Download 2007 Exam 3 1. The goal of the oxidative phase of the pentose

2007 Exam 3
1. The goal of the oxidative phase of the pentose phosphate pathway is to
a. produce NADPH for use in anabolic pathways.
b. regenerate NADP+ for use in catabolic pathways.
c. generate glucose for use in glycolysis.
d. make a variety of sugar products and intermediates for use in other pathways.
3. A medical student studied so hard for his / her biochemistry exam that he / she did not eat for one
whole day before the exam. What was the primary fuel source used for the student’s red blood cells
as he/she walked to the medical school to take the exam?
a. glucose
b. fatty acids
c. amino acids
d. cholesterol
e. pyruvate
5. In the presence of a mitochondrial uncoupler, which of the following is true?
a. The electron transport chain is activated.
b. ATP synthesis is inhibited.
c. Heat is generated.
d. All the above are true.
7. During times of fasting when the liver is producing glucose for the blood, this glucose does not
enter glycolysis in the liver cell because
a. it is phosphorylated and therefore can’t remain in the liver cell.
b. once it is released into the blood the glucose is used by another tissue before it comes back to the
liver.
c. liver hexokinase has a very low affinity for glucose, so the glucose does not get phosphorylated to
remain in the cell.
d. liver glucokinase has a very low affinity for glucose, so the glucose does not get phosphorylated to
remain in the cell.
8. Which one of the following statements is NOT true for nitric oxide (NO)?
a. NO is liberated in the conversion of L-arginine to citrulline.
b. The enzyme nitric oxide synthase (NOS) is a complex enzyme found in three major isoforms.
c. The inducible form of NOS (iNOS) is important in macrophages for generating NO for the
bactericidal activity.
d. The three forms of NOS are located in endothelial cells, neuronal cells and macrophages.
e. NO stimulated the influx of Ca2+ into vascular endothelial cells resulting constriction of vascular
smooth muscle.
10. A pregnant woman who is lactose intolerant can still produce lactose for her breast milk because
a. she doesn’t need to consume lactose to make lactose in her mammary glands.
b. her body can produce lactose using glucose alone as a starting material.
c. lactose is made in the mammary gland, whereas lactose intolerance is a digestion and absorption
problem.
d. all of the above.
11. Humans cannot convert acetyl CoA from even-chain fatty acid oxidation to glucose. However,
oxidation of odd-chain fatty acids can lead to glucose formation because
a. they produce one mole of propionyl CoA per mole of fatty acid oxidized.
b. their acetyl CoA can be converted directly to pyruvate.
c. gluconeogenesis occurs simultaneously with fatty acid oxidation.
d. the brain can utilize odd-chain fatty acids to make its own supply of glucose.
12. The primary agent of energy transduction in metabolic pathways is
a. the acetyl group
b. the electron
c. glucose
d. pyruvate
Questions 13 – 16 refer to the graphs depicted below, which correspond to four individual patients
(patient A, patient B, etc). The graphs show the source of the primary fuel used by that patient’s brain
while fasting over the time course shown. The differences in the four graphs are due to specific
enzyme deficiencies that three of the patients have compared to one patient that has a more normal
profile. Use these graphs to answer the following questions below. Any letter can be used more than
once, if necessary.
13. Which patient most likely has a liver phosphorylase deficiency?
14. Which patient most likely has a liver fructose 1,6-bisphosphatase deficiency?
15. Which patient exhibits the most normal profile for brain fuel utilization?
16. Which patient most likely has an HMG-CoA synthetase deficiency?
17. It is said that hexokinase commits glucose to the cell because
a. ATP is utilized during this reaction.
b. once formed, the product glucose 1-phosphate cannot leave the cell.
c. once formed, the product glucose 6-phosphate cannot leave the cell.
d. the eventual product of glycolysis, phosphoenolpyruvate, has such a high energy the cell must use
this molecule or risk losing the stored energy.
