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NS103 Spring 2007
Midterm Exam 3 (5 pages, 100 pts)
I.(2.5 pts each for 30 pts total) Choose the SINGLE best answer to each of the following questions:
1. In the urea cycle, nitrogen enters the cycle via the molecule ___________, and exits the cycle as
__________, while carbon exits the cycle via ____________.
A. Ornithine, arginine, fumarate
B. Carbamoyl phosphate, ammonia, CO2
C. Ammonia, urea, fumarate
D. Carbamoyl phosphate, urea, fumarate
E. Ornithine, urea, CO2
2. What combination of reactions is required to correctly synthesize arachadonic acid (20:4) from linoleic
acid (18:2)?
A. Two desaturation steps and two elongation steps
B. Two desaturation steps and one elongation step
C. One elongation step and three desaturation steps
D. One desaturation step and one elongation step
E. Two elongation steps and one desaturation step
3. In which physiological condition is there most likely to be positive nitrogen balance?
A. Wasting disease
B. Positive energy balance
C. Pregnancy
D. Starvation
E. Infection
4. Which statement is true about protein turnover?
A. Increased transamination can create a negative nitrogen balance.
B. Elevated creatinine levels in blood is indicative of positive nitrogen balance
C. Increased activity of PALP would produce a harmful excess of ammonia
D. Growth hormone and testosterone together increase protein degradation
E. Elevated protein turnover would be associated with elevated levels of carbamoyl phosphate
5. Which enzyme catalyzes key nitrogen incorporation reactions?
A. Glutamate dehydrogenase
B. Aspartate aminotransferase
C. Glutaminase
D. Alanine aminotransferase
E. Asparaginase
6. Which of the following statements is true about the pentose phosphate pathway?
A. The pathway produces fructose-5-phosphate that is used for nucleic acid biosynthesis
B. Reducing equivalents are produced to be used for oxidative phosphorylation
C. The pentose phosphate pathway requires riboflavin as a cofactor
D. The pentose phosphate pathway is an anapleurotic salvage pathway
E. NADPH equivalents from the pentose phosphate pathway are required for cholesterol synthesis
Pg 1 of 6
NS103 Spring 2007
Midterm Exam 3 (5 pages, 100 pts)
7. What is the correct order for the PALP ping-pong reaction?
A. Schiff base formation, amine transfer to PALP, amine transfer to ketoacid, amino acid enters
PALP binding site, amino acid accepts nitrogen
B. Amino acid enters PALP binding site, Schiff base formation, amine transfer to ketoacid, amino
acid leaves PALP binding site
C. Schiff base formation, amino acid enters PALP binding site, amine transfer to PALP, amine
transfer to ketoacid, amino acid leaves PALP binding site
D. Schiff base formation, amine transfer to PALP, amino acid enters PALP binding site, amine
transfer to ketoacid, amino acid leaves PALP binding site
E. Amino acid enters PALP binding site, amine transfer to PALP, amine transfer to ketoacid, amino
acid accepts nitrogen, Schiff base formation, amino acid leaves PALP binding site
8. Biotin is a required coenzyme for which metabolic step?
A. PEPCK’s conversion of oxaloacetate to phosphoenolpyruvate
B. Pyruvate carboxylase’s conversion of pyruvate to oxaloacetate
C. Pyruvate dehydrogenase’s coversion of lactate to pyruvate
D. Glucose-6-phosphatase’s conversion of glucose 6-P to glucose
E. Pyruvate kinase’s conversion of phophoenolpyruvate to pyruvate
9. What is rate limiting of the urea cycle?
A. Availability of ornithine
B. Activity of arginase
C. Transfer of citrate from the mitochondria
D. Availability of carbamoyl phosphate
E. Activity of arginosuccinase
10. Which desaturases are not present in mammalian cells?
A. 5, 9, 12
B. 9, 12
C. 9, 12, 15
D. 5, 6
E. 12, 15
11. Which of the following steps in -oxidation are regulated?
A. Uptake of free fatty acids into the mitochondria
B. Activation of free fatty acids in the mitochondria
C. The oxidation of a fatty acid into in metabolic products
D. Uptake of free fatty acids into the cell from the blood
E. Transport of free fatty acids in the blood
12. Which of the following reactions does not require pyridoxine as a cofactor?
A. Racemization
B. Transamination
C. Deamidation
D. Dehydration
E. Decarboxylation
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NS103 Spring 2007
Midterm Exam 3 (5 pages, 100 pts)
II.(25 pts) Fill in the blanks or circle the correct emboldened choices:
1. The role of 5-phosphoribosyl-1-pyrophosphate (PRPP) in the transamidation of amino acids is to
accept a nitrogen group.
