Exam 3

Glycolysis is a major contributor to cellular respiration via the formation of
pyruvate.Which of the following describes the last step of glycolysis forming pyruvate?
a. 2-Phosphoglycerate undergoes a dehydration reaction
b. 1, 3-Bisphosphoglycerate and ADP undergo substrate-level phosphoryation
c. 3-Phosphoglycrate undergoes an isomerization reaction
d. Phosphoenolpyruvate and ADP undergo substrate-level phosphorylation
e. None of the above

d. Phosphoenolpyruvate and ADP undergo substrate-level phosphorylation

Which of the following is NOT true about the phosphorylation reactions in glycolysis?
a. In the preparatory phase 2 ATP are used while in the payoff phase 2 ATP are
made per one glucose molecule
b. Kinases are the enzymes which commonly transfer phosphoryl groups
c. ATP exists in a complex with Mg2+ during phosphorylation reactions
d. PFK-1 is involved in the first committed step in glycolysis and utilizes ATP to
form fructose 2,6-bisphosphate
e. More than one are incorrect

A and D are incorrect. In the payoff phase 4 ATP molecules are done per one glucose molecule
Then PFK-1 catalyzes the conversion of F6P to F16BP

During the preparatory phase, cleavage occurs between C3 and C4 of fructose
1,6-bisphosphate. What type of reaction is responsible for this cleavage and what are the
products?
a. Phosphorylation; phosphoenolpyruvate and fructose 6-phosphate
b. Hydrolysis reaction; dihydroxyacetone phosphate and glyceraldehyde
3-phosphate
c. Aldol condensation; glyceraldehyde 3-phosphate and 1-3 bisphosphoglycerate
d. Reverse aldol condensation; dihydroxyacetone phosphate and 3-phosphoglycerate
e. None of the above

None of the above, it is a reverse aldol condenstion, but the products are dihydroxyacetone phosphate and glyceraldehyde-3-phosphate

Which of the following occurs in the presence of glyceraldehyde 3-phosphate
dehydrogenase?
a. Substrate-level phosphorylation
b. Isomerase reaction
c. Reduction of NAD+
d. Loss of H2O
e. None of the above

Reduction of NAD+

Remember that this enzyme catalyzes the conversion of glyceraldehyde-3-phosphate to glyceraldehyde 1,3 bisphosphate
and it uses an inorganic phosphate that is going to phosphorylate the first carbon of glyceraldehyde

How many ATP and NADH will be produced for two glucose molecules in the payoff
stage only?
a. 4 ATP, 2 NADH
b. 2 ATP, 1 NADH
c. 6 ATP, 4 NADH
d. 8 ATP, 4 NADH
e. None of the above

d. 8 ATP, 4 NADH

One glucose molecule will produce 4 ATP and 2 NADH in the
payoff stage

Bob has a rare genetic mutation that inhibits the function of alanine aminotransferase
meaning they cannot convert Alanine to Pyruvate in the liver. Which of the following
would you predict to be a consequence of this mutation?
a. It will hinder the ability of NH4+ to be transported out of the liver
b. It will have no effect because lactate can be converted to glucose via
gluconeogenesis
c. It will affect the transport of the three carbon molecules that are important for
gluconeogenesis
d. Both a and c are correct
e. Both b and c are correct

d. Both a and c are correct

Remember that NH4+ is produced in the liver by glutamate, which is a product of alanine transamination with alpha-KG

And alanine carries the 3C (Pyruvate) molecules to the liver

WITHOUT the enzyme malate dehydrogenase, which is involved in the conversion of pyruvate to phosphoenolpyruvate, which of the following would occur?
a. Oxaloacetate could not be transported out of the mitochondria
b. Malate could not be converted into Oxaloacetate
c. Oxaloacetate could not be converted into phosphoenolpyruvate
d. Both a and b are correct
e. All of the above

e) All of the above

Malate dehydrogenase catalyzes the conversion of Oxaloacetate to L-malate so it can leave the mitochondria via a malate transporter. Malate is then converted back to Oxaloacetate by malate dehydrogenase. Without malate dehydrogenase
oxaloacetate could not be formed outside the mitochondria and be converted to PEP.

Glucose-6-phosphatase deficiency (G6P deficiency) is a group of inherited metabolic
diseases characterized by poor tolerance to fasting. Which of the following would be a
result of glucose-6-phosphatase deficiency?
a. Fructose-6-phosphate can not be converted to Glucose-6-phosphate
b. Glycolysis could not be completed
c. Glucose-6-phosphate could not be converted to Glucose
d. Fructose-1,6-bisphosphate could not be converted to Fructose-6-phosphate
e. None of the above

c. Glucose-6-phosphate could not be converted to Glucose

Glucose-6-phosphatase is the enzyme used in the 3 bypass reaction of Gluconeogenesis, which is the hydrolysis of G6P to Glucose

The graph below depicts the relationship between fructose 6-phosphate concentration and
phosphofructokinase-1 activity. Which of the following answer choices correctly predicts
the energy state of the cell for the green line?
a. No inhibitors and low [ATP]
b. Some [ATP] and some [AMP]
c. High [ATP]
d. High [AMP] and high [ADP]
e. High [citrate]

b. Some [ATP] and some [AMP]

The black line with the largest slope represents the PFK-1
activity when no inhibitors are present or there is a high concentration of AMP or ADP. The line with the smallest slope (red-dashed line) represents PFK-1 activity when there is
high ATP or citrate concentrations.
The green line would occur if there were both inhibitors such as ATP and activators such as AMP present in the cell.

10. Which of the following are inhibitors of pyruvate kinase?
I. Glucagon
II. Fructose 1,6-bisphosphate
III. ATP
IV. Acetyl-CoA
a. I, II, and III
b. II and III
c. III only
d. II, III, and IV
e. III and IV

Pyruvate kinase is inactivated by high energy molecules and those are ATP, acetyl-coA (allosteric regulation)

11. Glycogen stores glucose in a polymeric form to prevent high osmotic pressures in cells.
Glycogenolysis will breakdown cellular glycogen to glucose 1-phosphate. Which
enzyme’s activity in this process will result in the production of glucose 6-phosphate?
a. Transferase activity of the debranching enzyme
b. Glycogen phosphorylase a/b
c. Glucosidase activity of the debranching enzyme
d. Phosphoglucomutase
e. Phosphoprotein phosphatase 1

d. Phosphoglucomutase

Phosphoglucomutase catalyzes the convertion of glucose-1-phosphate to glucose-6-phosphate

12. McArdle's disease, otherwise known as glycogen storage disease type V is caused by a
deficiency in the enzyme myophosphorylase which prevents glycogenolysis in the
muscles. Which of the following is false regarding this condition?
a. This will result in a deficiency of glucose 6-phosphate in the muscles
b. Symptoms include exercise-induced cramps and pain
c. Myoglobin will be found in urine
d. Glucose 6-phosphatase activity will be normal
e. All of the above are true

e. All of the above are true

A is true because decreased
phosphorylase activity in the muscles will result in decreased production of glucose-6-phosphate. B and C are all symptoms of McArdle’s disease. D is true because glucose 6-phosphatase only acts in the liver and kidneys so it would be unaffected by McArdle’s disease

13. Glycogen synthesis creates glycogen chains by linking glucose monomers. Which of the
following is FALSE regarding this process?
a. UDP-Glucose Pyrophosphorylase creates a sugar nucleotide
b. Glycogen synthase a/b forms (α1⟶4) linkages
c. The glycogen-branching enzymes forms (α1⟶6) linkages
d. The phosphorylated form of glycogen synthase a/b is active
e. Two of the above are false

d. The phosphorylated form of glycogen synthase a/b is active

Glycogen synthase a/b is active when it is not phosphorylated, in the other hand, glycogen phosphorylase is active when it is phosphorylated

