Biochem Evals 8 Set G

SUBJECT: BIOCHEMISTRY TOPIC: EVALS 8 SET G LECTURER: DR. UY DATE: MARCH 2011 item answer number a

1

c

explanation 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

c

phosphoenolpyruvate is a substrate of glycolysis but cannot be formed from glycerol

d

pyruvate is already the end product of glycolysis; nonetheless, it cannot be formed form glycerol

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

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 better answer because this attacks the storage capacity of the brain and not quite its dependency on glucose (basta better answer ung A)

b

there 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

2

b

3

UDP 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)

c

in Embden-Meyerhoff pathway (glycolysis), the products are pyruvate (aerobic) or lactate (anaerobic)

d

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

c 4

5

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

d

it starts with g6p and ends with g6p so we cannot really say there has been 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 primary substrate of non-oxidative reaction in PPP a

BIOCHEMISTRY: Evaluations 8 (set G)

part of the oxidative reaction Page 1

d

6

d 7

b

product of the first reaction in the non-oxidative reaction through the enzyme isomerase

d

product of the first reaction in the non-oxidative reaction through the enzyme epimerase

isomerase is utilized in the reaction of ribulose5phosphate to ribose5phosphate a

3-epimerase in utilized in the reaction of ribulose5phosphate to xylulose5phosphate

b

transaldolase 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

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

8

b

combinations of enzymes are faulty; other enzymes are not involved in the 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 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

a

9

10

11

c

inappropriate combination

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 of GSSG b

there 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 it’s 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

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

c

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

b 12

13

b

these substrates are not common among the 2 pathways

these enzymes are not involved in the production of vit C

xylulose5phosphate 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

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

BIOCHEMISTRY: Evaluations 8 (set G)

these enzymes are not affected by F26BP Page 2

14

a

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

a

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

glycogenesis doesn’t involve synthesis of a protein primer though it is a used 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

d

this can also be an answer however this only describes the branching mechanism of the pathway

15

c 16

abd c

17

c

18

d 19

d 20

fructose must first be phosphorylated before its metabolism enzymes are found in the middle of the pathway so they are not really in the INITIAL REACTION of fructose metabolism

glycogenolysis 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

d

g6pase is used in the cleavage of phosphate in G6P at the end of 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 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 :( ) 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 doesn’t 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)

the 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

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 abc

BIOCHEMISTRY: Evaluations 8 (set G)

all of which are products of non-reversible reactions which cannot be considered as a committed step Page 3

d 21

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 abc

22

d

all of which are not bifunctional and only regulates either of the pathways 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 mitochondria 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

23

c

glucose is first phosphorylated before metabolized abd

d 24

25

basta hindi ito :) all of which happens after phosphorylation of glucose

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 pyruvate carboxylase is a enzyme for gluconeogenesis which is activated in starvation state not in a high glucose environment

c

abd 26

d

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

not true. Haha

d 27

28

all reactions are involved in glycolysis a

no enolization

b

no mutarotation

c

no tautomerization

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 :)

b

glucokinase 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

29

a

glucokinase has a high km

cd

PFK1 is not regulated by allosterically

b 30

all of which are precursors of gluconeogenesis a

leucine is ketogenic

cd

fatty 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

BIOCHEMISTRY: Evaluations 8 (set G)

Page 4

c 34

d

35

36

42 43-44 45

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 promoted in increased levels of insulin 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 1,3bisphosphoglycerate which is converted to 2,3BPG. This product competes with oxygen in binding to hemoglobin a

acetyl 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 be metabolized and there are available enzymes which can utilize it so its accumulation is least likely

b

FRUCTOSE..YUM! I couldn’t elaborate more :) Joke lang :)

c

fructose 1,6 bisphosphatase is inhibited by F26BP

37

38-41

a

a

synthesis is induced by cAMP

b

synthesis is inhibited during starvation

d

synthesis is induced by fasting

NOT INCLUDED IN THE COVERAGE OF BIOCHEM COMPREHENSIVE EXAM :) *ENDOCRINE PART* 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

NOT INCLUDED IN THE COVERAGE OF BIOCHEM COMPREHENSIVE EXAM :) *ENDOCRINE PART* 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

46

a

losing the allosteric site for ATP in phosphofuctokinase renders it immune to 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

c

reactions from ribose5phosphate generates a lot of products however only F6P and G3P can enter glycolysis

BIOCHEMISTRY: Evaluations 8 (set G)

Page 5

49

d

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

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

b

aldose reductase converts glucose to sorbitol

51

c 52

53

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 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 promotes 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

a

pyruvate carboxylase utilizes the cofactor biotin in a key step in synthesizing glucose from pyruvate

a

the 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

54

55-70

seen in starved state; lowers levels of F26BP

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 PART*

71

a

since the conversion of pyruvate to OXAA is catalyzed by pyruvate carboxylase it consumes carbon dioxide (it's in the name ;))

72

b

also the enzyme pyruvate carboxylase requires biotin as its cofactor for optimal activity

73

b

remember 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

d

conversion of OXAA to phosphoenolpyruvate also releases carbon dioxide as a by product

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

a

in fed state, there is increased insulin:glucagon ration therefore increasing glycolytic activity

76

79-88

NOT INCLUDED IN THE COVERAGE OF BIOCHEM COMPREHENSIVE EXAM :) *ENDOCRINE PART*

BIOCHEMISTRY: Evaluations 8 (set G)

Page 6

89

c

in 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

b

in 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

b

in 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

d

in using sucrose, you can metabolize 2 sugars: fructose + glucose. Fructose yields to 2 ATP and Glucose yields to 2ATP. So 2+2=4 :)

94

a

hemolysis 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

c

cataract 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

d

Cori'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

===========================END OF TRANSCRIPTION=========================== OOOOOOOOOOOOOOOOOOOOOOOMMMMMMMMMMMMMMMMMMMMMMGGGGGGGGGGGGGGGGGGGGG LAST NA TO. AS IN TOTOO NA TALAGA NA LAST NA TO!!! SUUUMMMMMMMMEEEEEERRRRR NA!!!

BIOCHEMISTRY: Evaluations 8 (set G)

Page 7