2. The cellular site of fatty acid synthesis is the _cytosol_. In order to initiate fatty acid synthesis, a
supply of _acetyl-CoA__ is needed to make malonyl-CoA to elongate _acetyl-ACP_ to make free fatty
acids. This supply of starting material is transferred to the cellular site of fatty acid synthesis in the form
of _citrate_ coming primarily from the _TCA__ cycle in the _mitochondria__ (subcellular
3. Ketone body biogenesis and cholesterol synthesis are related in that they share the metabolic
intermediate, _HMG-CoA/acetoacetyl-CoA_, and utilize _acetyl-CoA__ as a substrate for their
biogenesis. The synthetic pathway for ketone bodies takes place in the __mitochondria__ (subcellular
compartment), while cholesterol is synthesized in the __cytosol_ (subcellular compartment).
4. Ketone bodies can pass readily through external cell membranes.
5. How many malonyl-CoA molecules are required to produce a 16 carbon palmitate via fatty acid
synthesis? ____7______.
If, on the other hand, a 16C palmitate molecule is -oxidized, how many acetyl-CoA molecules will be
produced? ____8________. Each cycle of -oxidation produces a single acetyl-CoA, _____1_____ (a
number) FADH2 molecule(s), and _____1______ (a number) NADH molecule(s).
6. Amino nitrogen is transported out of muscle primarily in the form of what two amino acids?
__alanine_____ and __glutamine______.
7. In the __fasted or starving__ metabolic condition, amino acid catabolism generates glucogenic and
ketogenic carbon backbones that can be used to produce energy directly via __ketone body synthesis__
and __TCA cycle/oxidative phosphorylation_ or indirectly via gluconeogenesis.
8. Two tissues where fatty acid synthesis takes place are _liver_ and _adipose_(also accept lactating
mammary gland)
9. The rate-limiting enzyme for cholesterol biogenesis is __ HMG-CoA reductase___.
10. The enzyme responsible for activating free fatty acids for -oxidation is __Acyl CoA synthetase_.
III.(7 pts) Match each answer from the right column with one answer from the left column
A. Cyclic AMP
__F__ Stimulates protein kinase C
B. Phosphoenolpyruvate
__E__ The metabolic precursor of IP3
C. Isoprenoid
__A__ Stimulates protein kinase A
D. Glucagon
__B__ Has cytosolic and mitochondrial synthetic pathways within
E. Phosphatidyl inositol
__C__ Intermediate in cholesterol synthesis
F. Diacyglycerol
__G__ Provides reducing equivalents for gluconeogenesis
G. Lactate
__D__ Binds to a G-protein receptor
Pg 3 of 6
NS103 Spring 2007
Midterm Exam 3 (5 pages, 100 pts)
IV. (4 pts) Complete the analogy by filling in the blank with the appropriate response:
1. Pyruvate is to Alanine as -Ketoglutarate is to __Glutamate__
2. Phosphofructokinase-1 is to Fructose-1,6-Bisphosphatase as Hexokinase is to Glucose-6phosphatase_
3. Marasmus is to inadequate protein and energy as Kwashiorkor is to ___inadequate protein intake_
4. Ketogenic amino acids are to ketone bodies as mevalonate is to __ cholesterol_
IV.(34 pts) Provide short answers to the following questions:
1. (6pts) Describe 2 reactions that can be used to remove the nitrogens from an asparagine molecule. List
the names of the substrates, products and enzymes for each and classify them as a deamination,
deamidation, transamination or transamidation (structures are not necessary).
Asparagine  Aspartate + NH3 via the enzyme aspariginase (DEAMIDATION)
Aspartate  Oxaloacetate via the enzyme aspartate amino-transferase (TRANSAMINATION)
Also accepted was: Asparagine + PRPP  Aspartate + 5-Phospho ribosylamine
(TRANSAMIDATION) even though this is likely not a legitimate reaction in vivo the correct
thinking was aceepted as correct
2. (4 pts) Name one anabolic and one catabolic hormone produced by the body. For one of them explain a
mechanism whereby its action has the ability to alter lean body mass.