18. Which one of the following statements regarding Reactive Oxygen Species (ROS) is NOT correct?
a. Cellular defenses against ROS include both large molecular enzymes and some small molecular
weight vitamins
b. The macromolecular antioxidants are superoxide dismutase, catalase and glutathione peroxidase
c. ROS are the cause of many diseases processes
d. Oxidative stress occurs when the rate at which the ROS are removed by antioxidants exceeds the
capacity of the cell to generate ROS.
e. ROS include superoxide radicals, hydrogen peroxide and hydroxyl radicals
20. For the energy charge of a cell, the actual [ATP] is considered to be the sum of [ATP] + ½ [ADP]
because
a. ADP has a high energy phosphate bond that can be used in place of ATP if necessary.
b. ADP has only half the free energy of ATP.
c. half of the cellular pool of ADP is converted to ATP by the ATP synthase.
d. half of the cellular pool of ADP is converted to ATP by adenylate kinase.
e. half of the cellular pool of ADP is converted to ATP by pyruvate kinase.
21. A palmitate molecule has entered fatty acid oxidation. How many rounds of β-oxidation are
required to completely oxidize this molecule to 8 molecules of acetyl CoA?
a. 6
b. 7
c. 8
d. 9
22. Which of the following statements is TRUE concerning Cytochrome P450?
a. It is a component of mitochondrial electron transport chain
b. It is involved in the process of hydroxylation of drugs
c. As an oxidase, molecular oxygen is a substrate of P450
d. A single Cytochrome P450 can metabolize variety of drugs and lipids
e. Reduction-oxidation of P450 is coupled to the pumping out of protons
23. One week after an episode of bronchitis, a 7-year-old girl with insulin-dependent diabetes
mellitus (i.e., a deficiency of insulin) is brought to the emergency room in a coma. Her breathing is
rapid and deep, and her breath has a fruity odor. Her blood glucose is 37 mM (normal: 4-6 mM). The
physician administers IV fluids that includes insulin among other things. One effect of insulin in this
situation would most likely be to stimulate
a. gluconeogenesis in the liver.
b. fatty acid release from adipose.
c. ketone body utilization in the brain.
d. glucose transport into muscle.
24. You and your study partners are having an argument about the ATP synthase. Which one of you is
correct?
a. You say ATP synthesis by the ATP synthase represents substrate-level phosphorylation, because
molecular oxygen is not directly involved in the reaction.
b. Partner 1 says ATP synthesis by the ATP synthase is not substrate-level phosphorylation because a
higher energy phosphate molecule was not used to form the ATP.
c. Partner 2 says this ATP synthesis is not substrate level phosphorylation because molecular oxygen
consumption is absolutely required for the ATP synthesis to operate.
d. None of you are correct this time.
26. During fasting, ATP levels are generally high due to the large amount of acetyl CoA produced by
fatty acid oxidation. Ignoring insulin and glucagon considerations, high ATP helps to restrict catabolic
activity by inhibiting
a. glycolysis.
b. the fatty acid oxidation.
c. the TCA cycle.
d. all the above.
27. Propionyl CoA is
a. a three carbon fatty acyl CoA that is produced during oxidation of fatty acids with an odd number
of carbons.
b. metabolite that can enter the glycolytic pathway and produce PEP for glucose synthesis.
c. is the reduced form of acetyl CoA that is produced during oxidation of fatty acids with an odd
number of carbons.
d. a reduced intermediate of the TCA cycle that is formed during when NADH levels are very high.
28. Cells utilize high energy biomolecules because
a. they are easily made and store energy for later use.
b. they are formed by substrate-level phosphorylation, so the cell does not need oxygen to synthesize
them.
c. they provide the necessary free energy required to drive energetically unfavorable reactions.
d. they possess chemical groups not found in enzyme active sites, allowing the enzyme to carry out
complex chemical reactions.
29. A 3 year old boy has ingested a toxin that completely inhibits the bifunctional enzyme in his cells.
What will be the most likely effect of this toxin on glycolysis in his cells?
a. No effect.
b. A futile cycle will develop whereby fructose 1,6-bisphosphate produced by PFK-1 will be
dephosphorylated to fructose 6-phosphate.
c. Glycolysis will run more quickly due to allosteric inhibition of fructose-2,6 bisphosphate.
d. Glycolysis will stop completely due to the loss of the bifunctional enzyme.
Questions 31 – 35 are based on the following scenario. A 4 year old girl has become lethargic and has
a swollen abdomen, and she has not eaten for over two days. The parents take her to the emergency
room. Physical examination shows the girl has massive hepatomegaly (enlarged liver) and enlarged
kidneys with normal spleen and heart. Laboratory studies show she has extremely low blood sugar
(hypoglycemia). Biopsy of liver and muscle shows excess glycogen is present in the liver but
essentially no glycogen is present in muscle. A glycogen-related disease is suspected, but further tests
reveal that the glycogen phosphorylase and phosphoglucomutase enzymes are functional in the
patient.
