SUBJECT: BIOCHEMISTRY

TOPIC: EVALS 8 SET G

LECTURER: DR. UY

DATE: MARCH 2011

item
answer explanation
number
TAG can be catalyzed to form 3 FFA and glycerol. When glycerol is oxidized it can
form glyceraldehyde or dihydroxyacetone which can be phosphorylated into
a
glyceraldehyde -3-phosphate or dihydoxyacetonephosphate which then is a
substrate in glycolysis
acetaldehyde a product of pyruvate decarboxylation (outside of the
1 b glycolytic pathway) to form ethanol with the enzyme pyruvate
decarboxyalase and cofactor thiamine
phosphoenolpyruvate is a substrate of glycolysis but cannot be formed
c
from glycerol
pyruvate is already the end product of glycolysis; nonetheless, it cannot be
d
formed form glycerol
c the brain is highly dependent on the circulating glucose for its energy generation
in the first place, the brain doesn’t have the capacity to store fuel (only
liver and muscle stores glycogen). Pwede rin sya kaya lang letter c is a
a
better answer because this attacks the storage capacity of the brain and not
quite its dependency on glucose (basta better answer ung A)
2
there is no block in the transport of glucose in the brain since, we all know,
b
that the brain depends greatly on glucose for energy
since the brain nga needs glucose, even at a very low concentration as such
d in hypoglycemia, the brain can still utilize glucose, so this choice is unlikely
to be considered
UDP glucoronates which is conjugated with bilirubin for excretion and L-ascorbate
b
(vitamin C) are synthesized in the uronic pathway
in citric acid cycle (TCA cycle), glucoronates and L-ascorbates are not
a generated (its primary goal is to produce energy in forms of ATP,
3 NADH,FADH etc)
in Embden-Meyerhoff pathway (glycolysis), the products are pyruvate
c
(aerobic) or lactate (anaerobic)
d in Cori's cycle, the main product is glucose (gluconeogenesis)
c it is the main producer of NADPH+H
a it allowed conversion of different monosaccharides other than triose
4 b it supplies RIBOSE PHOSPHATES to for nucleic acid synthesis
it starts with g6p and ends with g6p so we cannot really say there has been
d
a breakdown but there were conversions along the pathway
ribulose 5 phosphate is the end product of the oxidative reaction in the PPP and the
c
5 primary substrate of non-oxidative reaction in PPP
a part of the oxidative reaction

BIOCHEMISTRY: Evaluations 8 (set G) Page 1

 product of the first reaction in the non-oxidative reaction through the
b
enzyme isomerase
product of the first reaction in the non-oxidative reaction through the
d
enzyme epimerase
d isomerase is utilized in the reaction of ribulose5phosphate to ribose5phosphate
3-epimerase in utilized in the reaction of ribulose5phosphate to
a
xylulose5phosphate

6 transaldolase is used in the transfer of 3 carbons to form

b
fructose6phosphate and erythrose4phosphate
transketolase is used in the transfer of 2 carbons to form
c sedoheptulose7phosphate and glygeraldehyde3phosphate,
fructiose6phosphate and glyceraldehyde3phosphate
transketolase and transaldolase are responsible for interconversions of 3-,4-,5-,6-
d ,7-carbon sugars throug transfer of carbon groups (remember the prefix TRANS for
7 transfer haha wala lang :) )
combinations of enzymes are faulty; other enzymes are not involved in the
abc
interconversions
G6PDH is inhibited by high conc of NADPH though negative feedback; by high GSH
because high GSH (glutathione in sulfhydryl form) means that GSSG (glutathione in
disulfide form) has already been converted to GSH with the help of NADPH--this
b
8 signifies that a lot of NADPH has been produced; high palmitoyl CoA signifies that
there was an increase production of NADPH, this NADPH was used for synthesis of
Fatty acid such as palmitoyl coA
acd inappropriate combination
without G6PDH there is a decreased production of NADPH which is needed to
a convert GSSG to GSH; so with the deficiency in G6PDH there is an accumulation of
GSSG
there is an increase in H2O2 since glutathione is at its GSSG form which
b
9 cannot reduce the H2O2
NADPH keeps the Fe at hemoglobin at Fe2+; with it’s the deficiency in
c G6PDH Fe2+ is converted to Fe3+ which cannot bind to oxygen blah blah
blah
d there is a low concentration of GSH in the absence of NADPH
c L-xylulose5phosphate are both substrate of uronic acid pathway and HMP shunt
10
abd these substrates are not common among the 2 pathways
L-gluconolactone oxidase in needed for the production of Vit C. this enzyme is
c
11 deficient in humans
abd these enzymes are not involved in the production of vit C
xylulose5phosphate cannot be converted to xylitol(uronic pathway) in the event of
b
essential pentosuria so it is excreted in the urine
12 a it is the product of the inhibited reaction in the event of pentosuria
no information was gathered that pointed to an effect of pentosuria on
cd
these molecules
glucagon decreases the production of fructose2,6bisphosphate which is a potent
b inhibitor of fructose1,6bisphosphatase; therefore it cannot inhibit the action of
13 f16bp thus promote gluconeogenesis
acd these enzymes are not affected by F26BP