Anabolic – insulin, growth hormone, testosterone (among others)
Catabolic – glucagon, glucocorticoides, cytokines (among others)
Anabolic hormones will positively affect lean body mass whereas catabolic hormones will decrease
lean body mass
3. (3 pts) What is the rate-limiting enzyme for fatty acid synthesis? Describe the reaction that this enzyme
catalyzes, and name one allosteric activator or inhibitor of the enzyme.
Acetyl-CoA Carboxylase
Acetyl-CoA + HCO3-  Malonyl-CoA (Biotin is a necessary cofactor)
(requires the utilization of 1 mol of ATP per mol of malonyl-CoA produced ATP  ADP + Pi)
Allosteric activator: citrate Allosteric inhibitor: long chain acyl CoA’s
Note: Insulin is also an activator of ACC and AMPK and glucagon are inhibitors but they are not
allosteric inhibitors/activators.
4. (3 pts) What are 2 compounds that provide a link between the urea cycle and citric acid cycle. Decribe
how these compounds can intercoverted to be used in the two cycles.
Fumarate and Oxaloacetate
Fumarate is directly released from the urea cycle as a metabolic product and can be utilized as an
intermediate in TCA cycle (although there is a transport step involved since fumarate from urea
cycle is released to cytosol whereas fumarate entering the TCAC would need to be in the
Oxalacetate can be aminated to make aspartate which is used in urea cycle to convert citrulline to
arginosuccinate whereas OAA is directly used a a primary TCA intermediate
Pg 4 of 6
NS103 Spring 2007
Midterm Exam 3 (5 pages, 100 pts)
5. (4 pts) In the spaces provided, indicate the number of carbons in the corresponding molecules.
2 C Acetyl-CoA
6. (2 pts) How does this diagram help to describe why acetyl-CoA produced from amino acid degradation
or -oxidation cannot be utilized to make net glucose via gluconeogenesis?
Acetyl-CoA cannot be used to make glucose via gluconeogenesis because it will deplete the TCA
cycle of oxaloacetate and thus slow or stop the flux generating ability of the TCA cycle. The
fundamental reason is because of a carbon shortage (due to carbon loss from production of CO2 in
exchange for energetic molecule production) coming from the incoming acetyl-CoA substrate
which requires terminal utilization of oxaloacetate to meet the carbon needs of gluconeogenesis.
7. (6 pts) Describe the process by which palmitoyl-CoA outside the mitochondria makes it way into the
mitochondrial matrix. Name the transporters involved, any cofactors that are required and any products
that are produced in the process.
See lecture 13,14 slide 42 for diagram
Palmitate  Palmitoyl CoA which binds carnitine palmitoyl transferase-1 (CPT1). CPT1 transfers
the long chain acyl group from CoA to carnitine, releasing free CoA. Palmitoyl-carnitine enters the
intermembrane space.
Carnitine-acylcarnitine translocase (CAT) translocates palmitoylcarnitine through the inner
mitochondrial membrane into the mitochondrial matrix in exchange for a free carnitine molecule
from the matrix. Once on the matrix side of the membrane, CPTII replaces the carnitine group for
a CoA molecule, and this free carnitine molecule becomes available for CAT for another round of
Cofactors: CoA, Carnitine, (CPT 1 is inhibited by malonyl CoA), ATP to generate palmitoyl CoA
initially (but wasn’t required for full credit)
Transporters: CPT1, CPTII, and CAT
8. (6 pts) Some of the energetic ketone bodies do not contain chemical ketone groups. What is it about
their metabolism that, despite their chemistry, makes their name relevant? Knowing what you know
about diabetes propose a reason why type I diabetics are at risk for ketoacidosis.
The name ketone bodies is relevant to their biochemical processing because some of the ketone
bodies do in fact contain ketone groups while others, via an accessory pathway, get metabolized into
ketones (particularly acetone). A type I diabetic is at risk for ketoacidosis because in the lack on
insulin to take up glucose from the blood the body senses an energy shortage and produces ketone
bodies from protein and fatty acid catabolism to provide metabolic fuel for the brain and other
Pg 5 of 6
NS103 Spring 2007
Midterm Exam 3 (5 pages, 100 pts)
glucose dependent tissues. The buildup of ketone body biogenesis byproducts (such as acetone) and
the high concentration of ketone bodies in the blood can then lower blood pH to cause ketoacidosis.
Pg 6 of 6

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