Unit 11 Chapter Question
During fasting or exercise, fatty acids need to enter the mitochondria. All of the following will increase entry EXCEPT A. insulin B. AMP C. increased active protein kinase A D. epinephrine E. glucagon in the liver
Answer: A. insulin. Chapter 33, Objective 2: Be able to write the equation for the control step in fatty acid synthesis. What is the name of the enzyme and how is this enzyme step controlled?
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 A. The more muscles contract, the higher the concentration of ADP and AMP B. An active AMP-dependent protein kinase results in phosphorylation and activation of hexokinase C. The more glucose transporters in muscle cell membrane, the more glucose can enter the cell D. A lower ATP/ADP ratio activated phosphofructokinase-1 and increased the rate of glycolysis E. Even with increased Β-oxidation, there was a decrease in the inhibitors of pyruvate dehydrogenase
Answer: B. An active AMP-dependent protein kinase results in phosphorylation and activation of hexokinase. 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.
Over the last six months, your patient has developed a habit of eating chocolates. He is eating about 600 calories a day in chocolates and his diet contains about 400 extra calories a day. He comes to you for advice because he does not want to "get fat." You would be safe in telling him all of the following EXCEPT A. His liver will convert excess carbohydrates in chocolates into fat that will be transported and stored in his fat (adipose) cells B. If he continues his present diet, he will gain another 15 pounds and then stop gaining weight C. He could continue one chocolate a day and not gain more weight if he will exercise vigorously every day D. If he consumes more calories than he uses, he will continue to gain weight. E. His best choice is to stop chocolates and exercise
Answer: B. If he continues his present diet, he will gain another 15 pounds and then stop gaining weight. Chapter 33, Objective 18: Concerning Percy Veere who is eating too much candy: Can he produce fat from a low fat, high carbohydrate diet? How about a high protein, low fat diet?
During the activation of fatty acids by fatty acid synthetase, pyrophosphate (PPI) is produced. Which of the following statements is NOT true? A. PPi is hydrolyzed to 2 Pi by inorganic pyrophosphatase B. PPi does not contain a high energy bond C. The hydrolysis of PPi provides the driving force for the activation of fatty acids D. Without the hydrolysis of PPi, the fatty acid synthetase reaction would be reversible E. In vivo, hydrolysis of PPi causes the fatty acid synthetase reaction to be irreversible
Answer: B. PPi does not contain a high energy bond. Chapter 23, Objectives 4: What are the reactants and products of the fatty acyl CoA synthetase reaction?
All of the following statements about essential fatty acids are true EXCEPT A. They can not be synthesized by humans cells B. They are essential for the synthesis of some prostaglandins and other eicosanoids C. They contain omega-3 or omega-6 double bonds D. They contain at least 4 double bonds E. They are linoleic and linolenic acid
Answer: D. They contain at least 4 double bonds. Chapter 33, Objective 8: What are the essential fatty acids and why are they essential?
Where does the elongation of most fatty acids take place? A. Cytosol B. Mitochondria C. Nucleus D. VLDL E. Endoplasmic reticulum
Answer: E. Endoplasmic reticulum. Chapter 33, Objective 6: Where does the elongation of most fatty acids take place?
If stearyl CoA (18 carbon fatty acyl group) were oxidized by Β-oxidation, all of the following would result EXCEPT A. 8 acetyl CoA B. 8 FADH2 C. 8 NADH D. 32 ATP E. The uptake of 8 CoAs into Acetyl CoA
Answer: A. 8 acetyl CoA. 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?
In the pathway for the conversion of propionyl CoA to a TCA cycle intermediate, all of the following are true EXCEPT? A. Acetyl CoA is the product B. Methylmalonyl CoA is an intermediate C. ATP is used D. CO2 is added to propionyl CoA in a reaction that requires biotin E. Coenzyme B12 is used
Answer: A. Acetyl CoA is the product. 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.)
Acyl carrier protein and CoA have all of the following in common EXCEPT A. Both incorporate ADP into their structure B. Both incorporate pantothenic acid into their structure C. Both have a functional SH group (thiol group) D. Both form thioester bonds with fatty acids E. Both form high-energy bonds with fatty acids
Answer: A. Both incorporate ADP into their structure. Chapter 33, Objective 4: What do acyl carrier protein and CoA have in common?