31. Why would a glycogen-related disease be suspected?
a. When blood sugar is low, glucagon is high and glycogen breakdown should be activated, but
glycogen levels in the liver are above normal.
b. Despite the low blood sugar, insulin is high which should activate glycogen synthesis in the muscle,
but muscle glycogen is depleted.
c. Liver glycogen levels are higher than normal, suggesting no glucose is going toward glycogen
synthesis but rather is directed into glycolysis for cellular energy needs.
d. Muscle glycogen levels are lower than normal, suggesting that muscle glucose should be directed
to replenishing the glycogen store, but it is apparently is not working.
32. Based on the fact that the patient’s blood sugar is low, why does it make sense that muscle
glycogen would be depleted?
a. It doesn’t make sense – if glycogen is abnormal, it should be abnormal to the same extent in muscle
and liver.
b. Due to the low blood glucose level, muscle glycogen was used to produce free glucose units that
were released into the blood for use by other tissues.
c. The patient must have exercised prior to his examination by the pediatrician, which depleted the
muscle glycogen stores.
d. Due to the low blood glucose level, muscle was getting no glucose to use as energy. It used its own
supply of glycogen to help meet its energy needs until it was all gone.
33. If glycogenolysis is not able to produce glucose for the body, what would be the primary source of
blood glucose for this patient?
a. glycolysis.
b. gluconeogenesis
c. muscle glycogen breakdown.
d. acetyl CoA from fatty acid oxidation.
34. A defect in which enzyme could explain the liver’s inability to supply glucose to the blood?
a. glucose-6-phosphate dehydrogenase
b. phosphofructokinase-1
c. glycogen phosphorylase
d. glucose-6-phosphatase
35. If this patient is given an IV treatment containing glucose sufficient to raise her blood glucose
level to around 200 mg/dL, which of the following most likely happen?
a. Her pancreas will release insulin.
b. Her muscles will import glucose and regenerate their glycogen stores.
c. Her brain will take up the glucose and use it as the primary energy source.
d. All of the above are true.
36. Which one of the following reactions can generate deadly hydroxyl radicals (OH.)?
a. Fenton’s reaction
b. superoxide dismutation reaction
c. hydroxylation of H2O2
d. glutathione dependent peroxidation
e. Pauli’s exclusion reaction
37. What does it mean that the reactions malate to oxaloacetate and NAD+ to NADH are coupled
reactions for malate dehydrogenase?
a. That the energy required by the malate to oxaloacetate reaction can be obtained from the electron
transport chain via NADH.
b. That the NAD+ produced in another TCA cycle reaction can be used in this step.
c. That the protons liberated in this step can be used to drive ATP synthesis by the ATP synthase.
d. That the two reactions occur simultaneously within the active site of the enzyme and one reaction
will not happen unless the other reaction also occurs.
38. A 50 year old man in his second post-operative day after an appendectomy has not eaten since
the day of his surgery. Which of the following enzymes is most likely in an inactive state?
a. glycogen phosphorylase
b. glycogen phosphorylase kinase
c. glycogen synthase
d. phosphoenolpyruvate carboxykinase
39. Which of the following characterizes the first phase of glycolysis?
a. 2 ATP molecules s are used, 2 molecules of pyruvate are produced, fructose-1,6-bisphosphate is an
intermediate
b. 2 ATP molecules are produced, 2 molecules of lactate are produced, and 2 molecules of NADH are
produced
c. 1 molecule of glucose is converted to 2 molecules of pyruvate
d. 2 molecules of glyceraldehyde-3-phosphate are converted to 2 molecules of 1,3bisphosphoglycerate and 2 molecules of NADH are produced
e. none of the above are correct.
