biochem evals 8 set g

8/7/2019 Biochem Evals 8 Set G

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BIOCHEMISTRY: Evaluations 8 (set G) Page 1

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numberanswer explanation

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a

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

glyceraldehyde -3-phosphate or dihydoxyacetonephosphate which then is a

substrate in glycolysis

b

acetaldehyde a product of pyruvate decarboxylation (outside of the

glycolytic pathway) to form ethanol with the enzyme pyruvate

decarboxyalase and cofactor thiamine

cphosphoenolpyruvate is a substrate of glycolysis but cannot be formed

from glycerol

dpyruvate is already the end product of glycolysis; nonetheless, it cannot be

formed form glycerol

2

c the brain is highly dependent on the circulating glucose for its energy generation

a

in the first place, the brain doesnt have the capacity to store fuel (only

liver and muscle stores glycogen). Pwede rin sya kaya lang letter c is a

better answer because this attacks the storage capacity of the brain and not

quite its dependency on glucose (basta better answer ung A)

bthere is no block in the transport of glucose in the brain since, we all know,

that the brain depends greatly on glucose for energy

d

since the brain nga needs glucose, even at a very low concentration as such

in hypoglycemia, the brain can still utilize glucose, so this choice is unlikely

to be considered

3

bUDP glucoronates which is conjugated with bilirubin for excretion and L-ascorbate

(vitamin C) are synthesized in the uronic pathway

a

in citric acid cycle (TCA cycle), glucoronates and L-ascorbates are not

generated (its primary goal is to produce energy in forms of ATP,NADH,FADH etc)

cin Embden-Meyerhoff pathway (glycolysis), the products are pyruvate

(aerobic) or lactate (anaerobic)

d in Cori's cycle, the main product is glucose (gluconeogenesis)

4

c it is the main producer of NADPH+H

a it allowed conversion of different monosaccharides other than triose

b it supplies RIBOSE PHOSPHATES to for nucleic acid synthesis

dit starts with g6p and ends with g6p so we cannot really say there has been

a breakdown but there were conversions along the pathway

5c

ribulose 5 phosphate is the end product of the oxidative reaction in the PPP and the

primary substrate of non-oxidative reaction in PPP

a part of the oxidative reaction

SUBJECT: BIOCHEMISTRYTOPIC: EVALS 8 SET GLECTURER: DR. UYDATE: MARCH 2011


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bproduct of the first reaction in the non-oxidative reaction through the

enzyme isomerase

dproduct of the first reaction in the non-oxidative reaction through the

enzyme epimerase

6

d isomerase is utilized in the reaction of ribulose5phosphate to ribose5phosphate

a3-epimerase in utilized in the reaction of ribulose5phosphate to

xylulose5phosphate

btransaldolase is used in the transfer of 3 carbons to form

fructose6phosphate and erythrose4phosphate

c

transketolase is used in the transfer of 2 carbons to form

sedoheptulose7phosphate and glygeraldehyde3phosphate,

fructiose6phosphate and glyceraldehyde3phosphate

7

d

transketolase and transaldolase are responsible for interconversions of 3-,4-,5-,6-

,7-carbon sugars throug transfer of carbon groups (remember the prefix TRANS for

transfer haha wala lang :) )

abc combinations of enzymes are faulty; other enzymes are not involved in theinterconversions

8b

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

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

9

a

without G6PDH there is a decreased production of NADPH which is needed to

convert GSSG to GSH; so with the deficiency in G6PDH there is an accumulation ofGSSG

bthere is an increase in H2O2 since glutathione is at its GSSG form which

cannot reduce the H2O2

c

NADPH keeps the Fe at hemoglobin at Fe2+; with its the deficiency in

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

10

c L-xylulose5phosphate are both substrate of uronic acid pathway and HMP shunt

abd these substrates are not common among the 2 pathways

11c

L-gluconolactone oxidase in needed for the production of Vit C. this enzyme is

deficient in humans

abd these enzymes are not involved in the production of vit C

12

bxylulose5phosphate cannot be converted to xylitol(uronic pathway) in the event of