14. PHKB-related Phosphorylase kinase deficiency results in the deficiency of the enzyme
phosphorylase b kinase and leads to an enlarged liver, hypoglycemia and diminished
muscle tone. Which of the following is FALSE regarding the disease condition?
a. There will be increased glycogen phosphorylase activity
b. This will increase breakdown of glycogen
c. This will prevent full signal amplification of the enzyme cascade
d. Protein Kinase A will have a diminished effect on glycogenolysis
e. None of the above are false

b. This will increase breakdown of glycogen

Remember that phosphorylase B kinase phosphorylates phosphorylase b turning it into phosphorylase a which is the active form,and this drives the breakdown of glycogen in the gylcogenolysis pathway.


deficiency of phosphorylase b kinase will inhibit glycogen production by favoring dephosphorylation of glycogen
phosphorylase

15. GSD type 0 disease is a disorder of the enzyme Glycogen synthase that impairs
production of glycogen and results in muscle pain, weakness and syncopal episodes.
Which of the following is TRUE regarding this condition?
a. This disease primarily acts on skeletal muscle tissue
b. Type 0 results in high blood glucose
c. This result in high ketone bodies
d. There will be an abundance of UDP-glucose
e. Two of the above are true

c. This result in high ketone bodies

one of the symptoms of type 0 involves
high ketone bodies.

You have been studying for your biochemistry exam all day at Marston library, and you
notice that it has been over 8 hours since the last time you ate anything. What is occurring
in your liver during this time?
a. Glycogen synthase is dephosphorylated
b. Phosphofructokinase-1 is inactivated
c. The levels of fructose 2,6-bisphosphate are decreased
d. Insulin is released and acts on the hepatocyte receptor tyrosine kinases
e. More than one of the above are correct

e. More than one of the above are correct

b. Phosphofructokinase-1 is inactivated
c. The levels of fructose 2,6-bisphosphate are decreased

as we have not eaten for more than 8 hours, we are gonna have low blood glucose levels, and this is going to inhibit glycolysis, and the PFK-1 activity is going to be inactivate as well as the activate of F26BP is going to decrease, this stimulates gluconeogenesis and inhibits glycolysis.

low blood glucose level activates glucagon, and glucagon phosphorylates glycogen synthase a, therefore inhibiting glycogenesis as well

17. After completing your biochemistry exam, you decide to treat yourself because you
studied for many hours and felt you did really well. That night, you end up eating 2
pizzas and watching all the tv shows you need to catch up on. What is occurring in your
leg muscles during this time?
a. Gluconeogenesis is decreased
b. Glycogen phosphorylase a is activated
c. Glycogen synthase a is dephosphorylated
d. Epinephrine binds to the beta-adrenergic receptors on muscle cells
e. Glycolysis is significantly increased

c. Glycogen synthase a is dephosphorylated

During this period, there is a low energy demand. With high
levels of glucose, glycogen synthase a, the active form of the enzyme, will be activated to store glucose in the form of glycogen. Remember that gluconeogenesis does not occur in our muscles, only in the liver. Glycolysis is not warranted due to the lack of energy demand not because of a lack of glucose.

18. How do the levels of NADPH affect the partitioning of glucose 6-phosphate?
a. Under high levels of NADPH, glucose 6-phosphate is oxidized in the pentose
phosphate pathway
b. Under high levels of NADPH, glucose 6-phosphate is used in glycolysis to form
ATP
c. Under low levels of NADPH, glucose 6-phosphate is reduced in the pentose
phosphate pathway
d. Under low levels of NADPH, glucose 6-phosphate is used to form pentose
phosphates
e. More than one of the above are correct

b. Under high levels of NADPH, glucose 6-phosphate is used in glycolysis to form ATP
d. Under low levels of NADPH, glucose 6-phosphate is used to form pentose phosphates
e. More than one of the above are correct

NADP+ and NADH levels determine wether G6P enter glycolysis (more NADPH) or the Pentose Phosphate pathway (more NADP+ or less NADPH)

19. Red blood cells are susceptible to the formation of damaging oxidative species, such as
hydrogen peroxide and hydroxyl free radicals. This can occur when exposed to ionizing radiation, antimalarials, and herbicides. These oxidative species can cause damage to
lipids, proteins, and DNA. If our red blood cells lack important organelles, such as the nucleus and mitochondria, how are they able to undergo detoxification and combat this
oxidative damage?
a. The production of ribose 5-phosphate is activated to produce more nucleotides,
which will play a detoxification role in red blood cells
b. Red blood cells rely on mitochondrial respiration to produce oxygen and form a
hydroxyl free radical, which spontaneously converts to water and detoxifies the
cell
c. Glucose 6-phosphate is reduced to form NADP+, which will act as an electron
and proton acceptor in red blood cells, removing any free electrons and protons
that could potentially cause the formation of a damaging oxidative species
d. NADPH is used to detoxify red blood cells by reducing glutathione via
glutathione reductase, and then the reduced form of glutathione is used to convert
hydrogen peroxide to water via glutathione peroxidase
e. Unfortunately, red blood cells are not able to be detoxified when exposed to high
levels of ionizing radiation, antimalarials, and herbicides, and will therefore be
degraded

d. NADPH is used to detoxify red blood cells by reducing glutathione via
glutathione reductase, and then the reduced form of glutathione is used to convert hydrogen peroxide to water via glutathione peroxidase

Red blood cells use NADPH to prevent oxidative damage

20. Which of the following is FALSE regarding the phases of the pentose phosphate
pathway?
a. The oxidative phase involves the oxidation of glucose 6-phosphate and the
formation of ribose 5-phosphate, which is used to produce nucleotides,
coenzymes, DNA, and RNA
b. The oxidative phase involves 2 rounds of oxidation to produce NADPH
c. The nonoxidative phase is used for cells that need NADPH and will use ribose
5-phosphate to produce glucose 6-phosphate
d. Once NADPH is produced in the oxidative phase, it can be used for fatty acid
synthesis
e. All of the answer choices are correct

c. The nonoxidative phase is used for cells that need NADPH and will use ribose
5-phosphate to produce glucose 6-phosphate

While the nonoxidative phase of the pentose phosphate pathway
is used for cells when we are not in periods of growth, but we still need the reducing equivalents such as NADPH, ribulose 5-phosphate, and not ribose 5-phosphate that will be used to produce glucose 6-phosphate.