BIOCHEMISTRY: Evaluations 8 (set G) Page 2

 gluconeogenesis is an energy requiring pathway and in the action of PEPCK it
a utilizes GTP as a source of phosphate to be transferred to OXAA to produce
14 Phosphoenolpyruvate
bcd not used by the enzyme (ayaw nya eh, bakit ba?!? Haha joke lang :| )
in glycogenesis, UDP-glc is added to the NON-REDUCING end of a small glycogen
a
molecule this is applicable in both elongation (linear) and branching of the chain
glycogenesis doesn’t involve synthesis of a protein primer though it is a
b
used to start the process
15 though this can be an answer, letter A choice discussed how the elongation
c happens; in addition amylopectin chains are linear and glycogenesis
involves both elongation in a linear pattern and branching pattern
this can also be an answer however this only describes the branching
d
mechanism of the pathway
c fructose must first be phosphorylated before its metabolism
16 enzymes are found in the middle of the pathway so they are not really in
abd
the INITIAL REACTION of fructose metabolism
glycogenolysis is the removal of glucose residues in glycogen and in order to do this
c
the enzyme glycogen phosphorylase is used.
a glycogen synthase is used in glycogenesis
17
b hexokinase is used in phosphorylation of glucose
g6pase is used in the cleavage of phosphate in G6P at the end of
d
glycogenolysis
the formation of NADH in glycolysis is a source of energy. In the event of low
oxygen concentration such as in exercise, NADH is utilized by lactated
dehydrogenase to form lactate from pyruvate. This decreases the source of energy
c
of muscles since NADH is equivalent to 3ATPs; thus, less energy generated, more
prone to fatigue (disclaimer: not sure if this is really the explanation but
nonetheless it makes sense so...you could look it up if you want. sorry :( )
in exercise, energy is utilized and exhausted but then, ATP is produced in a
normal rate. ATP can be exhausted but this may not be primarily the cause
18 a
of muscle fatigue, it contributes though (hindi kasi ito ung answer sa
answer key eh :) hahaha joke :)
sodium-potassium imbalance doesn’t contribute to the energy production
b pathways so there might not be a connection with these ions and fatigue
(not sure)
accumulation of ADP is not directly correlated to energy utilization (haha
d not sure.sorry ulit. Nevermind this na lang, di naman ito ang sagot eh :)
haha)
the reaction that links glycolysis to TCA cycle is: pyruvate (glycolysis) to Acetyl CoA
d
(TCA cycle) through the enzyme pyruvate dehydrogenase
19 a enzyme in TCA cycle
b link between TCA and gluconeogenesis
c enzyme in TCA cycle
there are 3 irreversible steps in glycolysis. They are catalyzed by (1) glucose kinase,
d (2) phosphofructokinase (3)pyruvate kinase. The committed step is the reaction
20 catalyzed by PFK1 which produces fructose 1,6 bisphosphate
all of which are products of non-reversible reactions which cannot be
abc
considered as a committed step