40. Atractyloside is a toxic glycoside from a Mediterranean thistle that inhibits the mitochondrial
ATP/ADP translocase. Which of the following metabolic pathways will be inhibited (directly or
indirectly) in cells exposed to atractyloside?
a. electron transport chain.
b. TCA cycle
c. Glycolysis
d. Fatty acid oxidation
e. All these pathways will be inhibited
42. Fructose is metabolized using many of the same enzymes involved in glucose metabolism. Why
doesn’t fructose stimulate an insulin response?
a. It is glucose-6-phosphate that stimulates pancreatic β-cells to release insulin.
b. Blood fructose concentrations are never high enough to stimulate glucokinase to convert fructose
to glucose 6-phosphate.
c. Fructose is imported into cells using the GLUT5 transporter.
d. Aldolase B isn’t present in pancreas cells, which prevents fructose from being phosphorylated,
which prevents stimulation of an insulin response.
43. A patient has a defect in her carnitine palmitoyl transferase 1 (CPT-1) enzyme, making it inactive.
Because of this
a. the patient can oxidize fatty acids, but only in the cytosol.
b. oxidized fatty acids cannot be transported out of the mitochondria.
c. newly synthesized fatty acids may be immediately oxidized in the patient’s mitochondria.
d. the patient will most likely have a markedly elevated level of fatty acids in her blood.
44. Which one of the following enzymes catalyzes the conversion of hydrogen peroxide to water?
a. Superoxide dismutase
b. Dioxygenase
c. Catalase
d. Cytochrome P450
e. Oxidoperoxidase
45. The oxidative decarboxylation of pyruvate to acetyl-CoA is catalyzed by
a. pyruvate carboxylase.
b. pyruvate decarboxylase.
c. pyruvate dehydrogenase complex.
d. acetyl CoA synthetase.
46. A patient fasted for approximately 18 hours, then consumed a protein-only meal. What effect
would this meal have on gluconeogenesis in the patient’s liver?
a. Gluconeogenesis would stop since the patient consumed a meal.
b. The dietary amino acids would be used as a starting material for gluconeogenesis instead of amino
acids donated from muscle.
c. The patient could supply glucose to the liver from glycogen instead of gluconeogenesis.
d. All the above are true.
47. Ketone bodies are utilized by the brain when
a. a person has been fasting between 4 and 12 hours.
b. the level of ketone bodies in the blood gets sufficiently high.
c. acetyl CoA levels start to decline during a fast.
d. a person consumes more fat than carbohydrate.
49. Muscle cells do not respond to glucagon. Which metabolic signal(s) stimulate(s) glycogen
breakdown in muscle?
a. epinephrine
b. AMP
c. Ca2+
d. All of the above are stimulatory.
50. The enzyme that commits glucose to glycolysis is ___________ whereas the enzyme that commits
glucose to the pentose phosphate pathways is ___________.
a. hexokinase, glucose-6 phosphatase.
b. glucokinase, glucose-6 phosphate dehydrogenase.
c. phosphofructokinase-1, glucose-6 phosphate dehydrogenase.
d. aldolase B, glucose-6 phosphate dehydrogenase.
51. Pyruvate carboxylase attaches a CO2 group onto pyruvate to make oxaloacetate. For this to
happen, one molecule of ATP must be split to ADP + Pi simultaneously. Knowing this, which
statement is TRUE regarding the conversion of pyruvate à oxaloacetate?
a. It is a substrate-level phosphorylation reaction.
b. Pyruvate carboxylase is a kinase.
c. ΔGo′ is positive for the reaction.
d. ΔGo′ is negative for the reaction.
55. Which one of the following endogenous small molecules (antioxidants) can NOT protect the body
against ROS attack?
a. Uric acid
b. Vitamin B12
c. HDL
d. Melatonin
e. Glutathione (GSH)
63. Which enzyme of the TCA cycle is an integral membrane protein?
a. succinyl-CoA synthetase
b. succinate dehydrogenase
c. fumarase
d. malate dehydrogenase
65. Which of the following statements is TRUE about Reactive Oxygen Species (ROS)?
a. Reduction of oxygen by a single electrons is not subject to the kinetic barrier imposed by spin
restriction.
b. ROS can not damage DNA and intracellular proteins as these macromolecules are protected by
plasma membrane
c. Over 90% of oxygen consumed by the body is converted to free radicals by mitochondrial electron
transport chain.
d. The Fenton reaction and the Haber-Weiss reaction generate the deadly ROS, the singlet oxygen.
e. Mitochondrial DNA is not sensitive to ROS attack
Questions 66 – 70 refer to the following scenario. While working on her furnace, a 24 year old female
is exposed to a high level of carbon monoxide. Within minutes she becomes listless and confused.