Phosphatidic acid is an intermediate in both the synthesis of triacylglycerol and glycerophospholipids (membrane lipids). To convert phosphatidic acid to phosphatidylinositol, you would react phosphatidic acid with A. CTP and then with inositol B. UTP and then with inositol C. CTP and then with inositol trisphosphate D. CDP and then with inositol trisphosphate E. UDP and then with inositol
Answer: A. CTP and then with inositol. Chapter 33, Objective 15: How would you make phosphatidylinositol from inositol and phosphatidic acid?
During fatty acid mobilization, glycerol is used by the liver for gluconeogenesis because adipose does not have A. Glycerol kinase B. Hormone sensitive lipase C. Protein kinase A D. Phosphofructokinase-1 E. Glycerol transporters
Answer: A. Glycerol kinase. Chapter 33, Objective 10: During fatty acid mobilization, glycerol is not used by adipose tissue but is used by the liver for gluconeogenesis. Why?
The rate of beta oxidation is decreased by all of the following except? A. High concentrations of oxygen B. High concentrations of NADH C. High concentrations of FAD (2H) D. High concentrations of malonyl CoA E. High concentrations of insulin
Answer: A. High concentrations of oxygen. Chapter 23, Objectives 9:What are the major factors that control the synthesis of acetyl-CoA by B-oxidation muscle and/or liver?
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 A. Insulin increases and activates lipolysis B. Glucagon increases and increases lipolysis C. With long term fasting or exercise, epinephrine increases and activates lipolysis D. With long term fasting or exercise, cortisol increases and activates lipolysis
Answer: A. Insulin increases and activates lipolysis. 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?
Select the statement that is not true. As a person in a resting state (no exercise) enters a fast after a mixed meal A. Most tissues switch from using mostly fatty acids as fuel to using mostly glucose as fuel B. The decrease in insulin inhibits the production of malonyl CoA and this activates CPT1 so more fatty acids can enter the mitochondria C. The decrease in insulin/glucagon increases blood free fatty acids D. The increased utilization of fatty acids causes inhibition of pyruvate dehydrogenase and hexokinase E. Exercise would increase both the use of blood fatty acids and blood glucose for energy production
Answer: A. Most tissues switch from using mostly fatty acids as fuel to using mostly glucose as fuel. 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?
Concerning the fatty acid synthase complex, all of the following are true EXCEPT A. Products include NADP+ and CoA B. Products include stearate (C18:0) and CO2 C. Substrates include acetyl CoA D. Substrates include malonyl CoA E. Substrates include NADPH
Answer: B. Products include stearate (C18:0) and CO2. Chapter 33, Objective 3: What are the substrates and products of the fatty acid synthase complex?
In the normal oxidation of an odd chain fatty acid, all of the following would be part of the process EXCEPT A. Each odd chain fatty acyl CoA will produce one propionyl CoA B. Propionyl CoA enters the mitochondria using the Carnitine: palmitoyltransferase I system C. Propionyl CoA is converted to methylmalonyl CoA D. Methylmalonyl CoA is converted to succinyl CoA E. There is an increase in the number of 4 carbon intermediates in the TCA cycle
Answer: B. Propionyl CoA enters the mitochondria using the Carnitine: palmitoyltransferase I system. 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.)
When the liver converts excess glucose into fatty acids, all of the following are true EXCEPT A. Glucose is converted by glycolysis into pyruvate in the cytosol B. Pyruvate is converted to acetyl CoA by pyruvate dehydrogenase in the cytosol C. Acetyl CoA and oxaloacetate form citrate that leaves the mitochondria D. Citrate lyase converts citrate, CoA and ATP into oxaloacetate, acetyl CoA, ADP and Pi E. The acetyl CoA is converted to palmitate and the oxaloacetate is converted to pyruvate
Answer: B. Pyruvate is converted to acetyl CoA by pyruvate dehydrogenase in the cytosol. Chapter 33, Objective 1: What is the pathway for the conversion of glucose to acetyl CoA in the cytosol in preparation for fatty acid synthesis?