21. Thiamine pyrophosphate (TPP) is one of the five coenzymes involved in the production
of Acetyl-CoA in the Pyruvate Dehydrogenase pathway. TPP’s structure allows it to react
with pyruvate because TPP contains a(n)_____
a. Adenine ring
b. Thiazolium ring
c. Benzene ring
d. Isoalloxazine ring
e. Guanine ring

b. Thiazolium ring

22. Pyruvate Dehydrogenase (PDH) creates Acetyl CoA, CO2
, and a form of energy. Which
form of energy is released and in which enzyme complex?
a. ATP; Dihydrolipoyl transacetylase (E2)
b. ATP; Dihydrolipoyl dehydrogenase (E3)
c. NADH; Dihydrolipoyl transacetylase (E2)
d. NADH; Dihydrolipoyl dehydrogenase (E3)
e. None of the above

23. You are working in a lab analyzing how your mysterious toxin can affect the Citric Acid
Cycle. You look at the last product created and see Succinyl-CoA. Which immediate
product(s) would that enzyme form under normal conditions?
a. Succinyl-CoA synthetase; succinate, GTP, CoA-SH
b. Succinyl-CoA synthetase; succinate, NADH
c. Succinate dehydrogenase; fumarate, FADH2
d. Succinate dehydrogenase; fumarate, GTP, CoA-SH
e. Succinyl-CoA synthetase; succinate, ATP

Dr. House is studying how to regulate the Citric Acid Cycle. What conditions will cause
the formation of this molecule and with which enzyme?

a. Low NADH, alpha-ketoglutarate dehydrogenase
b. High ATP, citrate synthase
c. Low ATP, citrate synthase
d. High succinyl-CoA, aconitase
e. None of the above

25. The human body is a master at using specific molecules to adapt to different energy
conditions. At times when cells are deprived of energy, which of the following
intermediates can be used to replenish molecules necessary for the Citric Acid Cycle?
a. Pyruvate
b. Malate
c. Oxaloacetate
d. Phosphoenolpyruvate (PEP)
e. More than one of the above

25. The human body is a master at using specific molecules to adapt to different energy
conditions. At times when cells are deprived of energy, which of the following
intermediates can be used to replenish molecules necessary for the Citric Acid Cycle?
a. Pyruvate
b. Malate
c. Oxaloacetate
d. Phosphoenolpyruvate (PEP)
e. More than one of the above

Pyruvate and Phosphoenolpyruvate can create anaplerotic
reactions that replenish Malate and Oxaloacetate, respectively.

26. Which of the following is TRUE about the Electron Transport Chain?
a. Complex II is Succinate Dehydrogenase and is involved in TCA
b. Complex I pumps 2 protons into the intermembrane space
c. Complex IV pumps 4 protons into the intermembrane space
d. Electrons in Complex I pass through Fe-Si centers
e. None of the above

a. Complex II is Succinate Dehydrogenase and is involved in TCA

Complex II is succinate dehydrogenase and is also a part of
the TCA cycle.

27. O2 is required for obligate aerobes to live. Humans fall under this category as being
deprived of oxygen will lead to adverse effects. Acquiring proper levels of O2 is also
important for the Electron Transport Chain to proceed. In the absence of oxygen, which is
least likely to occur?
a. Water is not formed as a product of Complex IV
b. Fumarate will be produced
c. Cytochrome C will be oxidized
d. The ETC will decrease in function
e. None of the above

c. Cytochrome C will be oxidized

Without the presence of O2, Complex IV will fail to act
accordingly and not produce water and Cytochrome C will not be oxidized.

28. ATP Synthase has multiple structural subunits. Which of the following correctly matches
the subunit to its correct function?
a. α subunits bond ADP + P and ATP
b. γ subunit is the side stalk that serves as structural support
c. F0
is the integral membrane subunit
d. β subunits are left unoccupied
e. F1 Subunit extends into the intermembrane space

c. F0 is the integral membrane subunit

α subunits are left unoccupied and β subunits bind ADP + P and ATP. γ subunit is the central stalk that rotates. The F1 subunit extends in the mitochondrial matrix.

29. The Electron Transport Chain increases the concentration of protons in the
intermembrane space. The protons then flow down their concentration gradient through
ATP Synthase, providing the kinetic energy necessary for ATP Synthase to synthesize
ATP. Which of the following correctly describes the route protons take through ATP
Synthase from entry to exit?
a. Enters subunit a, binds to asparagine in ring of C, travels through the ring of C,
exits subunit a
b. Enters subunit a, binds to aspartate in ring of C, travels through the ring of C,
exits subunit a
c. Enters subunit a, binds to aspartate in ring of C, travels through the ring of C,
exits subunit β
d. Enters subunit a, binds to asparagine in ring of C, travels through the ring of C,
exits subunit β
e. None of the above

b. Enters subunit a, binds to aspartate in ring of C, travels through the ring of C,
exits subunit a

30. Which of the following is FALSE?
a. The malate-aspartate shuttle utilizes NAD+ / NADH as its electron carrier
b. Glycerol 3-Phosphate shuttle products can be used by Complex III of ETC
c. Glycerol 3-Phosphate shuttle forms FADH2
d. In the intermembrane space, malate dehydrogenase converts oxaloacetate to
malate oxidizing NADH to NAD+ in the process
e. All of the above are true

e. All of the above are true

The oxidation of fatty acids occurs in multiple regions within the cells of the human
body. Particularly in eukaryotes, β-oxidation is the catabolic process that takes place in
the ____________, where fatty acids are broken down to generate molecules used in the
electron transport chain.
a. Lysosomes
b. Mitochondria
c. Cytosol
d. Peroxisomes
e. None of the above

b. Mitochondria

Fatty acid β-oxidation occurs in the mitochondria in
eukaryotes.

32. Lipid anabolism synthesizes lipids from amino acids on certain cells. These lipids can
then serve as precursors for other cell processes. Which of the following molecules is the
precursor to the synthesis of fatty acids?
a. Triacylglycerols
b. Cholesterol
c. Malonyl-CoA
d. Glycerophospholipids
e. Acetyl-CoA

e. Acetyl-CoA

Acetyl-CoA is directly responsible for being the precursor to fatty
acids.

33. ATP is the main source of energy for most cellular processes. The body produces
different amounts of ATP depending on location and circumstance of production.
Oxidation of a carbon in a fatty acid would yield _______ molecules of ATP; whereas a
carbon in glucose would yield _______ molecules of ATP.
a. 2; 5
b. 4; 7
c. 7; 5
d. 5; 7
e. 4; 2

c. 7; 5

Oxidation of a carbon in a fatty acid yields ~ 7 ATPs whereas a carbon in glucose yields ~ 5 ATPs. General lipids will provide more energy return than carbohydrate metabolism.

34. Triacylglycerol, also known by its common abbreviation of TAG, is a very important
source of energy in the body. Measuring the amount of triacylglycerosl in the blood is
one way to monitor the risk for cardiovascular disease. Several organs participate in the
active catabolism of triacylglycerol in the body. Which of the following options does
NOT include an organ that commonly synthesizes triacylglycerol?
a. Liver
b. Skeletal muscle
c. Spleen
d. A & C
e. None of the above

c. Spleen

The liver, heart, and skeletal muscle are all common places where
triacylglycerols are synthesized.

35. The first stage of beta oxidation to break down a fatty acid into numerous acetyl-CoA
molecules requires multiple rounds. Stage one of beta oxidation begins with an oxidation
reaction that reduces FAD, and ends in attack by CoA-SH. How many times must
CoA-SH attack to fully break down our original molecule, Palmitoyl-CoA, a 16 carbon
long fatty acid?
a. 2
b. 6
c. 7
d. 8
e. None of the above, the reaction does not have to be repeated to progress to Stage

c. 7

In total, this cycle happens 7 times. The process is repeated 6 times after the first in order to fully break down the fatty acid. This generates a
total of 8 acetyl-CoA molecules, 7 NADH molecules, and 7 FADH2 molecules

36. While on a ketogenic diet is a diet that involves low carbohydrate and high fat intake.
During the ketogenic diet, the body burns fat reserves to form ketone bodies. Which
molecules are these fats being broken down to?
a. Acetone
b. Pyruvate
c. Acetoacetate
d. A & C
e. B & C

d. A & C

Acetone (a) and acetoacetate (c) are the ketone bodies.