Knowing something is wrong, she tries to move out the room to get some fresh air, but she collapses
and becomes unconscious. She is not found for over an hour. She is taken to the hospital emergency
room and aggressive treatment is started. Sadly, she dies shortly after reaching the hospital. The
autopsy shows that the carbon monoxide completely saturated her tissues.
66. The lethal effect of carbon monoxide for this patient most likely was
a. inhibition of Complex I of the electron transport chain.
b. inhibition of Complex II of the electron transport chain.
c. inhibition of Complex III of the electron transport chain.
d. inhibition of Complex IV of the electron transport chain.
67. Due to the carbon monoxide poisoning, how would the patient’s oxygen consumption most likely
change?
a. There would be no change in oxygen consumption.
b. She would consume more oxygen.
c. She would consume less oxygen.
68. At the time of her death, which of the following electron transport chain components would most
likely be in an oxidized state for the patient?
a. Complex I
b. Complex II
c. Complex III
d. None of these components would be in an oxidized state
69. As the patient’s time of death drew near, was it likely possible for her to generate ATP by
oxidative phosphorylation?
a. Yes: even though Complex I was inhibited, electrons could enter the electron transport chain via
Complex II.
b. Yes: even though Complex II was inhibited, electrons could enter electron transport chain via
Complex I.
c. Yes: even though Complex IV is inhibited, electrons can still enter the electron transport chain
through “other” flavoproteins.
d. No: regardless of how electrons could enter the electron transport chain, electrons could not move
through the chain to molecular oxygen.
70. As the patient’s time of death drew near, which of the following would likely be true?
a. Anaerobic glycolysis would be the only source of ATP production for her brain (assume blood
glucose is available).
b. Anaerobic fatty acid oxidation would be a major source of ATP production for her muscles.
c. The TCA cycle in her cells would be strongly inhibited.
d. All the above would be true.
71. The figure below depicts the conversion of fructose 6-phosphate to fructose 1,6-bisphosphate by
the enzyme phosphofructokinase 1 during glycolysis, and the reconversion of fructose 1,6bisphosphate to fructose 1-phosphate by the enzyme fructose 1,6-bisphosphatase during
gluconeogenesis.
a.
b.
c.
d.
As written, this is a futile cycle that consumes ATP to make fructose 1,6-bisphosphate, only to have
fructose 1,6-bisphosphate degraded to fructose 6-phosphate right away by the phosphatase. In order
for this to be a substrate cycle that works only in one direction or the other at any given time, which
of the following statements MUST be true?
phosphofructokinase 1 and fructose 1,6-bisphosphatase are active all the time and depend only on
the presence of substrate for activation.
sugar phosphate molecules have a higher free energy than ATP, preventing the kinase from
proceeding as written.
sugar phosphate molecules have a lower free energy than ATP, allowing the kinase reaction to occur
as written.
phosphofructokinase 1 and fructose 1,6-bisphosphatase are reciprocally regulated enzymes under
hormonal control.
EXAM 5 2006
1. ATP production by glycolysis is considered anaerobic because
a. glycolysis takes place in the cytosol, whereas the electron transport chain (thus O2 consumption)
takes place in the mitochondrial matrix.
b. glycolysis will produce ATP only during times of extreme O2 deprivation.
c. ATP is formed by the pathway independent of O2.
d. O2 is required for ATP formation during key steps in the pathway.
2. A 27-year-old patient wishes to become pregnant, and hopes to breast feed her infant. She is
concerned because she has a lactase deficiency and cannot tolerate milk or dairy products in her diet.
She thinks here lactose intolerance will prevent her from producing milk of sufficient caloric value to
nourish her baby. You tell here not to worry because
a. she can produce lactose by degrading α-lactalbumin.
b. even though she can’t breast feed her baby, there are formulas available that are just as good as
breast milk.
c. she can consume pure galactose in order to produce the galactose moiety of lactose.
d. the mammary gland can produce lactose from non-dairy dietary carbohydrate.
3. Metabolism of large amounts of ethanol can inhibit fatty acid oxidation because ethanol
metabolism
a. metabolism uses NADPH.
b. produces NADH.
c. metabolism produces acetate.
d. metabolism uses acetyl CoA.