essential pentosuria so it is excreted in the urine

a it is the product of the inhibited reaction in the event of pentosuria

cd

no information was gathered that pointed to an effect of pentosuria on

these molecules

13b

glucagon decreases the production of fructose2,6bisphosphate which is a potent

inhibitor of fructose1,6bisphosphatase; therefore it cannot inhibit the action of

f16bp thus promote gluconeogenesis

acd these enzymes are not affected by F26BP


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14a

gluconeogenesis is an energy requiring pathway and in the action of PEPCK it

utilizes GTP as a source of phosphate to be transferred to OXAA to produce

Phosphoenolpyruvate

bcd not used by the enzyme (ayaw nya eh, bakit ba?!? Haha joke lang :| )

15

ain glycogenesis, UDP-glc is added to the NON-REDUCING end of a small glycogen

molecule this is applicable in both elongation (linear) and branching of the chain

b glycogenesis doesnt involve synthesis of a protein primer though it is aused to start the process

c

though this can be an answer, letter A choice discussed how the elongation

happens; in addition amylopectin chains are linear and glycogenesis

involves both elongation in a linear pattern and branching pattern

dthis can also be an answer however this only describes the branching

mechanism of the pathway

16

c fructose must first be phosphorylated before its metabolism

abdenzymes are found in the middle of the pathway so they are not really in

the INITIAL REACTION of fructose metabolism

17

cglycogenolysis is the removal of glucose residues in glycogen and in order to do this

the enzyme glycogen phosphorylase is used.

a glycogen synthase is used in glycogenesis

b hexokinase is used in phosphorylation of glucose

dg6pase is used in the cleavage of phosphate in G6P at the end of

glycogenolysis

18

c

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 energyof 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 :( )

a

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

of muscle fatigue, it contributes though (hindi kasi ito ung answer sa

answer key eh :) hahaha joke :)

b

sodium-potassium imbalance doesnt contribute to the energy production

pathways so there might not be a connection with these ions and fatigue

(not sure)

d

accumulation of ADP is not directly correlated to energy utilization (haha

not sure.sorry ulit. Nevermind this na lang, di naman ito ang sagot eh :)

haha)

19

dthe reaction that links glycolysis to TCA cycle is: pyruvate (glycolysis) to Acetyl CoA

(TCA cycle) through the enzyme pyruvate dehydrogenase

a enzyme in TCA cycle

b link between TCA and gluconeogenesis

c enzyme in TCA cycle

20

d

there are 3 irreversible steps in glycolysis. They are catalyzed by (1) glucose kinase,

(2) phosphofructokinase (3)pyruvate kinase. The committed step is the reaction

catalyzed by PFK1 which produces fructose 1,6 bisphosphate

abcall of which are products of non-reversible reactions which cannot be

considered as a committed step


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21

d

phosphofructokinase2 is a bifuctional enzyme(PFK2-FBP2 complex) which alter the

concentration of F26BP (an increase in F26BP promotes PFK1, increase rate of

glycolysis; a decrease in F26BP lifts the inhibition on F16BPase, increase rate of

gluconeogenesis

abcall of which are not bifunctional and only regulates either of the pathways

not both

22d

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 ofmitochondria thus it the metabolism of glucose ends in glycolysis. Since glycolysis

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 :)

23c glucose is first phosphorylated before metabolized

abd all of which happens after phosphorylation of glucose

24

d

pyruvic acid is the end product of glycolysis in an aerobic condition because the

conversion of pyruvate into the substrate of TCA cycle inhibits its conversion to

lactated

a lactic acid is produced in an anaerobic environment

bc not products of glycolysis

25c

pyruvate carboxylase is a enzyme for gluconeogenesis which is activated in

starvation state not in a high glucose environment

abd these enzymes are anabolic in nature. These are activated in fed state

26d

muscle glycogen doesnt have g6pase so it cannot release glucose in blood, so

glucose reserves in muscle can only be ulitized by the muscle itself (SELFISH!!)

