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x M1 Biochem Quiz 1 > Lectures 1-6 > Flashcards

Lectures 1-6 Flashcards

1
Q

4 functions of carbohydrates

A
  1. Metabolic fuel
  2. Components of DNA/RNA
  3. Components of proteins
  4. Cell wall structure in bacteria/plants
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2
Q

Carbohydrates are transported in blood in what form?

A

alpha-D-glucose (cyclic)

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3
Q

What is the storage form of glucose called?

A

Glycogen

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4
Q

2 ways glucose can be metabolized anaerobically

A
  1. glycolysis

2. pentose phosphate pathway

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5
Q

2 ways in which RBCs can metabolize glucose

A
  1. glycolysis
  2. pentose phosphate pathway
    (must be anaerobic)
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6
Q

glucose can be stored as glycogen in what parts of the body?

A
  1. liver

2. muscle

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7
Q

if glucose is metabolized aerobically, what is it metabolized to? what does this process require?

A

becomes CO2. requires that the cell use 02

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8
Q

liver cells have the special function of synthesizing what? from what starting materials?

A

can synthesize glucose, from lactic acid and some amino acids.

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9
Q

The 1-C of glucose is referred to what? why?

A

referred to as the reducing carbon, because it can be oxidized easily.

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10
Q

What is Benedicts reagent? What was it used for?

A

Used in past to measure ‘reducing sugar’ in urine. Benedicts reagent contains a blue salt that turns red in the presence of 1-C of glucose. 1-C is oxidized, Benedicts is reduced.

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11
Q

If glucose is oxidized at C-1, what will it become?

A

Gluconic acid

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12
Q

If glucose is oxidized at C-6, what will it become?

A

Glucuronic acid

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13
Q

What causes cataracts in diabetes?

A

Accumulation of sorbitol in the lens, since the lens lacks sorbitol dehydrogenase (glucose –> sorbitol –> fructose) and there is a lot of glucose around.

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14
Q

How is a glycosidic bond formed?

A

elimination of water between 2 sugar molecules

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15
Q

How is HbA1C formed?

A

Glucose in blood reacts with NH2 groups in hemoglobin.

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16
Q

What is HbA1C a measure of?

A

long-term glucose levels in blood.

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17
Q

Where is Sialic acid found?

A

Cell surface glycoproteins

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18
Q

what are glycosaminoglycans?

A

polysaccharides with carboxyl, sulfate and amino groups

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19
Q

What are proteoglycans?

A

proteins attached to glycosaminoglycans. Function as joint lubricants and structural components in connective tissue.

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20
Q

What type of glycosidic bonds can humans metabolize?

A

Can metabolize alpha-1,4 glycosidic bonds but not beta-1,4 glycosidic bonds. hence cannot digest cellulose.

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21
Q

Describe glycogen

A

storage form of glucose. Glucose molecules linked by alpha-1,4 and alpha-1,6 glycosidic bonds.

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22
Q

glycolysis is used to achieve what?

A

ATP production, pyruvate/lactate production.

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23
Q

the pentose phosphate pathway is used for what?

A

to create NADPH, ATP, and pentose

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24
Q

Glycogen synthesis is used to accomplish what?

A

storage of glucose

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25
Q

glycolysis: aerobic or anaerobic?

A

can be either

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26
Q

pentose phosphate pathway: aerobic or anaerobic?

A

anaerobic

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27
Q

citric acid cycle accomplishes what? aerobic or anaerobic?

A

recovers maximum amount of energy from carbohydrate. can convert glucose or lactate to CO2. requires oxygen.

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28
Q

Gluconeogenesis accomplishes what?

A

synthesis of glucose. allows liver to maintain constant blood glucose levels.

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29
Q

How is glucose trapped inside cells?

A

by phosphorylation

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30
Q

what cells have hexokinase?

A

all cells

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31
Q

what cells have glucokinase in addition to hexokinase?

A

liver, pancreatic cells

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32
Q

RBCs use what pathways to metabolize glucose?