Colleen Lakker was born 6 weeks prematurely and suffered from respiratory distress syndrome (RDS). All of the following help to explain her problem EXCEPT A. She cannot get enough oxygen to her tissues or exhale enough CO2 B. She cannot contract her alveoli (air sacks) C. The surface tension in the fluid inside her alveoli is too great D. She has not synthesized enough surfactants E. She has not synthesized enough dipalmitoylphosphatidylcholine, phosphatidylglycerol, cholesterol, and surfactant proteins
Answer: B. She cannot contract her alveoli (air sacks). Chapter 33, Objective 19: Concerning Colleen Lakker: What was the cause of respiratory distress syndrome of this premature infant? What specific compounds are missing? Are any derivatives of phosphatidic acid?
All of the following statements are true EXCEPT. There are a number of lipases that hydrolyze groups in glycerophospholipids in the cell membrane. A lipase that released A. Arachidonate and monoacylglycerolphosphate would be phospholipase A2 B. Inositol trisphosphate and diacylglycerol would be phospholipase C C. A phosphate that was attached to the number-2 (middle) carbon atom of glycerol would be phospholipase A1 D. An acyl group was attached to the number-2 (middle) carbon atom of glycerol would be phospholipase A2 E. A phosphate that was attached to diacylglycerol would be phospholipase C
Answer: C. A phosphate that was attached to the number-2 (middle) carbon atom of glycerol would be phospholipase A1. Chapter 33, Objective 17: What are the functions of phospholipase A1, Phospholipase A2, and Phospholipase C? Which one would release arachidonic acid? Which one would release diacylglycerol and inositol trisphosphate?
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 A. Blood Β-hydroxybutyrate enters the mitochondria non-liver cells where it will be catabolized B. Beta-hydroxybutyrate is oxidized to acetoacetate by beta-hydroxybutyrate dehydrogenase, NADH is produced C. Acetoacetate is activated using the enzyme acyl CoA synthetase and ATP D. Acetoacetyl CoA + CoA yield two acetyl CoAs which usually enter the TCA cycle and produce energy E. Acetoacetate is not catabolized by the liver because the liver lacks the enzyme succinyl CoA acetoacetate CoA transferase
Answer: C. Acetoacetate is activated using the enzyme acyl CoA synthetase and ATP. 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?
Your patient suffers from medium chain acyl CoA (MCAD) deficiency. Compared to a normal person, you would expect all of the following EXCEPT A. An increase in the rate at which liver glycogen stores are depleted and decrease time of onset of hypoglycemia following a mixed meal B. An increase in blood glucose utilization in the fasting state because the cells cannot get enough energy form Β-oxidation C. An increase in ketone body synthesis because of inhibition of the TCA cycle D. A decrease in gluconeogenesis in the liver because gluconeogenesis depends upon energy supplied by Β-oxidation E. Symptoms to appear anytime the patient does not eat regularly
Answer: C. An increase in ketone body synthesis because of inhibition of the TCA cycle. 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.
Five hours following a mixed meal, your patient begins vigorous exercise. All of the following would occur in striated muscle cells EXCEPT A. The AMP concentration would rise dramatically B. Increased AMP-Protein Kinase would inhibit acetyl CoA carboxylase C. Increased Malonyl CoA would inhibit Carnitine palmitoyl transferase D. More fatty acids would be used for energy E. More glucose would be used for energy
Answer: C. Increased Malonyl CoA would inhibit Carnitine palmitoyl transferase. 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?
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 A. Increased ADP concentration B. Increased ATP synthase activity as a result of increased ADP concentration C. Increased pumping of protons into the mitochondria by the electron transport chain D. Increased NADH and FADH2 utilization by the electron transport chain E. Increased NAD+ and FAD available as substrates for Β-oxidation
Answer: C. Increased pumping of protons into the mitochondria by the electron transport chain. 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.
Starting with an intermediate in glycolysis and acyl CoA, all of the following are intermediates in the synthesis of triacylglycerols EXCEPT A. Glycerol-3-phosphate B. Monoacylglycerol phosphate C. Monoacylglycerol D. Diacylglycerol phosphate E. Diacylglycerol
Answer: C. Monoacylglycerol. Chapter 33, Objective 9: Starting with an intermediate in glycolysis and acyl CoA, be able to name the intermediates in the synthesis of triacylglycerols in liver and adipose tissue.
