Glycogen is not made in the liver during fasting. Why not? Back to question 13.
14. Answer: A. Chapter 36, Objective 14: Glycolysis does not function when gluconeogenesis is functioning. What factors turn on gluconeogenesis and turn off glycolysis? Back to question 14.
15. Answer: C. Chapter 36, Objective 15: What is the control enzyme for the release of free fatty acids during a fast and how is this enzyme regulated? Back to question 15.
16. Answer: E. Chapter 36, Objective 16: Why are ketone bodies produced during a fast? Back to question 16.
17. Answer: C. Chapter 36, Objective 17: Besides providing ATP, how does increased b oxidation enable gluconeogenesis? Back to question 17.
18. Answer: C. Chapter 36, Objective 18: Explain how increased fatty acid oxidation and decreased insulin spares blood glucose by muscle in the fasting and resting state. Back to question 18.
19. Answer: E. Chapter 36, Objective 19: What is the effect of exercise upon the use of blood glucose by muscle in the fasting state? What is the mechanism? Back to question 19.
20. Answer: C. Chapter 36, Objectives 20: Concerning Di Beatty, who has type I diabetes and has developed ketoacidosis: On a molecular level, explain why she has opalescent serum. Why does she have high blood glucose? Why does she have ketonemia? Back to question 20.
21. Answer: C. Chapter 36, Objectives 21: Concerning Ann Sulin who has type II diabetes: On a molecular level, explain why she has high serum triacylglycerol. Why does she have high blood glucose? Would you expect ketoacidosis? Back to question 21.
22. Answer: A. Chapter 36, Objectives 10: What are the pathways for the synthesis of triacylglycerol in adipose from glucose and free fatty acids? How is the production of glycerol phosphate regulated? Back to question 22.
23. Answer: B. Chapter 36, Objectives 18: Explain how increased fatty acid oxidation and decreased insulin spares blood glucose by muscle in the fasting and resting state. Back to question 23.