A

glycolysis or pentose phosphate pathway

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33
Q

in RBCs, what happens to lactate and CO2?

A

exit the cell because they are not phosphorylated.

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34
Q

what are the 5 key enzymes in glycolysis?

A
  1. hexokinase/glucokinase
  2. phosphofructokinase
  3. glyceraldehyde-3P-dehydrogenase
  4. phosphoglycerokinase
  5. pyruvate kinase
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35
Q

What must be regenerated from NADH in order for glycolysis to proceed?

A

NAD+

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36
Q

Cells that have mitochondria can use O2 to regenerate NAD+ how?

A

by respiration

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37
Q

RBCs cannot use O2 for metabolism: why?

A

even though they are bathed in O2 they lack mitochondria

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38
Q

how do RBCs regenerate NAD+?

A

via lactate dehydrogenase (pyruvate –> lactate + NAD+)

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39
Q

RBCs constitutively form what from glucose?

A

lactate

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40
Q

when would muscle cells form lactate from glucose?

A

if deprived of O2

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41
Q

what does a kinase do in general?

A

phosphorylates a substrate

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42
Q

what do hexokinase/glucokinase do?

A

converts glucose into glucose-6P

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43
Q

how do the kinetic properties of hexokinase and glucokinase differ?

A

glucokinase in liver permits glucose uptake and glycogen synthesis at high blood glucose levels. glucokinase in pancreas functions as a blood glucose sensor. hexokinase reaches Vmax very quickly.

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44
Q

what happens to go from glucose-6P to fructose-6P? what enzyme catalyzes this reaction?

A

goes from an aldose to a ketose. enzyme = glucose phosphate isomerase.

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45
Q

what happens when fructose-6P goes to fructose-1,6-bisphosphate? what enzyme?

A

fructose-6P + ATP –> fructose-1,6-bisphosphate + ADP. enzyme is PFK-1. Not reversible. Main regulatory enzyme of glycolysis.

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46
Q

What activates PFK-1?

A

AMP, ADP, fructose-2,6-bisphosphate

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47
Q

What inhibits PFK-1?

A

ATP, citrate

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48
Q

How does glyceraldehyde-3P go to 1,3-bisphosphoglycerate? What enzyme/what is notable?

A

Enzyme is glyceraldehyde-3P dehydrogenase (GAPDH). Notable: the resulting molecule contains a high energy Acyl-P bond.

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49
Q

what will inhibit the GADPH reaction?

A

arsenate.

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50
Q

what enzyme catalyzes the reaction from 1,3-bisphosphoglycerate to 3-phosphoglycerate? what else results?

A

enzyme: phosphoglycerate kinase (named for reverse reaction). also yields ATP.

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51
Q

what enzyme catalyzes the reaction from phosphoenolpyruvate (PEP) to pyruvate? what else is produced?

A

enzyme: pyruvate kinase. also produces ATP.

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52
Q

what enzyme catalyzes the reaction from pyruvate to lactate? what else is produced?

A

lactate dehydrogenase (LDH). also produces NAD+ from NADH.

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53
Q

where does the equilibrium lie for the lactate dehydrogenase reaction?

A

far to the direction of lactate, which can then exit the cell.

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54
Q

what are the 2 isozymes of lactate?

A

H: occurs in heart. ideally suited to oxidize lactate (create pyruvate)
M: occurs in muscle, liver. ideal for reducing pyruvate (creating lactate)

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55
Q

how many ATPs are formed by glycolysis?

A

2 ATPs overall

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56
Q

what enzymes are the 3 main regulators of glycolysis?

A
  1. hexokinase
  2. PFK-1
  3. pyruvate kinase
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57
Q

which reaches Vmax more quickly: hexokinase or glucokinase?

A

hexokinase. reaches Vmax very quickly.

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58
Q

what inhibits hexokinase? does this inhibit glucokinase?

A

glucose-6P. does not inhibit glucokinase.