When the liver converts excess glucose into fatty acids, all of the following are true EXCEPT A. The control enzyme is acetyl CoA carboxylase B. The enzyme is activated by protein phosphatase C. Protein phosphatase is activated as a result of glucagon binding to liver cells D. The control enzyme converts ATP, CO2, and acetyl CoA into malonyl CoA, ADP, and Pi E. The concentrations of glucagon, epinephrine, or AMP are low because high concentrations would inhibit the control enzyme
Answer: C. Protein phosphatase is activated as a result of glucagon binding to liver cells. Chapter 33, Objective 2: Be able to write the equation for the control step in fatty acid synthesis. What is the name of the enzyme and how is this enzyme step controlled?
In the synthesis of membrane lipids, what is the function of SAM? A. To add phosphate groups to phosphatidylinositol B. To convert phosphatidylethanolamine into phosphatidylserine C. To convert phosphatidylethanolamine into phosphatidylcholine D. To convert phosphatidylcholine into phosphatidylinositol E. To convert phosphatidylserine into phosphatidylethanolamine
Answer: C. To convert phosphatidylethanolamine into phosphatidylcholine. Chapter 33, Objective 16: In the synthesis of membrane lipids, what is the function of SAM?
All of the following about the fatty acyl CoA synthetase reaction are true EXCEPT A. Almost all free fatty acids use this reaction to become activated B. ATP is a substrate C. Free fatty acids are substrates D. ADP is a product E. Fatty acyl CoA is a product
Answer: D. ADP is a product. Chapter 23 , Objective 4: What are the reactants and products of the fatty acyl CoA synthetase reaction?
Concerning the pathway for ketone body synthesis, all of the following make sense EXCEPT A. Three acetyl CoA molecules can become 3-hydroxy-3-methyl glutaryl CoA (HMG CoA) B. HMG CoA is used for cholesterol and ketone body synthesis C. HMG CoA lyase produces acetoacetate and acetyl CoA D. Acetoacetate is oxidized to beta-hydroxybutyrate and acetone E. The rate of ketone body production is proportional to the excess acetyl CoA in the liver mitochondria
Answer: D. Acetoacetate is oxidized to beta-hydroxybutyrate and acetone. 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?
Otto Shape begins a 20-mile run. All of the following are true EXCEPT A. The uptake of blood glucose by muscle will increase within a minute and blood glucose will be lowered B. Low blood glucose and increased blood epinephrine and norepinephrine will both decrease insulin release C. Decreased insulin release will increase glucagon release D. Blood cortisol, which must be synthesized before it is released, will start to increase within seconds E. Cortisol, glucagon, epinephrine and norepinephrine will all cause increased release of free fatty acids from adipose tissue
Answer: D. Blood cortisol, which must be synthesized before it is released, will start to increase within seconds. 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?
All of the following statements are true about free fatty acids released from adipose tissue EXCEPT A. Fatty acids are hydrophobic B. Fatty acids are not soluble in blood, the cytosol, or any other water solution C. Fatty acids are transported in the blood by albumin D. Fatty acids bind to a hydrophilic binding pocket of albumin E. Fatty acids are transported in the cytosol bound to proteins
Answer: D. Fatty acids bind to a hydrophilic binding pocket of albumin. Chapter 23 , Objective 2: How are free fatty acids transported from adipose tissue to muscle or liver cells?
Your patient has type-1 diabetes. If she missed her regular inulin injection, you would expect all of the following EXCEPT A. A low insulin would contribute to the low activity of acetyl CoA carboxylase B. A high epinephrine would contribute to the low activity of acetyl CoA carboxylase in muscle cells C. A high glucagon would contribute to the low activity of acetyl CoA carboxylase in liver cells D. High malonyl CoA would increase the influx of acyl carnitine into the mitochondria E. High acetyl CoA would increase the production of ketone bodies in the liver
Answer: D. High malonyl CoA would increase the influx of acyl carnitine into the mitochondria. 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?