abc not true. Haha

27

d all reactions are involved in glycolysis

a no enolization

b no mutarotation

c no tautomerization

28 b

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

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 :)

29

bglucokinase is used to phosphorylate glucose in the liver. With its high km, at low

conventration of glucose such as in hypoglycemia, glucose cannot be utilized

a glucokinase has a high km

cd PFK1 is not regulated by allosterically

30

b all of which are precursors of gluconeogenesis

a leucine is ketogenic

cdfatty acid when oxidized (unless it is odd numbered--in form of proprionyl

CoA) cannot produce glucose

31 b

in the absence of G6Pase, G6P cannot be converted to glucose to be released in

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


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a active when phosphorylated

b not allosterically regulated, just activated by cAMP

c active when phosphorylated

34

cinsulin (produced in fed state) promotes anabolism. So glycogen synthase activity is

promoted in increased levels of insulin

ab these are produced in starved states

d glycogen synthase in inhibited in starved state

35

d

when pyruvate kinase is deficient, substrate before the reaction tends to

accumulate and look for other pathways to go to. One of which is

1,3bisphosphoglycerate which is converted to 2,3BPG. This product competes with

oxygen in binding to hemoglobin

aacetyl coa is produced form pyruvate but pyruvate production is inhibited

in the set up. So there is no accumulation of acetyl coa

b since pyruvate kinase is inhibited there is no production of pyruvate

c glucose should have entered the pathway because it needs to bemetabolized and there are available enzymes which can utilize it so its

accumulation is least likely

36 b FRUCTOSE..YUM! I couldnt elaborate more :) Joke lang :)

37

c fructose 1,6 bisphosphatase is inhibited by F26BP

a synthesis is induced by cAMP

b synthesis is inhibited during starvation

d synthesis is induced by fasting

38-41NOT INCLUDED IN THE COVERAGE OF BIOCHEM COMPREHENSIVE EXAM :) *ENDOCRINE

PART*

42 d

galactose is phosphorylated by galactokinase to produce galactose1phosphate.

Then, it is converted to glucose1phosphate by coupling with UDPglc which then

produces UDPgal. G1P is the converted to G6P then it enters glycolysis


PART*

45 a amylopectin is a linear chain composed of glucose residues linked by a1->4 linkage

46

d fructose 1,6 bisphosphatase has no effect in pyruvate kinase

alosing the allosteric site for ATP in phosphofuctokinase renders it immuneto ATP meaning ATP cannot inhibit its activity therefore rate of glycolysis

increases

b

losing the allosteric site for citrate in phosphofuctokinase renders it

immune to citrate meaning citrate cannot inhibit its activity therefore rate

of glycolysis increases

c

losing the phosphatase domain of phosphofructokinase-2 increases the

production of F26BP which increases PFK1 activity which increases rate of

glycolysis

47 c

PPP is the only source of carbon dioxide in the cytoplasm. So liberation of carbon

dioxided is seen when there is much NADPH is required meaning there is a drive

for PPP

48 creactions from ribose5phosphate generates a lot of products however only F6P and

G3P can enter glycolysis


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49d

fructose26bisphosphate is synthesized in fed state meaning increased

glucagon:insulin ratio (increased insulin, decreased FBP2 activity, increased PFK2

activity). This is observed just after the consumption of a large bowl of ice cream

abc seen in starved state; lowers levels of F26BP

50 a

during exercise there is an increased rate of glycolysis therefore increasing

NADH/NAD ratio. NADH is utilized by lactate dehydrogenase to form lactate to

pyruvate

51

b aldose reductase converts glucose to sorbitol

a sorbitol dehydrogenase converts sorbitol to fructiose

cd not mentioned at all

52

c

fasting for 12 hours would promote glycogenolysis. When glycogen phosphorylase

is phosphorylated, the enzyme is rendered active thus, glycogenolysis occur. When