BIOCHEMISTRY: Evaluations 8 (set G) Page 3

 phosphofructokinase2 is a bifuctional enzyme(PFK2-FBP2 complex) which alter the
concentration of F26BP (an increase in F26BP promotes PFK1, increase rate of
d
glycolysis; a decrease in F26BP lifts the inhibition on F16BPase, increase rate of
21 gluconeogenesis
all of which are not bifunctional and only regulates either of the pathways
abc
not both
1 mole of glyceraldehyde3phosphate yeilds to 1 mole of pyruvate and in the
process produces 2 moles of ATP; however in RBCs there is an absence of
d mitochondria thus it the metabolism of glucose ends in glycolysis. Since glycolysis
22 alone is an anaerobic pathway, pyruvate is converted to lactate. so, all in all the
products are 2 ATP and 1 lactate
abc basta hindi ito :)
c glucose is first phosphorylated before metabolized
23
abd all of which happens after phosphorylation of glucose
pyruvic acid is the end product of glycolysis in an aerobic condition because the
d conversion of pyruvate into the substrate of TCA cycle inhibits its conversion to
lactated
24
a lactic acid is produced in an anaerobic environment
bc not products of glycolysis
pyruvate carboxylase is a enzyme for gluconeogenesis which is activated in
c
25 starvation state not in a high glucose environment
abd these enzymes are anabolic in nature. These are activated in fed state
muscle glycogen doesn’t have g6pase so it cannot release glucose in blood, so
d
26 glucose reserves in muscle can only be ulitized by the muscle itself (SELFISH!!)
abc not true. Haha
d all reactions are involved in glycolysis
a no enolization
27
b no mutarotation
c no tautomerization
since the question asks for which requires ATP, first thing to consider is KINASE.
Then since 2 lang naman yung kinase pili na lang kayo haha joke lang. pyruvate
28 b
kinase is in glycolysis so it is not the answer. It should be phosphoglycerate kinase
which is an enzyme of gluconeogenesis which is the one asked for in the question :)
glucokinase is used to phosphorylate glucose in the liver. With its high km, at low
b
conventration of glucose such as in hypoglycemia, glucose cannot be utilized
29
a glucokinase has a high km
cd PFK1 is not regulated by allosterically
b all of which are precursors of gluconeogenesis
a leucine is ketogenic
30
fatty acid when oxidized (unless it is odd numbered--in form of proprionyl
cd
CoA) cannot produce glucose
in the absence of G6Pase, G6P cannot be converted to glucose to be released in
31 b blood so G6P will find another way for it to be metabolized and one pathway which
utilizes G6P is HMP. Increased levels of G6P will induce HMP
32 c transketolase perform optimally with the help of vitamin B1 (thiamine)
33 d pyruvate kinase is inactivated when phosphorylated

BIOCHEMISTRY: Evaluations 8 (set G) Page 4

 a active when phosphorylated
b not allosterically regulated, just activated by cAMP
c active when phosphorylated
insulin (produced in fed state) promotes anabolism. So glycogen synthase activity is
c
promoted in increased levels of insulin
34
ab these are produced in starved states
d glycogen synthase in inhibited in starved state
when pyruvate kinase is deficient, substrate before the reaction tends to
accumulate and look for other pathways to go to. One of which is
d
1,3bisphosphoglycerate which is converted to 2,3BPG. This product competes with
oxygen in binding to hemoglobin
acetyl coa is produced form pyruvate but pyruvate production is inhibited
35 a
in the set up. So there is no accumulation of acetyl coa
b since pyruvate kinase is inhibited there is no production of pyruvate
glucose should have entered the pathway because it needs to be
c metabolized and there are available enzymes which can utilize it so its
accumulation is least likely
36 b FRUCTOSE..YUM! I couldn’t elaborate more :) Joke lang :)
c fructose 1,6 bisphosphatase is inhibited by F26BP
a synthesis is induced by cAMP
37
b synthesis is inhibited during starvation
d synthesis is induced by fasting
NOT INCLUDED IN THE COVERAGE OF BIOCHEM COMPREHENSIVE EXAM :) *ENDOCRINE
38-41
PART*
galactose is phosphorylated by galactokinase to produce galactose1phosphate.
42 d Then, it is converted to glucose1phosphate by coupling with UDPglc which then
produces UDPgal. G1P is the converted to G6P then it enters glycolysis
NOT INCLUDED IN THE COVERAGE OF BIOCHEM COMPREHENSIVE EXAM :) *ENDOCRINE
43-44
PART*
45 a amylopectin is a linear chain composed of glucose residues linked by a1->4 linkage
d fructose 1,6 bisphosphatase has no effect in pyruvate kinase
losing the allosteric site for ATP in phosphofuctokinase renders it immune
a to ATP meaning ATP cannot inhibit its activity therefore rate of glycolysis
increases

46 losing the allosteric site for citrate in phosphofuctokinase renders it

b immune to citrate meaning citrate cannot inhibit its activity therefore rate
of glycolysis increases
losing the phosphatase domain of phosphofructokinase-2 increases the
c production of F26BP which increases PFK1 activity which increases rate of
glycolysis
PPP is the only source of carbon dioxide in the cytoplasm. So liberation of carbon
47 c dioxided is seen when there is much NADPH is required meaning there is a drive
for PPP
reactions from ribose5phosphate generates a lot of products however only F6P and
48 c
G3P can enter glycolysis