All of the following stimulate the storage of triacylglycerol in adipose tissue following a high carbohydrate meal EXCEPT A. A high insulin/glucagon ratio B. The activation of lipoprotein lipase C. Increased concentration of Glut4 transporters in the membrane D. Inhibition of glycolysis E. Increased synthesis of glycerol phosphate by glycerol-3-phosphate dehydrogenase
Answer: D. Inhibition of glycolysis. Chapter 33, Objective 11: How does the insulin/glucagon ratio stimulate the storage of triacylglycerol in adipose tissue following a high carbohydrate meal?
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? A. Less inhibition of Pyruvate dehydrogenase by acetyl CoA B. More pyruvate converted to acetyl CoA C. More glucose converted into pyruvate D. More inhibition of Phosphofructokinase-1 by ATP E. Less production of ATP and NADH via B-oxidation
Answer: D. More inhibition of Phosphofructokinase-1 by ATP E. Less production of ATP and NADH via B-oxidation. 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.
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 A. In the cytosol, the acyl group is transferred to carnitine by the enzyme carnitine palmitoyltransferase I B. Acylcarnitine enters the mitochondrion using carnitine acylcarnitine translocase C. In the mitochondrion, the acyl group is transferred to CoA by the enzyme carnitine palmitoyltransferase II D. The free CoA generated in the mitochondria travels back to the cytosol using carnitine acylcarnitine translocase E. The product of the carnitine palmitoyltransferase II reaction is oxidized by Β-oxidation
Answer: D. The free CoA generated in the mitochondria travels back to the cytosol using carnitine acylcarnitine translocase. 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.
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 A. The more muscles contract, the higher the concentration of ADP and AMP B. AMP-dependent protein kinase causes the phosphorylation of acetyl CoA carboxylase C. Phosphorylation of acetyl CoA carboxylase inhibits the production of malonyl CoA D. The malonyl CoA concentration drops and inhibition of carnitine: palmitoyltransferase II is removed E. Much more acyl carnitine is available to use the carnitine-acylcarnitine translocase
Answer: D. The malonyl CoA concentration drops and inhibition of carnitine: palmitoyltransferase II is removed. 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
All of the following help to explain the increased production of ketone bodies as a person enters a fast EXCEPT A. The insulin/glucagon ratio drops and release of free fatty acid from adipose tissue increases B. Decreased insulin results in phosphorylation of acetyl CoA carboxylase and decreased malonyl CoA C. Increased fatty acyl CoA enters the liver mitochondria because CPT I is not inhibited D. Β-oxidation produces too much NADH and FADH2 so Β-oxidation is inhibited E. More Acetyl CoA is produced than is needed by the TCA cycle so the excess it used to make ketone bodies
Answer: D. Β-oxidation produces too much NADH and FADH2 so Β-oxidation is inhibited. Chapter 23 , Objective 15: How can a decrease in the insulin/glucagon ratio explain the increased production of ketone bodies during a fast?
When the concentration of epinephrine or glucagon is high, they bind to receptors on adipose cell membrane and all of the following can be expected to occur EXCEPT A. Hormone-Receptor-Gαβγ-GDP + GTP = Hormone-Receptor + GDP + Gβγ +Gα-GTP B. Gα-GTP + Adenylate cyclase = Gα-GTP-Adenylate cyclase C. ATP = cAMP + PPi D. cAMP + PKARRCC = 2 cAMP-R + 2 PKA E. ATP + Lipoprotein Lipase (inactive) = Lipoprotein Lipase-Pi (active) + ADP
Answer: E. ATP + Lipoprotein Lipase (inactive) = Lipoprotein Lipase-Pi (active) + ADP. Chapter 33, Objective 12: Be able to list the sequence of events from the time epinephrine binds a receptor on the surface of an adipose cell until acetyl CoA is made in muscle or liver. Don't forget the key enzyme that controls the process.
Phosphatidic acid is an intermediate in both the synthesis of triacylglycerol and glycerophospholipids (membrane lipids). To convert phosphatidic acid to phosphatidyl choline, you would remove the phosphate and react diacylglycerol with A. ADP-choline B. UDP-choline C. TDP-choline D. GDP-choline E. CDP choline
Answer: E. CDP choline. Chapter 33, Objective 14: By this time, you know how to make phosphatidic acid from glucose. How would you make phosphatidylcholine from phosphocholine (head group) and phosphatidic acid?