pyruvate kinase and glycogen synthase are phosphorylated they are rendered to be

inactive this inhibiting glycolysis and glycogenesis and promoting glycogenolysis

a gluconeogenesis is not activated until 24 hours of fasting

b adenylate cyclase is activated by the presence of glucagon which promotesgluconeogenesis and this doesnt happen until 24 hrs of fasting

d glycogen synthas is activated in fed state which is not the case in the given

53 apyruvate carboxylase utilizes the cofactor biotin in a key step in synthesizing

glucose from pyruvate

54

athe km of glucokinase is high and it is above the fasting concentration of glucose in

blood; thus in fasting, glucose cannot be efficiently phosphorylated in the liver

b glucokinase is found only in the liver

c its activity is inhibited by F26BP since it favors the binding of GK to GKRPd it is less sensitive to inhibition of g6p


PART*

71 asince the conversion of pyruvate to OXAA is catalyzed by pyruvate carboxylase it

consumes carbon dioxide (it's in the name ;))

72 balso the enzyme pyruvate carboxylase requires biotin as its cofactor for optimal

activity

73 bremember the malate-aspartate shuttle? Oxaloacetate takes up NADH and forms

malate to be able to cross the mitochondrial membrane

74 c once inside the mitochondroa, malate gives off NADH and forms OXAA

75 dconversion of OXAA to phosphoenolpyruvate also releases carbon dioxide as a by

product

76 b

increased ATP means, there is no more need for generation of ATP therefore

inhibition of glycolysis. On the other hand, gluconeogenesis requires high levels of

ATP to produce glucose so increased ATP promotes gluconeogenesis

77 a

increased F26BP increases the activity if PFK1 thus increases rate of glycolysis. On

the other hand, high levels of F26BP inhibits the activity of F1,6BPase this

inhibiting gluconeogenesis

78 ain fed state, there is increased insulin:glucagon ration therefore increasing

glycolytic activity


PART*


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89 cin using G6P as substrate, 1 ATP is utilized by PFK; 4 ATPs are produced by (2

from) phosphoglycerate kinase and (2 from) pyruvate kinase. So -1 +4 =3

90 bin using DHAP as substrate, no ATP is utilized, 1 ATP is generated from

Phosphoglycerate kinase and another from pyruvate kinase. So, +1 +1 = 2

91 bin using G3P as substrate, no ATP is utilized, 1 ATP is generated from

Phosphoglycerate kinase and another from pyruvate kinase. So, +1 +1 = 2

92 b in using fructose as substrate, 1 ATP is used by hexokinase; 1ATP is used by PFK;4ATPs are produced: 2 from phosphoglycerate kinase and 2 fro) pyruvate kinase.

So -2 +4 =2

93 din using sucrose, you can metabolize 2 sugars: fructose + glucose. Fructose yields to

2 ATP and Glucose yields to 2ATP. So 2+2=4 :)

94 ahemolysis indicates a defect in the PPP since NADPH is not utilized to protect RBCs

from lysis. So we can conclude that this is a deficiency in G6PDH

95 ccataract formation can be associated with accumulation of galactose (galactosemia)

due to deficiency in galactokinase

96 b galactose1phosphate uridyltransferase deficiency leads to severe liver disease

97 d

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

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

98 dCori's disease is caused by a defect in the debranching enzyme (glucosyl 4:6

transferase) Thus, glycogen accumulates. This manifests as liver disease.

99 b

Anderson's disease on the other hand is a deficiency in the branching enzyme

resulting to accumulation of glycogen with long outer chains but the branches

contains only few glucose molecules

100 c

McAdle's disease is caused by the deficiency of skeletal muscle glycogen

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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biochem evals 8 set g

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