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 fructose26bisphosphate is synthesized in fed state meaning increased
d glucagon:insulin ratio (increased insulin, decreased FBP2 activity, increased PFK2
49 activity). This is observed just after the consumption of a large bowl of ice cream
abc seen in starved state; lowers levels of F26BP
during exercise there is an increased rate of glycolysis therefore increasing
50 a NADH/NAD ratio. NADH is utilized by lactate dehydrogenase to form lactate to
pyruvate
b aldose reductase converts glucose to sorbitol
51 a sorbitol dehydrogenase converts sorbitol to fructiose
cd not mentioned at all
fasting for 12 hours would promote glycogenolysis. When glycogen phosphorylase
is phosphorylated, the enzyme is rendered active thus, glycogenolysis occur. When
c
pyruvate kinase and glycogen synthase are phosphorylated they are rendered to be
inactive this inhibiting glycolysis and glycogenesis and promoting glycogenolysis
52 a gluconeogenesis is not activated until 24 hours of fasting
adenylate cyclase is activated by the presence of glucagon which promotes
b
gluconeogenesis and this doesn’t happen until 24 hrs of fasting
d glycogen synthas is activated in fed state which is not the case in the given
pyruvate carboxylase utilizes the cofactor biotin in a key step in synthesizing
53 a
glucose from pyruvate
the km of glucokinase is high and it is above the fasting concentration of glucose in
a
blood; thus in fasting, glucose cannot be efficiently phosphorylated in the liver
54 b glucokinase is found only in the liver
c its activity is inhibited by F26BP since it favors the binding of GK to GKRP
d it is less sensitive to inhibition of g6p
NOT INCLUDED IN THE COVERAGE OF BIOCHEM COMPREHENSIVE EXAM :) *ENDOCRINE
55-70
PART*
since the conversion of pyruvate to OXAA is catalyzed by pyruvate carboxylase it
71 a
consumes carbon dioxide (it's in the name ;))
also the enzyme pyruvate carboxylase requires biotin as its cofactor for optimal
72 b
activity
remember the malate-aspartate shuttle? Oxaloacetate takes up NADH and forms
73 b
malate to be able to cross the mitochondrial membrane
74 c once inside the mitochondroa, malate gives off NADH and forms OXAA
conversion of OXAA to phosphoenolpyruvate also releases carbon dioxide as a by
75 d
product
increased ATP means, there is no more need for generation of ATP therefore
76 b inhibition of glycolysis. On the other hand, gluconeogenesis requires high levels of
ATP to produce glucose so increased ATP promotes gluconeogenesis
increased F26BP increases the activity if PFK1 thus increases rate of glycolysis. On
77 a the other hand, high levels of F26BP inhibits the activity of F1,6BPase this
inhibiting gluconeogenesis
in fed state, there is increased insulin:glucagon ration therefore increasing
78 a
glycolytic activity
NOT INCLUDED IN THE COVERAGE OF BIOCHEM COMPREHENSIVE EXAM :) *ENDOCRINE
79-88
PART*

BIOCHEMISTRY: Evaluations 8 (set G) Page 6

 in using G6P as substrate, 1 ATP is utilized by PFK; 4 ATPs are produced by (2
89 c
from) phosphoglycerate kinase and (2 from) pyruvate kinase. So -1 +4 =3
in using DHAP as substrate, no ATP is utilized, 1 ATP is generated from
90 b
Phosphoglycerate kinase and another from pyruvate kinase. So, +1 +1 = 2
in using G3P as substrate, no ATP is utilized, 1 ATP is generated from
91 b
Phosphoglycerate kinase and another from pyruvate kinase. So, +1 +1 = 2
in using fructose as substrate, 1 ATP is used by hexokinase; 1ATP is used by PFK;
92 b 4ATPs are produced: 2 from phosphoglycerate kinase and 2 fro) pyruvate kinase.
So -2 +4 =2
in using sucrose, you can metabolize 2 sugars: fructose + glucose. Fructose yields to
93 d
2 ATP and Glucose yields to 2ATP. So 2+2=4 :)
hemolysis indicates a defect in the PPP since NADPH is not utilized to protect RBCs
94 a
from lysis. So we can conclude that this is a deficiency in G6PDH
cataract formation can be associated with accumulation of galactose (galactosemia)
95 c
due to deficiency in galactokinase
96 b galactose1phosphate uridyltransferase deficiency leads to severe liver disease
deficiency in fructokinase means there is no formation of F1P and instead, fructose
will be enter the glycolytic pathway though F6P via hexokinase activity. F6P is can
97 d be used both in glycolysis and gluconeogenesis. If glyconeogenesis is favored then
there can be increased glucose level which can manifest in increased glucose levels
in urine
Cori's disease is caused by a defect in the debranching enzyme (glucosyl 4:6
98 d
transferase) Thus, glycogen accumulates. This manifests as liver disease.
Anderson's disease on the other hand is a deficiency in the branching enzyme
99 b resulting to accumulation of glycogen with long outer chains but the branches
contains only few glucose molecules
McAdle's disease is caused by the deficiency of skeletal muscle glycogen
100 c phosphorylase; thus, there is an accumulation of glycogen in skeletal muscle but not
in liver. This results to muscle cramps and weakness

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