37. What is the correct order of the following steps of fatty acid synthesis?
i. Oxidation of NADPH
ii. Acetyl-CoA is converted to malonyl-CoA
iii. Acetyl-CoA binds to β-Ketoacyl-ACP Synthase
iv. Condensation reaction via nucleophilic attack of carbonyl carbon of
Acetyl-S-KS
a. II, IV, I, III
b. III, II, IV, I
c. II, III, IV, I
d. III, II, I, IV
e. None of the abov

c. II, III, IV, I

The first step in fatty acid synthesis is the conversion of acetyl-CoA to malanoyl-CoA through ACC (one atp molecule is used)
Biotin coenzyme

Then malanoyl-CoA is converted to palmitic acid/ palmitae through an enzyme called Fatty acid synthase

ACR DR

38. Epileptic encephalopathy is a disease that can cause many seizures at the time of birth.
This disease is caused by a lack of citrate transporter in mitochondrial membranes. What
process is likely inhibited by individuals with this disorder?
a. Ketogenesis
b. Fatty acid synthesis
c. Kreb’s cycle
d. Fatty acid oxidation
e. None of the above

Citrate transporter is integral to transporting citrate out of the
mitochondria. Once out of the mitochondria, it can undergo fatty acid synthesis. If
individuals could not transport citrate out of the cell, they would not be able to synthesize
fatty acids.

39. Palmitoyl-CoA is a 16 carbon long fatty acid. We typically store energy in the form of
palmitoyl-CoA. One of the first steps in the synthesis of palmitoyl-CoA is the conversion
of acetyl-CoA to malonyl-CoA via acetyl-CoA carboxylase. Which of the following
would activate this enzyme?
a. Glucagon
b. Phosphorylation of acetyl-CoA carboxylase
c. Palmitoyl-CoA
d. Citrate
e. None of the above

d. Citrate
ciitrate being a precursor for fatty acid synthesis activates
acetyl-CoA carboxylase. High citrate levels would indicate sufficient cellular energy
levels which promotes its cleavage into acetyl-CoA and oxaloacetate which can then be
used in fatty acid synthesis.

40. Individuals with type I diabetes must take insulin in order to utilize glucose properly.
When these patients take insulin during periods of high glucose intake, there is an
increased production of what molecule?
a. Acetone
b. Fatty acids
c. Malonyl-CoA
d. Triacylglycerols
e. All of the above

e. All of the above

Insulin helps up-regulate the process of glycolysis which increases
acetyl-CoA levels and in turn ketone body levels like acetone. Insulin also upregulates
ACC for fatty acid synthesis, which leads to more fatty acids and therefore more
triacylglycerols so E is the best answer.

41. Oxysterols are oxidized derivatives of the traditional cholesterol structure. Oxysterols
have been linked to multiple chronic pathologies in the human body, including metabolic
disorders, and cardiovascular disease. These molecules additionally play a role in general
cholesterol metabolism as a regulatory component, inhibiting which enzyme?
a. AMP kinase
b. Squalene monooxygenase
c. HMG-CoA reductase
d. Acyl-CoA-cholesterol acyl transferase
e. None of the above

c. HMG-CoA reductase

42. The ACAT enzyme is responsible for the conversion of cholesterol to a(n) _____
a. Steroid hormone
b. Biliary acid
c. Cholesteryl ester
d. Hydroxysterol
e. ACAT serves as a precursor enzyme contributing to the formation of all of these
molecules.

c. Cholesteryl ester

43. Rickets is a disease caused by deficiency of vitamin D3 leading to insufficient calcium
uptake in the necessary tissues. Vitamin D3 is formed from a cholesterol derivative.
Given what you know of cholesterol structure, what type of receptor does Vitamin D3
bind to.
a. G-protein coupled receptor
b. Nuclear hormone receptor
c. Receptor tyrosine kinase
d. More than one of these can bind Vitamin D3
e. None of these can bind Vitamin D3

b. Nuclear hormone receptor

Steroids are able to pass through the lipid bilayer because of its
small uncharged nature. There it will either form a homo or hetero steroid nuclear
complex affecting transcription of gene products as a result. Since cholesterol derivatives
are hydrophobic, they can simply diffuse through the cell membrane and bind to a
receptor located within the cell.

44. A low energy state of the cell would result in the inhibition of which enzyme involved in
cholesterol biosynthesis?
a. ACAT
b. HMG-CoA reductase
c. AMPK
d. Cholesterol dehydrogenase
e. Sterol synthetase

b. HMG-CoA reductase

Glucagon is the signal for a low energy state, and glucagon
inhibits HMG-CoA reductase. Although AMPK is an effector enzyme that senses the
system for low ATP, it is AMPK that goes to alter HMG-CoA reductase and inhibit
cholesterol synthesis due to the high cost energy needed for this biosynthetic pathway.

45. After three equivalences of acetyl-CoA are condensed, what is the name of this
significant structure in the cholesterol biosynthetic pathway?"
a. Beta-Hydroxy-beta-methyl-glutaryl-CoA
b. Oxysterol
c. Mevalonate
d. Cholesterol Esters
e. Cholesterol

a. Beta-Hydroxy-beta-methyl-glutaryl-CoA

HMG-COA

46. A patient that is admitted to the emergency room is complaining of chest pain. A
coronary calcium scan is performed using specialized X-ray technology to reveal a
significant build up of fatty plaque on the walls of the patient’s arteries. Which of the
following is the patient most likely experiencing?
a. Increase levels of HDL
b. atherosclerosis
c. Increased levels of LDL
d. B and C only
e. All of the above

b. atherosclerosis
c. Increased levels of LDL

Arteriosclerosis is a build up of fatty plaque on the walls of the
arteries and a common symptom of this cardiovascular disease is chest pain, therefore the
patient most likely has arteriosclerosis, so option B is correct. VLDL and LDL are the
types of lipids responsible for the accumulation of plaque in the arteries (not HDL)

47. Gaucher disease is a common lysosomal storage disorder that results in the lack of
enzymes that break down lipids in the body cells, specifically lytic enzymes.Which of the
following would be the LEAST likely consequence of this disease?
a. Increased levels of apoB-100
b. Reduced levels of released fatty acids
c. Increased levels of released amino acids
d. Reduced levels of released cholesterol
e. Increased levels of cholesteryl esters

c. Increased levels of released amino acids


Lytic enzymes in the lysosome degrade apoB-100 and cholesterol
esters, therefore a lack in lytic enzyme activity would result in an increase of these
molecules, so options A and E are true. Lytic enzymes also release amino acids, fatty
acids, and cholesterol, therefore a decrease in lytic enzyme activity would result in
reduced levels of these molecules, so options B and D are true, but option C is false.