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59
Q

how is glucose metabolism coupled to insulin secretion?

A

glucokinase is not inhibited by glucose-6P, so the rate of glycolysis in pancreatic beta-cells tracks with blood glucose levels. the more ATP formed in pancreatic beta cells by glycolysis –> K+ channel closes –> depol –> Ca2+ channel opens –> Ca2+ rushes in –> insulin released.

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60
Q

what enzyme catalyzes Fructose-6P to Fructose 2,6-bisphosphate?

A

PFK-2.

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61
Q

What is special about PFK-2?

A

it is a bifunctional enzyme: in one direction a kinase, the other is a phosphatase. catalyzes formation and degradation of Fructose 2,6-bisphosphate.

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62
Q

what would be the effect if both the kinase and the phosphatase of PFK-2 work simultaneously?

A

would generate heat in a futile cycle. hence these two need regulation so that they work at different times.

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63
Q

what enzyme cleaves Fructose 1,6P in half to form two 3C molecules?

A

aldolase

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64
Q

the conversion of glucose to 1,3 bisphosphoglycerate requires the investment of how many ATP/glucose?

A

2 ATP/glucose.

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65
Q

RBCs synthesize what from 1,3 bisphosphoglycerate?

A

both 3-phosphoglycerate (like other cells) and 2,3 bisphosphoglycerate (BPG) which decreases oxygen affinity of hemoglobin.

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66
Q

What inhibits pyruvate kinase?

A

ATP. this is impt in skeletal muscle.

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67
Q

What are the 3 enzymes in glycolysis that exist as different isozymes?

A
  1. hexokinase/glucokinase
  2. pyruvate kinase
  3. lactate dehydrogenase
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68
Q

what activates pyruvate kinase in the liver?

A

liver isozyme of pyruvate kinase is activated by Fructose-1,6-P

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69
Q

What favors the formation of lactate from pyruvate in cells?

A

the exit of the product (lactate) from the cell, and the large negative free energy of the reaction.

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70
Q

how many different isozymes are there for lactate dehydrogenase?

A

there are 5.

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71
Q

what is the clinical significance of having an LDH isozyme that is specific to heart muscle?

A

to diagnose an MCI, can draw blood and test for the H4 (heart-specific) LDH isozyme.

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72
Q

in the absence of O2, what regenerates NAD and allows glycolysis to proceed?

A

LDH and the pyruvate -> lactate reaction.

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73
Q

Lactose is what 2 monosaccharides?

A

galactose + glucose

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74
Q

Sucrose is what 2 monosaccharides?

A

glucose + fructose

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75
Q

Maltose is what 2 monosaccharides?

A

2 glucose

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76
Q

What is lactose intolerance?

A

an acquired deficiency of lactase

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77
Q

what is galactosemia?

A

loss of uridyl transferase enzyme, causing galactol to accumulate

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78
Q

what is fructose intolerance?

A

loss of liver-specific aldolase causing Fructose-1P to accumulate

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79
Q

what is the most common enzymopathy?

A

G6PDH

80
Q

what do most G6PDH individuals experience?

A

usually asx

81
Q

what are the most common manifestations of G6PDH deficiency?

A

adult: hemolytic anemia
neonatal: jaundice

82
Q

what is the first enzyme in the pentose phosphate pathway?

A

G6PDH

83
Q

what is the importance of the first part of the pentose phosphate pathway/G6PDH?

A

forms NADPH

84
Q

why is NADPH important?

A

required to generate reduced glutathione (which protects RBCs against oxidative damage)

85
Q

what does the pentose phosphate pw form (3 things)?

A

ATP, pentoses, NADPH

86
Q

what can pentoses be converted to that is part of the glycolytic and gluconeogenic pws?

A

glyceraldehyde-3P

87
Q

what 2 things can glyceraldehyde-3P be converted to?

A
  1. glucose

2. lactate (via glycolysis)

88
Q

what is the only source of NAPDH in RBCs?