4. Which one of the following statements is NOT correct?
a. Amino acids in proteins that are particularly resistant to ROS attack include Pro, His, Arg, Cys, Met.
b. The macromolecular antioxidant enzymes are superoxide dismutase, catalase and glutathione
peroxidase.
c. Oxidative stress occurs when the antioxidants present in the cell are overwhelmed by the over
production of ROS.
d. Reperfusion injury generates excessive amounts of ROS.
e. The phagocytes (polymorphonuclear neutrophils) of Chronic Granulomatous Disease (CGD)
patients can not generate sufficient amounts of ROS for effective killing of the engulfed bacteria.
Questions 5-11 relate to the following scenario: You are evaluating a patient that has a problem with
mitochondrial energy metabolism in her muscles. Lab tests show that her muscles can make ATP by
oxidative phosphorylation, but the amount of ATP she produces in her muscles is much lower than
expected based on her metabolic rate. When questioning her, you learn that she is an avid gardener.
She tells you that it drives her crazy when insects eat her plants and ruin her vegetables. Therefore,
over the last few weeks, she has been using a pesticide powder on her plants. She does not wear any
protective clothing or a breathing mask when she sprinkles the powder on her plants, so you suspect
she has ingested some form of toxin from the pesticide. She shows you the pesticide bottle’s warning
label, and you find the pesticide contains rotenone. You tell her you now understand the problem.
5. Which protein is directly affected by the rotenone?
a. complex I
b. complex III
c. complex IV
d. ATP synthase
6. Which metabolic pathway(s) will be indirectly affected by rotenone?
a. TCA cycle
b. fatty acid oxidation
c. glycolysis
d. all of the above pathways.
7. In the presence of rotenone, electrons enter the electron transport chain
a. by NADH only.
b. by both NADH and FADH2.
c. by FADH2 only.
d. by a route independent of NADH and FADH2.
8. In the presence of rotenone, what is the maximum number of protons that can be transported out
of the mitochondrial matrix into the inter-membrane space for each 2 electrons that enter the
electron transport chain?
a. 4
b. 6
c. 10
d. 12
9. In the presence of rotenone, what is the maximum number of ATP molecules that can be
synthesized per 2 electrons that enter the electron transport chain?
a. 1
b. 1.5
c. 2
d. 2.5
10. Assume glycolysis will continue to produce ATP and NADH even in the presence of rotenone.
Under these conditions, which shuttle system will most likely transfer the electrons from cytoplasmic
NADH to the electron transport chain?
a. the malate-aspartate shuttle
b. the Cori cycle
c. the glycerol-3-phosphate shuttle
d. the pyruvate carboxylase system
11. What effect does rotenone have on the mechanism of ATP synthesis by the ATP synthase?
a. No effect: ATP synthesis proceeds as normal.
b. ATP synthesis stops because there is an insufficient H+ gradient.
c. ATP synthesis is more rapid because less electron energy is used to make the H+ gradient.
d. The binding change mechanism is replaced by an alternating sites mechanism.
12. The difference(s) between alcohol dehydrogenase (ADH) and the microsomal ethanol oxidizing
system (MEOS) is (are)
a. ADH is a cytoplasmic enzyme whereas MEOS is located in the ER membrane.
b. ADH produces acetaldehyde + NADH whereas MEOS consumes NADPH to produce acetaldehyde.
c. ADH has high affinity for ethanol whereas MEOS has low affinity for ethanol.
d. All of the above are correct differences.
13. Which one of the following enzymes can generate superoxide radicals while acting on its
substrates?
a. superoxide dismutase
b. catalase
c. glutathione peroxidase
d. glutathione reductase
e. xanthine oxidase
14. Which common dietary sugar is taken up by the liver, phosphorylated at carbon 1 by
fructokinase, split into dihydroxyacetone phosphate (which enters glycolysis) and glyceraldehyde,
which is phosphorylated to glyceraldehyde 3-phopsate (and enters glycolysis)?
a. glucose
b. galactose
c. mannose
d. fructose
15. What is the outcome of the glycolysis pathway?
a. 2 ATP, 2 NADH, 2 pyruvate
b. 4 ATP, 2 NADH, 2 pyruvate
c. 2 ATP, 4 NADH, 1 pyruvate
d. 4 ATP, 4 NADH, 1 pyruvate
16. Select the INCORRECT statement about Reactive Oxygen Species (ROS):
a. UV, X-rays and gamma-rays generate excessive amounts of ROS in human tissues.