All of the following are glycerophospholipids that are typically found in the cell membrane EXCEPT A. Phosphatidylcholine (lecithin) B. Phosphatidylethanolamine C. Phosphatidylserine D. Phosphatidylinositol E. Diphosphatidylglycerol (cardiolipin)
Answer: E. Diphosphatidylglycerol (cardiolipin). Chapter 33, Objective 13: Be able to name 4 glycerophospholipids found in cell membranes.
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 A. During a fast because of increased glucagon B. During starvation because of increased glucagon, epinephrine and cortisol C. During exercise because of increased epinephrine D. During stress because of increased glucagon, epinephrine and cortisol E. During a regular meal because of the increased insulin/glucagon ratio
Answer: E. During a regular meal because of the increased insulin/glucagon ratio. Chapter 23 , Objective 12: What is the effect of insulin, glucagon, or epinephrine upon lipolysis in adipose tissue?
Where does the desaturation of fatty acids take place in humans? A. Cytosol B. Nucleus C. Mitochondria D. VLDL E. Endoplasmic reticulum
Answer: E. Endoplasmic reticulum. Chapter 33, Objective 7: Where does the desaturation of fatty acids take place in humans?
There are several factors that regulate the rate of Β-oxidation. All of the following make sense EXCEPT A. In the fed state, insulin inhibits the release of free fatty acids from adipose tissue and therefor limits substrate for Β-oxidation B. In the fed state, insulin will cause dephosphorylation and activation of acetyl CoA carboxylase that produces malonyl CoA, an inhibitor of CPT1 C. If the ATP/ADP ratio is low, AMP dependent protein kinase will phosphorylate and inactivate acetyl CoA carboxylase D. In the fasting state, the low insulin/glucagon ratio will result in the disappearance of malonyl CoA and activation of CPT1 E. If the ATP/ADP ratio is low, then high concentrations of FADH2 and NADH will inhibit Β-oxidation
Answer: E. If the ATP/ADP ratio is low, then high concentrations of FADH2 and NADH will inhibit Β-oxidation. Chapter 23 , Objective 9: What are the major factors that control the synthesis of acetyl-CoA by Β-oxidation muscle and/or liver?
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 A. Active in the fed state because insulin activates phosphatases that dephosphorylate the enzyme B. Inactive in the fasting state because Protein kinase A phosphorylates and inactivates the enzyme C. Inactive if the fasting state if epinephrine has activated the cAMP cascade D. Inactive if cellular concentrations of AMP are high because AMP-activated protein kinase will phosphorylate and inactivate the enzyme E. Inactive if cellular concentrations of citrate are high because citrate is an allosteric inhibitor of the enzyme
Answer: E. Inactive if cellular concentrations of citrate are high because citrate is an allosteric inhibitor of the enzyme. Chapter 23, Objectives 9:What are the major factors that control the synthesis of acetyl-CoA by B-oxidation muscle and/or liver?
Your patient suffers from type-1 diabetes. If she missed her regular insulin injection, you would expect all of the following EXCEPT A. Decreased insulin and increased stress hormones (glucagon, epinephrine, norepinephrine, cortisol, and others) B. Increased mobilization of fatty acids from adipose tissue and increased entrance of fatty acids into all cells of the body except brain C. Low insulin and high glucagon to both result in the inhibition of acetyl CoA carboxylase and decreased concentrations of malonyl CoA D. Low malonyl CoA would result in faster entrance of acyl CoA into the mitochondria, more Β-oxidation, and more acetyl CoA E. Increased ketone body synthesis will result in an increase in blood pH
Answer: E. Increased ketone body synthesis will result in an increase in blood pH. 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?
When the concentration of epinephrine or glucagon is high, they bind to receptors on adipose cell membrane and all of the following can be expected to occur EXCEPT A. The cAMP cascade activates hormone sensitive lipase B. Triacylglycerol is hydrolyzed to free fatty acids and glycerol C. Free fatty acids are carried to most tissues of the body by albumin D. Fatty acids are activated, enter the mitochondria, and are oxidized by beta-oxidation and the TCA cycle E. Increased Β-oxidation increases glycolysis in resting muscle
Answer: E. Increased Β-oxidation increases glycolysis in resting muscle. Chapter 33, Objective 12: Be able to list the sequence of events from the time epinephrine binds a receptor on the surface of an adipose cell until acetyl CoA is made in muscle or liver. Don't forget the key enzyme that controls the process.