A

pentose phosphate pw

89
Q

can RBCs that are G6PDH deficient form ribose?

A

yes, the pentose reactions are reversible

90
Q

what tissues have high amounts of pentose phosphate pw activity?

A

adipose, liver, lactating mammary, adrenal cortex, thyroid, testis, RBCs

91
Q

what tissues have LOW amounts of pentose phosphate pw activity?

A

heart, skeletal muscle

92
Q

how are disaccharides converted to monosaccharides?

A

by enzymes on the surface of intestinal mucosal cells

93
Q

what causes fructose intolerance?

A

loss of liver-specific form of aldolase, which results in accumulation of Fructose-1P and depletion of ATP in liver cells

94
Q

what causes galactosemia?

A

the loss of a Galactose-1P uridyl transferase

95
Q

G6PDH deficiency results in the lack of what in RBCs?

A

NADPH and therefore glutathione reductase and therefore glutathione.

96
Q

Anabolic (constructive) pathways usually use what as a cofactor?

A

NADPH

97
Q

Catabolic (breakdown) pathways usually use what as a cofactor?

A

NAD+

98
Q

In the course of forming Ribose-5P, is NADPH created? ATP?

A

NADPH: Yes
ATP: No

99
Q

In the course of forming pentoses into glucose-6P, is NADPH created? ATP?

A

NADPH: Yes??
ATP: No

100
Q

The pentose phosphate pw is linked to glycolysis via what enzyme reactions?

A

transketolase and transaldolase

101
Q

In the course of forming pentoses to lactate via glycolysis, is NADPH created? ATP?

A

NADPH: Yes
ATP: Yes

102
Q

where is most fructose metabolized?

A

liver

103
Q

what does accumulation of Fructose-1P cause?

A

liver damage; depletion of P (and depletion of ATP); inhibition of glycogen phosphorylase (which catalyzes glycogen -> glucose-1P); hypoglycemia (because liver glycogen cannot be used to replace blood glucose)

104
Q

name 4 symptoms of lactose intolerance

A
  1. abdominal discomfort, cramps
  2. bloating
  3. increased urination (trying to release stomach contents)
  4. diarrhea
105
Q

What is the role of glutathione in RBCs?

A

protects from oxidative damage

106
Q

what is the result of oxidative damage in RBCs?

A

hemolysis –> anemia.

107
Q

What are Heinz bodies?

A

inclusions in RBCs comprised of denatured hemoglobin (could be due to oxidative damage)

108
Q

why does G6PDH deficiency only affect RBCs?

A

Other cells have alternate means/enzymes of forming NADPH.

109
Q

define gluconeogenesis

A

the synthesis of glucose from precursors other than glycogen

110
Q

where does gluconeogenesis primarily occur?

A

LIVER, sometimes kidney

111
Q

what does pyruvate dehydrogenase do?

A

converts pyruvate to Acetyl CoA and CO2 in the mitochondria.

112
Q

What does pyruvate dehydrogenase use as cofactors? (5 things)

A

TPP, Lipoic Acid, FAD, NAD, Coenzyme A

113
Q

what is pyruvate dehydrogenase’s composition?

A

composed of 3 enzymes (E1, E2, E3)

114
Q

3 fates of pyruvate, and the enzymes that catalyze those reactions?

A
  1. lactate (lactate dehydrogenase)
  2. CO2 and Acetyl CoA (pyruvate dehydrogenase)
  3. oxaloacetate (pyruvate carboxylase)
115
Q

What is the point of gluconeogenesis?

A

replenish blood glucose for use by the brain (cannot use Fatty Acids)

116
Q

name 3 carbon sources for gluconeogenesis

A
  1. lactate (from RBCs and exercising muscle)
  2. some Amino Acids (from muscle protein)
  3. Glycerol (from triglycerides)
117
Q

What are the 3 enzymes that are used for glycolysis but are sidestepped for gluconeogenesis?