b. ROS can damage DNA, proteins and carbohydrates but not membranes because of their high
unsaturated fat content.
c. Over 90% of oxygen consumed by the body is used for the mitochondrial electron transport chain.
d. The Fenton reaction and the Haber-Weiss reaction generate the deadly hydroxyl radical.
e. Most oxidations occur by the transfer of a single electron to O2 as a one electron reduction of
oxygen, which is not subject to the kinetic barrier imposed by spin restriction.
17. Which of the following is NOT a reversible covalent modification of glycogen phosphorylase that
regulates its activity?
a. Phosphorylation of glycogen phosphorylase by phosphorylase kinase.
b. Dephosphorylation of glycogen phosphorylase by protein phosphatase.
c. AMP binding to glycogen phosphorylase.
d. None of the above apply.
20. People who are galactose intolerant should avoid which of the following disaccharides?
a. sucrose
b. maltose
c. lactose
d. galactose
22. One of the primary outcomes of epinephrine binding to α receptors in the liver is
a. inhibition of glycogen degradation.
b. stimulation of glycogen synthesis.
c. inhibition of glycogen synthesis.
d. inhibition of glycolysis.
24. Glucose 1-phosphate is activated by UTP to facilitate glycogen synthesis because
a. UDP-glucose is more reactive than glucose 1-phosphate.
b. UDP-glucose incorporation into glycogen is irreversible.
c. UDP-glucose can readily interconvert with galactose.
d. glucose 1-phosphate could be dephosphorylated prior to utilization for glycogen synthesis.
25. When glucose 6-phosphate dehydrogenase is active, which of the following pathways is active?
a. glycolysis
b. gluconeogenesis
c. pentose phosphate
d. fatty acid oxidation
26. What is the primary difference between normal glycogen breakdown in liver and glycogen
breakdown in lysosomes?
a. Lysosomes use digestive enzymes to break down glycogen, whereas normal glycogen degradation
in liver utilizes glycogen phosphorylase.
b. Lysosomes break down substances to base units.
c. Lysosomes utilize lysosomal glucosidase, whereas as normal glycogen degradation in liver utilizes
glycogen phosphorylase.
d. Lysosome degradation of glycogen is not under hormonal control, whereas
Questions 28-30 use the following scenario. A patient comes to see you because he notices he has a
fruity odor in his breath. He has tried mouthwash, several types of toothpaste, and even breath mints
to get rid of this smell. When you question him, you learn that he has not eaten any carbohydrates for
seven days because he is trying to lose 10 pounds quickly before his wedding and honeymoon. He
asks you what he can do to get rid of this problem: looking great in a bathing suit is not as critical as
having bad breath during the honeymoon.
28. The most likely source of this fruity odor is
a. acetone
b. free fatty acids
c. undigested lactose
d. urea
29. What metabolic conditions favor this condition?
a. high glucagon à low acetyl CoA à high ketone body levels
b. high glucose à high insulin à high acetyl CoA à high ketone body levels
c. high glucagon à high acetyl CoA à high ketone body levels
d. very low glucose à high glucagon à low acetyl CoA à low ketone body levels
30. What would be a very simple way for this patient to eliminate the problem?
a. consume fats
b. consume carbohydrates
c. consume protein
d. eliminate lactose
EXAM 6 2006
1. You are arguing with your study partner about a fasting person who has been exposed to a
compound that completely inhibits fructose 1,6-bisphosphatase. You say glucose production by
gluconeogenesis will halt completely, but your study partner says that in the absence of fructose 1,6bisphosphatase, PFK-1 will simply run backwards to allow glucose formation. You know you are
right because
a. PFK-1 is deactivated by multiple mechanisms during fasting.
b. the kinase activity of the bifunctional enzyme is stimulated by glucagon.
c. the bifunctional enzyme can convert fructose 1,6-phosphate directly to fructose 6-phosphate, thus
bypassing fructose 1,6-bisphosphatase.
d. all of the above reasons are true.