During starvation, when the brain uses more ketone bodies, all of the following are true EXCEPT A. Total energy usage by the brain is about the same as the fed state B. Ketone bodies supply much more energy than they normally do C. Less glucose needs to be used to maintain normal levels of ATP D. Less glucose is removed from blood by brain cells E. Less gluconeogenesis occurs in muscle cells
Answer: E. Less gluconeogenesis occurs in muscle cells. 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.
Compared to a 24 hour fast, all of the following would be true for after five days of starvation EXCEPT A. Brain cells use less glucose and more ketone bodies to synthesize ATP B. The brain takes up less Glucose C. Less glucose is made in the liver to maintain blood glucose levels D. Less amino acids are used for gluconeogenesis E. More protein is catabolized to supply substrate for gluconeogenesis
Answer: E. More protein is catabolized to supply substrate for gluconeogenesis. 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
Colleen Lakker was born 6 weeks prematurely and suffers from respiratory distress syndrome (RDS). An arterial blood sample revealed a low partial pressure of oxygen (pO2) and a slightly elevated partial pressure of carbon dioxide (pCO2). Her arterial pH was low. All of the following help to explain her condition EXCEPT A. Her hypoxia is inhibiting the cytochrome oxidase reaction in the electron transport chain B. The ATP to ADP ratio of most cells in her body will be low C. The TCA cycle and pyruvate dehydrogenase will be inhibited D. Phosphofructosekinase-1 and anaerobic glycolysis will be activated and produce lactic acid E. Respiratory alkalosis has somewhat compensated for the lactic acidosis
Answer: E. Respiratory alkalosis has somewhat compensated for the lactic acidosis. Chapter 33, Objectives 20: Concerning Colleen Lakker who suffers from respiratory distress syndrome: Explain her lactic acidosis using what you have learned in previous chapters. Use the terms cytochrome oxidase, electron transport chain, NADH, Acetyl CoA, pyruvate dehydrogenase, ATP level, phosphofructokinase, anaerobic glycolysis, and lactate in your answer.
All of the following would be expected during an extended fast (starvation) EXCEPT A. After about a day, blood glucose levels would remain constant at the low end of the normal range B. Blood ketone bodies would rise to very high concentrations over the first 20 days C. Blood fatty acids would rise during the first 3 days and very little after that time D. The use of blood ketone bodies by the brain would spare the use of blood glucose E. The catabolism of muscle protein to produce glucose would increase every day
Answer: E. The catabolism of muscle protein to produce glucose would increase every day. 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.
All of the following statements about Β-oxidation are true EXCEPT A. The pathway helps to generate energy and acetyl CoA from fatty acyl CoA B. The pathway produces NADH and FADH2 as products C. The pathway is found in all tissues that contain mitochondria D. 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 E. The pathway is reversible
Answer: E. The pathway is reversible. 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
The fatty acids produced by the fatty acid synthase complex are not substrates for beta-oxidation because A. They are immediately activated to palmitoyl CoA B. Acetyl CoA, one substrate for the fatty acid synthase complex, inhibits carnitine: palmitoyltransferase-2 C. High NADPH, a requirement for fatty acid synthesis, inhibits beta-oxidation D. High glucagon causes phosphorylation of acetyl CoA carboxylase whenever fatty acid synthase is active E. The product of the control step for fatty acid synthesis also inhibits carnitine: palmitoyltransferase-1
Answer: E. The product of the control step for fatty acid synthesis also inhibits carnitine: palmitoyltransferase-1. Chapter 33, Objective 5: What prevents the fatty acids made by fatty acid synthesis from undergoing B-oxidation?
The major pathway used to oxidize free fatty acids in humans is called A. The ketone body catabolic pathway B. The phosphatidic acid catabolic pathway C. Lipolysis D. The carnitine:palmitoyl transferase I and II pathway E. Β-oxidation
Answer: E. Β-oxidation. Chapter 23 , Objective 3: Name the major pathway used to oxidize fatty acids into acetyl CoA.