A
  1. pyruvate kinase (oxaloacetate circle)
  2. PFK-1 (Fructose-1,6-bisphosphatase)
  3. hexokinase/glucokinase (glucose-6-phosphatase)
118
Q

how much energy is used to convert pyruvate to PEP?

A

2 high-energy intermediates: 1 ATP, 1 GTP

119
Q

pyruvate carboxylase is located where?

A

mitochondria

120
Q

pyruvate carboxylase requires what to activate it, and what as a cofactor?

A

Acetyl-CoA activates it, and Biotin is a cofactor

121
Q

PEP carboxykinase is located where?

A

cytoplasm

122
Q

why does oxaloacetate need to be transformed to malate?

A

oxaloacetate cannot cross the mito membrane, but malate can. once malate has crossed out, it is changed back to oxaloacetate.

123
Q

what mitochondrial conditions favor gluconeogenesis?

A

high NADH

124
Q

What inhibits Fructose-1,6-bisphosphatase?

A

Fructose-1,6-bisphosphate and ADP

125
Q

What activates Fructose-1,6-bisphosphatase?

A

Citrate and ATP

126
Q

what both activates Fructose-1,6-bisphosphatase AND inhibits PFK-1?

A

Citrate and ATP

127
Q

What conditions will favor gluconeogenesis and slow down glycolysis?

A
  1. High ATP levels will do both

2. High blood lactate/high mitochondrial NADH will favor gluconeogenesis.

128
Q

Why do we need to transform Glucose-6P to glucose during gluconeogenesis?

A

Glucose-6P cannot exit the cell.

129
Q

what organs have Glucose-6-Phosphatase?

A

Liver and kidney, but NOT muscle

130
Q

Where does the Cori Cycle take place? what happens?

A

in Liver. Takes up blood lactate (formed by exercising muscle) and converts it to blood glucose for use by brain.

131
Q

what 3 reactions/enzymes require ATP in gluconeogenesis?

A
  1. pyruvate carboxylase
  2. PEP carboxykinase
  3. 3-Phosphoglycerate kinase
132
Q

Gluconeogenesis from lactate requires how many ATP per glucose?

A

6

133
Q

why is the pyruvate dehydrogenase reaction irreversible?

A

because CO2 leaves, and because there is a large negative free energy.

134
Q

Deficiency of the E1 subunit of PDH is the most common cause of what?

A

genetic lactic acidosis

135
Q

What is the order in which the cofactors are used in the Pyruvate Dehydrogenase reaction? What part swings?

A

TPP, Lipoic Acid, Coenzyme A, FAD, NAD. It is the Lipoic Acid/Lysine that swings from E2 that accepts part of the complex formed by TPP.

136
Q

How is PDH regulated?

A

There is a protein kinase (inhibitory) and a protein phosphatase (activating) that regulate PDH

137
Q

What inhibits/activates the protein kinase which inhibits PDH?

A

Inhibits: Pyruvate and ADP
Activates: ATP, acetyl CoA, NADH

138
Q

What inhibits/activates the protein phosphatase that activates PDH?

A

Inhibits: nothing
Activates: calclum, insulin

139
Q

quantitatively, what is the most impt precursor for gluconeogenesis?

A

lactate

140
Q

how is pyruvate converted to PEP?

A

enzymes: pyruvate carboxylase and PEP carboxykinase. Oxaloacetate –> malate –> Oxaloacetate.

141
Q

why can’t pyruvate be converted directly back to PEP?

A

the pyruvate kinase reaction is irreversible

142
Q

What is Von Gierke’s disease?

A

Type I storage disease due to the genetic loss of glucose-6Pase.

143
Q

Where is most glycogen stored?

A

muscle and liver

144
Q

what does muscle glycogen provide? what does it not provide?

A

provides Glucose-6P for muscle. NOT a source of blood glucose

145
Q

liver glycogen can be a source of what?

A

blood glucose

146
Q

the glycogen polymer overall is attached to a small protein called what?