4. A 14-yr old boy has been experiencing progressive onset of muscle fatigue and cramping. You find
no evidence for hypoglycemia and a muscle biopsy reveals that all the enzymes required for fatty
acid metabolism are present and functional in muscle. However, following an overnight fast and
glucagon challenge, free fatty acids do not appear in the blood. The most likely cause of these
symptoms is a deficiency of
a. hormone sensitive lipase.
b. lipoprotein lipase.
c. apoB48 and apoB100.
d. carnitine-palmitoyl transferase I
6. If a person has a phosphoenolpyruvate carboxykinase (PEPCK) defect, which of the following
cannot be used as starting material for gluconeogenesis?
a. alanine
b. lactate
c. glycerol
d. neither alanine nor lactate
7. In cystic fibrosis, the pancreatic ducts become obstructed by viscous mucus. Consequently,
digestion of which of the following would be most impaired?
a. fat and protein
b. carbohydrate and starch
c. carbohydrates and fat
d. protein and carbohydrates
8. The committed step in fatty acid synthesis, formation of malonyl-CoA, is catalyzed by
a. pyruvate carboxylase.
b. fatty acid synthase.
c. citrate lyase.
d. acetyl-CoA carboxylase.
10. How does adipose tissue utilize glycerol?
a. synthesis of triglycerides
b. glycolysis intermediate
c. gluconeogenesis intermediate
d. adipose tissue does not utilize glycerol.
13. A person with a deficiency of the bifunctional enzyme would
a. waste ATP in a PFK-1 / fructose 1,6-bisphosphatase futile cycle.
b. waste ATP in a pyruvate kinase / PEP phosphatase futile cycle.
c. be unable to synthesize glucose.
d. be unable to form fructose-6 phosphate.
14. A young child presents with a metabolic disorder manifesting as a significantly decreased ability
to synthesize cholesterol. Specific clinical tests indicate that the enzymes in the cholesterol synthesis
pathway are all present and functional, but cytoplasmic levels of HMG-CoA are elevated well above
normal. A defect in which enzyme could cause this problem?
a. HMG-CoA reductase
b. glucose 6-phosphate dehydrogenase
c. citrate lyase
d. mevalonate reductase
17. A person has an apoprotein CII deficiency. Which of the following would be a metabolic
consequence of this deficiency?
a. VLDL and chylomicron hyperlipidemia.
b. Decreased dietary fat absorption and fatty stools.
c. VLDL and chylomicron hypolipidemia.
d. Decreased VLDL and chylomicron endocytosis.
18. In a fasting individual, which of the following conditions stimulates the production of blood
glucose by gluconeogenesis?
a. a cAMP-mediated inactivation of pyruvate kinase.
b. a decreased supply of substrates.
c. an increase in the portal vein glucose level above the Km for glucokinase.
d. decreased levels of phosphoenoylpyruvate carboxykinase.
19. Phosphofructokinase-1 (PFK-1) is activated by ATP at low levels (1-2 mM) but inhibited by ATP
at higher levels ( > 3 mM) because
a. ATP is a substrate for the enzyme, thus a necessary component for activity.
b. ATP is a negative allosteric modulator that binds to its allosteric binding site on PFK-1 only when
ATP levels are high ( > 3 mM ).
c. PFK-1 activity depends on the adenylate charge of the cell.
d. All the above are true.
20. A 5-year old girl presents with a metabolic disorder manifesting as a significantly decreased
ability to synthesize cholesterol, fatty acids, triglycerides, and lipids. Specific clinical tests indicate
that the enzymes for these synthesis pathways are all present and functional, but at markedly
decreased levels relative to normal patients. The girl has sufficient adenylate charge to drive the
synthesis pathways, and NADH and NADPH levels are fine. A defect in which of the following account
for all the observed deficiencies?
a. glucose 6-phosphate dehydrogenase
b. phosphofructokinase-1
c. SREBP cleavage-activating protein
d. cAMP response element binding protein
26. Which of the following statements regarding the digestion of dietary lipids is TRUE?
a. Bicarbonate ions increase the pH of the intestinal tract so that pancreatic lipase and bile salts are
more active.
b. 2-Monoacylglycerols and free fatty acids are produced by lipoprotein lipase.
c. A deficiency of pancreatic lipase would eventually lead to a prostaglandin deficiency.
d. Phospholipids act as detergents for micelle formation.