48. Statins are a class of medication that are commonly used to decrease levels of LDL
cholesterol. Which lipid metabolic pathway will most likely be affected by a patient’s
consumption of statin medication?
a. Endogenous
b. Exogenous
c. Forward
d. Reverse
e. None of the above

a. Endogenous

49. Familial Hypercholesterolemia (FH) is a genetic disorder that is associated with
decreased uptake of LDL cholesterol from plasma, premature atherosclerosis, and
increased likelihood of early on heart disease. Which of the following receptors is most
likely mutated as a result of this genetic disorder?
a. Free fatty acid receptor
b. SR-B1 receptor
c. Low-density lipoprotein (LDL) receptor
d. Beta adrenergic receptor
e. More than one of the above

c. Low-density lipoprotein (LDL) receptor

A decreased uptake in LDL would mean that any receptor
specific to LDL uptake would most likely be mutated. Since the low-density lipoprotein
(LDL) receptor is responsible for uptake of LDL from the plasma, option C is correct.
Free fatty acid receptors sense the concentration of fatty acids in the plasma, SR-B1
receptors control the uptake of HDL, and beta adrenergic receptors bind epinephrine for
signaling purpose,

50. A researcher is studying an unknown disease of the small intestine that supposedly
impairs the organ’s ability to synthesize important lipoproteins. Which of the following
would most likely be affected by this disease?
I. VLDL
II. HDL
III. Chylomicrons
a. I, II
b. I, III
c. II, III
d. III only
e. I only

d. III only
III. Chylomicrons


The disease targets specifically the small intestine so any lipid
formed in the small intestine will be affected. VLDL and HDL are both formed in the
liver

1. The first step of glycolysis is the phosphorylation of glucose to glucose-6-phosphate.
However, Glucose phosphorylation is an energetically unfavorable process, indicated by
a ΔG value of + 13.8. Which of the following statements explains how this reaction is
able to proceed?
a. Glucose has high group transfer potential, which drives its phosphorylation
b. The phosphorylation of glucose is coupled with the phosphorylation of ADP, an
energetically favorable reaction
c. The phosphorylation of glucose is coupled with substrate level phosphorylation,
an energetically favorable reaction
d. The phosphorylation of glucose is coupled to ATP hydrolysis, an energetically
favorable reaction
e. None of the above

d. The phosphorylation of glucose is coupled to ATP hydrolysis, an energetically
favorable reaction

2. When our muscle cells contract, there is about 5 seconds worth of available ATP before it
is all used up. In order to keep contracting, the muscle cells must next use __________ to
generate ATP.
a. Phosphoenolpyruvate
b. Phosphocreatine
c. Pyruvate
d. Creatine
e. 3-Phosphoglycerat

b. Phosphocreatine

3. Which of the following statements is/are TRUE regarding the reaction depicted below?
a. The enzyme that catalyzes this reaction is pyruvate kinase
b. This reaction occurs during the preparatory phase of glycolysis
c. This is the first ATP generating step of glycolysis
d. This reaction involves the transfer of a phosphoryl from 2-phosphoglycerate
e. More than one of the above

a. The enzyme that catalyzes this reaction is pyruvate kinase

4. During times of strenuous exercise, oxygen cannot reach our muscle cells fast enough for
aerobic respiration to be maintained. Instead, anaerobic respiration occurs to generate
energy in the absence of oxygen. Which of the following is occurring in an individual
participating in a high intensity workout?
a. Lactate dehydrogenase catalyzes the oxidation of pyruvate to lactate
b. Lactate dehydrogenase catalyzes the oxidative decarboxylation of pyruvate to
acetyl-CoA
c. NAD+ is regenerated so glycolysis can continue making ATP
d. NADP+ is regenerated so glycolysis can continue making ATP
e. NADH is regenerated so glycolysis can continue making ATP

c. NAD+ is regenerated so glycolysis can continue making ATP

5. Phosphoglycerate kinase deficiency is a rare genetic disorder that affects the body’s
ability to break down glucose. This deficiency is caused by mutations in the PGK1 gene
and can lead to cell damage or cell death. Which of the following would be directly
affected by a mutation in the PGK1 gene?
a. Substrate level phosphorylation resulting in the first generation of ATP
b. The interconversion of dihydroxyacetone phosphate and
glyceraldehyde-3-phosphate
c. The phosphorylation of fructose-6-phosphate in order to generate a symmetrical
molecule for cleavage
d. The transfer of a high energy phosphoryl group to 3-phosphoglycerate
e. More than one of the above

a. Substrate level phosphorylation resulting in the first generation of ATP

Below is a graph showing activation and inhibition of phosphofructokinase-1. Curve A
represents activity with no effectors. Which of the following could lead to curve B?
I. High ATP
II. Low ATP
III. Citrate
IV. AMP
a. II only
b. I, III
c. II, III
d. II, IV
e. II, III, IV

d. II, IV

7. A patient presents with abdominal pain, yellowing of skin, and fatigue. Suspecting a liver
condition, the physician orders an alanine transaminase (ALT) blood test, which measures
a patient’s ALT levels. ALT levels can increase when your liver is damaged, and this
patient is found to have elevated ALT levels. Which of the following CORRECTLY
describes the effect these elevated ALT levels have on the patient’s glucose-alanine
cycle?
a. In the muscle, alanine would be converted into pyruvate at an increased rate
b. In the liver, alanine would be converted into pyruvate at an increased rate
c. Blood glucose levels would decrease due to increased levels of pyruvate in the
liver
d. In the liver, α-Ketoglutarate levels would be elevated
e. More than one of the above

b. In the liver, alanine would be converted into pyruvate at an increased rate

Alanine aminotransferase converts pyruvate into alanine in the
muscle. Alanine aminotransferase converts alanine into pyruvate in the liver. During this
process, alpha-ketoglutarate is converted into glutamate, which would lower levels of
alpha-ketoglutarate in the liver. An increase in alanine aminotransferase would increase
blood glucose levels by increasing liver pyruvate levels, since pyruvate forms glucose
through gluconeogenesis

8. Biotinidase deficiency is an inherited disorder in which the body is unable to recycle the
vitamin biotin. Biotinidase removes biotin that is bound to proteins in food, leaving the
vitamin in its free state. Free biotin is needed to act as a coenzyme for four carboxylation
enzymes in the body. Which step of gluconeogenesis requires biotin as a coenzyme?
a. Synthesis of phosphoenolpyruvate from oxaloacetate
b. Synthesis of fructose-6-phosphate from fructose 1,6-bisphosphate
c. Synthesis of glucose from glucose 6-phosphate
d. Synthesis of oxaloacetate from pyruvate
e. None of the above

d. Synthesis of oxaloacetate from pyruvate

9. Glucagon and insulin are hormones that bind cell surface receptors and regulate
metabolism. Which of the following statements regarding the way these hormones
regulate glycolysis and gluconeogenesis is FALSE?
a. Glucagon stimulates gluconeogenesis
b. Insulin inhibits gluconeogenesis
c. Glucagon inhibits glycolysis
d. More than one of the above
e. None of the above

e. None of the above

10. A child presents in your pediatric clinic with developmental delay, intermittent ataxia,
poor muscle tone, and abnormal eye movements. You diagnose the patient with pyruvate
dehydrogenase complex deficiency (PDCD). You explain to the patient’s family that the
pyruvate dehydrogenase complex is important in regulating carbohydrate metabolism.
Which of the following ACCURATELY describes a pathway involving pyruvate?
a. Acetyl-CoA allosterically stimulates pyruvate dehydrogenase, converting
pyruvate to acetyl-CoA
b. Acetyl-CoA allosterically inhibits pyruvate dehydrogenase, preventing conversion
of pyruvate to acetyl-CoA
c. Conversion of pyruvate to phosphoenolpyruvate is stimulated when Fatty Acids
are available as sources of energy
d. Acetyl-CoA allosterically stimulates pyruvate carboxylase, converting
oxaloacetate to pyruvate
e. More than one of the above

Both B and C are true statements.

11. John is an elite endurance athlete who is currently 30 minutes into running the New York
City marathon. Which of the following would be FALSE regarding John’s glycogen
metabolism?
a. Glycogen Phosphorylase would be cleaving glucose residues at the reducing end
of glycogen chains
b. The debranching enzyme would be transferring branches onto the main chain
c. The debranching enzyme would be cleaving residues at the ɑ1-6 branch as free
glucose
d. Phosphoglucomutase would be converting G1P into G6P for use in glycolysis in
the muscle
e. None of the above

a. Glycogen Phosphorylase would be cleaving glucose residues at the reducing end
of glycogen chains

12. The skeletal muscle and liver are the organs that account for the majority of glycogen
stored in our bodies. However, the utilization and metabolism of glycogen between these
organs differs. Which of the following does NOT describe a difference between glycogen
metabolism in the liver and skeletal muscle?
a. Glycogen in the liver is important for regulating blood glucose, whereas glycogen
in the muscle is used to sustain muscle contractions.
b. Glucose-6-phosphate is converted to glucose in the liver
c. Glucagon signals glycogenolysis in the liver
d. Epinephrine signals glycogenolysis in the muscle
e. None of the above

None of the above

13. A glycogenin dimer is a necessary primer in order to build a glycogen molecule. Which
of the following are TRUE about glycogenin?
I. It is an enzyme that catalyzes the assembly of new chains
II. Has a tyrosine residue that attacks Glucose-1-phosphate to form a glycosidic bond
III. It is autophosphorylated and dimerizes when bound by UDP-glucose
a. I
b. II
c. III
d. I and II
e. II and III

I. It is an enzyme that catalyzes the assembly of new chains

14. After John has finished the New York marathon he goes home to rest and recover because
he has spent lots of energy, his muscles need to recover, and his glycogen stores have
been depleted. Which of the following would NOT be a necessary step in order for John
to rebuild his glycogen?
a. UDP-Glucose Phosphorylase converts glucose-1 phosphate into UDP-Glucose
b. PP1 must deactivate Glycogen Synthase
c. Glycogen Synthase transfers the glucose residue from a UDP-glucose onto the
non-reducing end of a glycogen chain
d. Glycogen Branching Enzyme forms the ɑ1-6 glycosidic bonds necessary to form
branches
e. All of the above are necessary steps in glycogen synthesis

b. PP1 must deactivate Glycogen Synthase

Insuline - RTK - PP1 - activate glycogen synthase

15. Which of the following pairs of scenarios and metabolic outcomes are incorrect?
a. Kevin has just eaten a bowl of chili and has fallen asleep at his desk: Glycogen
synthase will be active.
b. Dwight is running from a bear: Epinephrine will activate phosphorylase b kinase
c. Stanley is on a fasting diet and has decided to take the stairs: His hepatocytes
(liver cells) will be releasing Glucose-6-phosphate through GLUT 2
d. Michael is running a race: Glycogen phosphorylase will be active
e. All of the above pairings are correct

c. Stanley is on a fasting diet and has decided to take the stairs: His hepatocytes
(liver cells) will be releasing Glucose-6-phosphate through GLUT 2


G6P has to be converted to Glucose

16. Hemolytic anemia is a condition where RBCs are destroyed faster than they are
produced. As a result, patients with this condition most typically present with symptoms
of fatigue, dizziness, and jaundice. Which biochemical process is most likely deficient
allowing for this deleterious disease to occur?
a. Ketone body synthesis
b. Cholesterol synthesis
c. Pentose phosphate pathway
d. Glutathione peroxidase pathway
e. None of the above

c. Pentose phosphate pathway

It is important to note that the enzymatic activity of glutathione
peroxidase which converts peroxide to water is because of the reducing equivalents
produced by the pentose phosphate pathway

17. Karen is a renowned biochemist from the esteemed Ramachandran Academy. After
receiving her degree with honors, she and her high school sweetheart Carl Wheezer
moved to the suburbs to raise a family. Shortly then after, Karen caught Carl in an act of
infidelity, where she then devised a sinister scheme to murder Carl without being caught.
She synthesized a small molecule possessing an aromatic nitrogenous ring that is
glycosidically bonded to a sugar molecule, mimicking NAD+. This molecule covalently
binds to the E3 component of the pyruvate dehydrogenase complex blocking the
movement of electrons; and as a result, Carl dies 5 hours later after it was fed to him.
What would most likely show on the toxicology report?
a. Oxidized lipoyllysine
b. High concentrations of acetyl-CoA
c. High concentration of NAD+
d. High concentrations of pyruvate
e. Two of the above

c. High concentration of NAD+
d. High concentrations of pyruvate

This question is very complex and it questions how well you
know this pathway forwards and backwards. First, you have to note that since it blocks
the reduction of NAD+, answer C is correct. Now, we have to look at this process going
in the reverse. Since you are not able to reoxidize FADH2, you are not able to reoxidize
the reduced lipoyllysine, making answer A incorrect. Since the E2 component is
compromised, that means acetyl-CoA would not be readily produced, making answer B
incorrect. Finally, since the E2 activity is compromised, the E1 activity will be
compromised as well, leading to a build-up of pyruvate and making answer D correct.

18. A patient who possesses the condition of chronic alcoholism typically also possess
vitamin deficiencies such as, thiamine. This is because the alcohol results in
inflammation of the stomach lining preventing the uptake of critical vitamins. Which of
the following would NOT be one of the effects on the pyruvate dehydrogenase complex
due to this deficiency?
a. Increased levels of acetyl-CoA
b. Decreased levels of acetyl-CoA
c. Less NADH present for the ETC
d. Higher concentration of pyruvate
e. None of the above

a. Increased levels of acetyl-CoA

If TPP is not readily available,
the product of acetyl-CoA will be slowed down, FADH2 will not be produced as quickly,
and the pyruvate levels will still rise.

. After this biochemistry exam, you and your friends decided to celebrate your two weeks
of freedom before the next exam by going on a Wawa run. You buy a deliciously high
calorie milkshake and a greasy quesadilla. You all head back to your apartment to feast
and watch a movie. What is the metabolic state of your liver?
a. Insulin is bound to liver receptors
b. Epinephrine binds to the livers receptors
c. Glucagon is released
d. Glycogen synthase is inactive
e. A and D

a. Insulin is bound to liver receptors

under a high energy state (mass
quantities of food put into the system) insulin binds to the liver and signals the body to
bring in this energy source through the transporters.

20. Which biosynthetic pathway(s) DOES NOT require reducing equivalents of NADPH?
a. Steroid synthesis
b. Fatty acid synthesis
c. Pyruvate dehydrogenase complex
d. Maintaining glutathione in its reduced state
e. Cholesterol synthesis

c. Pyruvate dehydrogenase complex

21. Identify the citric acid cycle intermediate below and the enzyme that produces it.
a. Succinate, succinyl-CoA synthase
b. Citrate, citrate synthase
c. α-ketoglutarate, α-ketoglutarate dehydrogenase
d. Succinate, succinate synthetase
e. None of the above are correct

None of the above

It is succinate, and the enzyme that produces it is succinyl-coA synthethase that uses a GDP + PI first substrate-level phosphorylation

22. The α-ketoglutarate dehydrogenase complex is mechanistically similar to the pyruvate
dehydrogenase complex that produces an important precursor to the citric acid cycle.
Which of the following is NOT a similarity between these two complexes?
a. Both are inactivated by phosphorylation
b. Both require NAD+ as a reactant
c. Both produce CO2 as a byproduct
d. Both are activated by Calcium in muscle cells
e. All of the above are correct similarities

a. Both are inactivated by phosphorylation

alpha-KG is not inactivated by phosphorylation

23. Succinate dehydrogenase deficiency is a rare genetic disorder that can result in severe
neurological and/or muscular degeneration. How many of the following would you
expect to occur in an individual with this disorder?
I. Increased cellular concentration of FAD
II. Decreased proton pumping of the ETC complex II
III. Decreased cellular concentration of malate
IV. Decreased cellular concentration of ATP
a. 1
b. 2
c. 3
d. All of the above would occur
e. None of the above would occur

I. Increased cellular concentration of FAD
III. Decreased cellular concentration of malate
IV. Decreased cellular concentration of ATP

24. List the following steps of the citric acid cycle in the correct order:
Substrate-level phosphorylation, formation of cis-aconitate, production of FADH2, Claisen
ester condensation
a. Claisen ester condensation, formation of cis-aconitate, production of FADH2,
substrate level phosphorylation
b. Substrate-level phosphorylation, formation of cis-aconitate, production of
FADH2, Claisen ester condensation
c. Claisen ester condensation, substrate level phosphorylation, formation of
cis-aconitate, production of FADH2
d. Claisen ester condensation, formation of cis-aconitate, substrate level
phosphorylation, production of FADH2
e. None of the above are the correct order

d. Claisen ester condensation, formation of cis-aconitate, substrate level
phosphorylation, production of FADH2

25. Lab tests that you run on a patient reveal an extremely low ratio of NADH/NAD+ in their
body. Which of the following enzymes would you expect to be inhibited?
a. Isocitrate dehydrogenase
b. Succinate dehydrogenase
c. Citrate synthase
d. Fumarase
e. More than one of the above is correct

a. Isocitrate dehydrogenase

26. Sarah is learning about the electron transport chain in her biochemistry class. More
specifically, she is learning about how succinate is converted to ubiquinone in Complex
II. Which of the following are TRUE regarding Complex II of the electron transport
chain?
I. FAD is used as the coenzyme
II. Protons are pumped into the intermembrane space
III. Q is oxidized
a. I, II and III
b. II and III
c. I and III
d. I only
e. III only

d. I only

27. You are currently working in a laboratory in the Chemistry department at the University
of Florida. In this laboratory you are working with the diester derivative of malonic acid
known as dimethyl malonate. Dimethyl malonate is responsible for inhibiting succinate
dehydrogenase. If succinate dehydrogenase is inhibited, what complex in the electron
transport chain would be also be inhibited?
a. Complex I
b. Complex II
c. Complex III
d. Complex IV
e. None of the above

b. Complex II

28. Which of the following is NOT associated with Complex III?
a. FAD
b. Succinate
c. Cytochrome C
d. Iron Sulfur centers
e. Two of the above

a. FAD
b. Succinate

29. Researchers use a variety of inhibitors in order to determine the sequence of electron
carriers. For example, researchers would use various inhibitors to see which compounds
in specific complexes would fail to reduce. Which of the following CORRECTLY
matches the inhibitor to the complex it inhibits?
a. Carbon monoxide inhibits Complex III
b. Rotenone inhibits Complex I
c. Antimycin A inhibits Complex IV
d. Cyanide inhibits Complex II
e. Both A and B are correct

b. Rotenone inhibits Complex I

30. Fatal neonatal lactic acidosis is a mitochondrial disease and it can be described as a
metabolic defect present in infants that ultimately results in their death. Fatal neonatal
lactic acidosis can be caused by an abnormality in complex III of the electron transport
chain. Which of the following would be an example of an abnormality in complex III of
the electron transport chain?
a. Electrons are transferred from ubiquinol to cytochrome c
b. 3 protons are pumped out per pair of electrons
c. Electrons are passed through the cytochromes via iron potassium centers
d. None of the answers are correct
e. Both B and C are correct

b. 3 protons are pumped out per pair of electrons
c. Electrons are passed through the cytochromes via iron potassium centers


4 protons are pumped
and it is iron sulfur centers

31. In the experiment proving Electron transport and ATP synthesis were coupled, what was
the reason for adding succinate into the experiment?
a. Uncoupler
b. ATP synthase inhibitor
c. Source of electrons
d. Mitochondria stabilizer
e. None of the above, NADH was used instead

c. Source of electrons

32. A rare mutation has been found for the gene encoding the b-subunits for ATP synthase.
This mutation has caused the b-subunits to misfold and work incorrectly. Assuming ATP
synthase were to still be assembled, what would most likely happen to ATP synthase as a
direct consequence?
a. Protons would no longer be able to bind to ATP synthase
b. The F1 and F0 complexes of ATP synthase would be loosely held together
c. The F1 complex would be unable to rotate properly
d. Protons would be unable to travel towards the F1 complex
e. ADP & Pi would no longer be able to be transported into the mitochondria

b. The F1 and F0 complexes of ATP synthase would be loosely held together

33. Which of the following statements is TRUE regarding oxidative phosphorylation?
a. Phosphate groups are brought into the intermembrane space via a
proton/phosphate symporter
b. The F1 complex of ATP synthase is embedded within the inner membrane of the
mitochondria
c. ATP is formed within mitochondrial matrix and is shuttled into the intermembrane
space by an antiporter
d. 𝛼-subunits of the F1 complex are where ADP & Pi groups bind
e. There are two distinct forms of the 𝛽-subunit in ATP synthase, an empty
conformation and full conformation

c. ATP is formed within mitochondrial matrix and is shuttled into the intermembrane
space by an antiporter

34. James has been found to have a rare condition in which his succinyl-CoA synthetase
enzymes are overactive (think back to the TCA cycle). What would most likely happen as
a direct result of his condition?
a. The rest of the TCA cycle enzymes would be upregulated in order to compensate
b. Glycolysis enzymes would be upregulated in order to provide more substrate for
the PDH complex
c. Increased succinyl-CoA levels would inhibit the 𝛼-ketoglutarate dehydrogenase
complex
d. Due to increased ATP levels, overall cellular respiration enzymes would be
downregulated
e. None of the above would occur

d. Due to increased ATP levels, overall cellular respiration enzymes would be
downregulated

35. Rigoberto read the results on the experiment proving how oxidation and phosphorylation
are coupled and decided to replicate the experiment himself. He adds ADP & Pi along
with succinate in a beaker with intact mitochondria to start. After a couple of minutes,
Rigoberto adds CN-
. Finally, after a couple more minutes he adds DNP to the reaction
beaker. What would be seen on the reaction graph after DNP is added in this scenario?
a. Both oxygen consumption and ATP levels would remain plateaued
b. Once DNP is added, ATP consumption would remain plateaued and O2
consumption would begin to increase once more
c. Once DNP is added, both ATP and O2
levels would begin to increase again
d. Once DNP is added, O2 consumption would remain plateaued and ATP
consumption would begin to increase once more
e. None of the above are true

a. Both oxygen consumption and ATP levels would remain plateaued

36. A triacylglycerol (TAG) is an ester derived from glycerol and three fatty acids. TAGs are
the main constituents of body fat in humans and other vertebrates. Why are
triacylglycerols stored over carbohydrates?
a. Triacylglycerols do not raise the osmolarity of the cytosol
b. Without storing triacylglycerols, cholesterol biosynthesis would not occur
c. Carbohydrate storage would directly diminish the rate of electron flow
d. TAGs provide 70% of the daily energy requirement
e. None of the above

a. Triacylglycerols do not raise the osmolarity of the cytosol

37. Adipocyte lipolysis encompasses the hydrolysis of triacylglycerols (TAG) and release of
fatty acids for use as an energy source by other tissues such as the heart and skeletal
muscle. The regulation of adipocyte lipolysis is an intricate balance of signaling cascades
to release fatty acids during times of energy need. Which of the following steps regarding
fatty acid release from adipocytes is in the correct order?
1. Hormone- sensitive lipase is activated by phosphorylation
2. Subsequent steps release free fatty acids and glycerol
3. Perilipin undergoes conformational change and allows access to
HSL
4. Protein Kinase A is activated
5. Glucagon binds to receptors on adipocytes
a. 5,4,2,3,1
b. 4,5,3,1,2
c. 5,4,1,3,2
d. 1,3,4,2,5
e. 1,3,5,4,2

c. 5,4,1,3,2

38. An important component of Triacylglycerol Catabolism involves the transports of TAGs.
Fats that are acquired through diet are mobilized in chylomicrons. What else is TRUE
about TAG transport?
a. Chylomicrons move from the tissues to the bloodstream
b. Bile salts emulsify the fats in the small intestine and form micelles
c. Lipoprotein lipase converts TAGs to fatty acids and glycerol
d. TAGS are taken up by the intestinal mucosa and converted into fatty acids to be
incorporated in chylomicrons
e. Two of the above are correct

a. Chylomicrons move from the tissues to the bloodstream
c. Lipoprotein lipase converts TAGs to fatty acids and glycerol

39. Beta-oxidation is the catabolic process by which fatty acid molecules are broken down to
generate acetyl-CoA, which enters the citric acid cycle, and NADH and FADH2
, which
are coenzymes used in the electron transport chain. Which of the following is NOT a step
in B-oxidation?
a. Oxidation resulting in FADH2
b. Thiolase catalyzing cleavage into Acyl-CoA and Acetyl-CoA
c. Dehydration of Acyl-Coa to produce a double bond
d. Addition of water to introduce a hydroxyl group
e. None of the above

c. Dehydration of Acyl-Coa to produce a double bond

40. If Myristoyl-CoA (a 14-carbon fatty acid) were to undergo Beta oxidation, what would
the total number of electron carriers, net gain of water, and total number of Acetyl Coas
be at the end?
a. 10,5,6
b. 12,6,7
c. 14,7,8
d. There is not enough information to determine how many Acetyl-Coas will be in
the final product
e. 16,8,9

b. 12,6,7

41. Diabetic ketoacidosis (DKA) is a serious complication of diabetes that can be
life-threatening. DKA develops when your body doesn't have enough insulin to allow
blood sugar into your cells for use as energy. Instead, ketone bodies are produced to
supply the body with energy; however, very high levels of ketone bodies makes the blood
acidic in the body. What compound leads to high production of ketone bodies in the body
if it is unused in other metabolic pathways?
a. Pyruvate
b. Oxaloacetate
c. Acetyl-CoA
d. Citrate
e. NADPH

c. Acetyl-CoA

2. In the synthesis of fatty acids, what role does the energy carrier NADPH play?
a. NADPH makes the transfer of malonyl-CoA to the acyl carrier protein (ACP) a
favorable process
b. NADPH reduces the alkene in the trans-Butenoyl-ACP molecule to an alkane
c. NADPH reduces the 𝛃-keto group on the 𝛃-ketobutyryl-ACP molecule, setting the
fatty acid for a dehydration reaction
d. Both B and C
e. All of the above

b. NADPH reduces the alkene in the trans-Butenoyl-ACP molecule to an alkane
c. NADPH reduces the 𝛃-keto group on the 𝛃-ketobutyryl-ACP molecule, setting the
fatty acid for a dehydration reaction

43. A new genetic disease results in the mutation of the acetyl-CoA carboxylase so that
acetyl-CoA no longer forms a working enzyme-substrate complex. As a result, there is a
lack of production of malonyl-CoA. What is most likely the impact of this mutation on
fatty acid synthesis and beta-oxidation activity?
a. Beta oxidation activity increases; fatty acid synthesis activity decreases
b. Beta oxidation activity decreases; fatty acid synthesis activity decreases
c. Beta oxidation activity increases; fatty acid synthesis activity increases
d. Beta oxidation activity decreases; fatty acid synthesis activity increases
e. The acetyl-CoA carboxylase enzyme has no impact on fatty acid metabolism

a. Beta oxidation activity increases; fatty acid synthesis activity decreases

44. Which of the following concerning the acetyl-CoA carboxylase (ACC) enzyme is
FALSE?
a. The reaction requires a biotin coenzyme
b. ACC is allosterically regulated by citrate levels
c. ACC is phosphorylated by both PKA and AMPK
d. The main reaction of ACC is to create acetyl-CoA from HCO3
- and malonyl-CoA
e. None of the above

d. The main reaction of ACC is to create acetyl-CoA from HCO3
- and malonyl-CoA

ACC and HCO3 produce malanoyl-coA

45. Mike was considering going on a low-carb diet in an effort to lose weight quicker for his
crazy beach bod. Which of the following statements are likely to occur due to his new
diet strategy?
I. Synthesis by acetyl-CoA carboxylase decreases
II. Synthesis by fatty acid synthase decreases
III. Carnitine acyltransferase I activity decreases
IV. The concentration of ketone bodies overall decrease
a. I and II
b. II and III
c. I and IV
d. III and IV
e. I, II, III, and IV

I. Synthesis by acetyl-CoA carboxylase decreases
II. Synthesis by fatty acid synthase decreases


low caloric intake - glucagon - phosphorylated

ACC is inactive when phosphorylated

46. One morning you wake up for class and realize that you’ve woken up an hour early! As a
result, you take the chance to relax and make a large pancake breakfast; you’re in no rush
to get to class, and your stomach is full. Following your relaxing morning, the hormone
_____ is released, which would ______ HMG-CoA Reductase by ________ it.
a. Glucagon, inhibit, dephosphorylating
b. Insulin, inhibit, phosphorylating
c. Glucagon, inhibit, phosphorylating
d. Insulin, stimulate, dephosphorylating
e. Epinephrine, stimulate, phosphorylating

d. Insulin, stimulate, dephosphorylating

47. Vitamin D₃ is necessary for the regulation of calcium uptake in the intestine and calcium
levels in kidney and bone. Deficiencies in Vitamin D₃ could potentially lead to the
development of Rickets, a condition which affects bone formation. Vitamin D₃ is derived
from which of the following essential molecules?
a. Cholesterol
b. Steroid hormones
c. Cholesterol esters
d. Glycerophospholipids
e. Sphingolipids

a. Cholesterol

48. Cholesterol biosynthesis is an intricate and important life-sustaining process that begins
with acetyl-CoA. Of the following, which is/are intermediate(s) of this biosynthetic
pathway?
i. Squalene
ii. Mevalonate
iii. Carnitine
iv. Palmitoyl-CoA
a. ii only
b. i and iii
c. i and ii
d. iii and iv
e. i, ii, and iii

i. Squalene
ii. Mevalonate

49. After performing a blood test on a patient, a physician finds that their blood contains a
very low amount of triacylglycerols. An insufficiency of which plasma lipoprotein would
the doctor most likely believe to be the culprit of this triacylglycerol deficiency?
a. Hemoglobin
b. VLDL
c. HDL
d. LDL
e. Chylomicrons

e. Chylomicrons

50. Plasma lipoproteins are molecules that our cells use for assistance in transporting lipids.
These molecules help differentiate the targets of specific lipids, and also grant lipids the
ability to exist in aqueous environments. The endogenous pathway utilizes the function of
plasma lipoproteins to carry out its goal of transporting triacylglycerols and cholesterol to
peripheral tissues. Which plasma lipoprotein(s) are most involved in the endogenous
pathway?
i. VLDL
ii. LDL
iii. HDL
iv. Chylomicrons
a. i only
b. i and ii
c. i and iii
d. i, ii, and iv
e. i, ii, and iii

i. VLDL
ii. LDL