A

glycogenin

147
Q

what are the 3 enzymes the synthesizes glycogen from glucose-1P?

A
  1. UDP-glucose pyrophosphorylase
  2. Glycogen synthase
  3. branching enzyme
148
Q

what are the 2 enzymes that degrade glycogen to glucose-1P?

A
  1. glycogen phosphorylase

2. debranching enzyme

149
Q

what are the regulated enzymes in the synthesis/degradation of glycogen?

A

glycogen phorphorylase and glycogen synthase

150
Q

why is muscle not a source of blood glucose?

A

does not contain glucose-6-phosphatase to convert glucose-6P to glucose -> bloodstream

151
Q

what are the 2 types of glycosidic bonds in glycogen?

A
  1. alpha-1,6 glycosidic linkage (branches)

2. alpha-1,4 glycosidic linkage (straight)

152
Q

what is the non-reducing end? what characterizes the reducing end?

A

the end that monosaccharides will be added to. the reducing end is connected to glycogenin

153
Q

why is it helpful to store glucose as glycogen?

A

less change to osmotic pressure of cell

154
Q

what is one difference between glycogen and fat?

A

glycogen can be metabolized and provide energy in the absence of oxygen

155
Q

what enzyme catalyzes Glucose-1P to Glucose-6P and back?

A

phosphoglucomutase

156
Q

UDP-glucose pyrophosphorylase does what?

A

Glucose-1P to UDP-glucose (which can be added to glycogen)

157
Q

glycogen synthase does what?

A

adds units of UDP-glucose to glycogen chains with alpha-1,4 linkages.

158
Q

what activates/inhibits glycogen synthase?

A

activates: dephosphorylation by protein phosphatase. inhibits: phorphorylation by a protein kinase

159
Q

what is the function of the branching enzyme?

A

transfers 7 or more glucosyl residues from the non-reducing end, leaving at least 4 behind as a primer. forms an alpha-1-6 glycosidic bond

160
Q

what does glycogen phosphorylase do?

A

breaks alpha-1,4 bonds of glycogen. yields single glucose-1P, trapped in cell

161
Q

what activates/inhibits glycogen phosphorylase?

A

activates: phosphorylation by protein kinase. inhibits: dephos by protein phosphatase

162
Q

what does the debranching enzyme do?

A

Bifunctional enzyme: 2 activities in one protein. once branches are shortened to 4 residues by glycogen phosphorylase, transfers 3 units to non-reducing end. Then breaks alpha-1.6 bond and liberates the final residue of glucose-1P

163
Q

where is glucose-6-phosphatase found? what does it do?

A

ER of liver cells. hydrolyzes Glucose-6P to glucose + free phosphate. Glucose then transported out of cell to cytoplasm.

164
Q

what is the limit dextran?

A

a short stretch of glucosyl residues connected to the glycogenin protein, that glycogen synthase adds further units to to form glycogen.

165
Q

glycogen synthesis and degradation: regulated the same way in muscle and liver or differently?

A

differently: in muscle, regulated based on energy status. in liver, regulated based on glucose availability (ie nutritional status)

166
Q

the protein kinase cascade that regulates phosphorylation/dephosphorylation of glycogen phosphorylase and glycogen synthase is controlled by what?

A

cAMP (in both muscle and liver)

167
Q

what permits rapid changes in muscle glycogen metabolism?

A

Ca transients

168
Q

what regulates liver glycogen metabolism?

A

glucose levels

169
Q

overall, what does glycogen synthase do?

A

regulates glycogen synthesis

170
Q

overall what does glycogen phosphorylase do?

A

regulates glycogen degradation

171
Q

what does glucose do to glycogen synthase in the liver?

A

activates it

172
Q

what does AMP do to glycogen phosphorylase in the muscle?

A

activates it

173
Q

what does glucose-6P do to glycogen phosphorylase in the muscle?

A

inhibits it (via blocking AMP activation)

174
Q

which is phosphorylated, glycogen phosphorylase a or b?

A

a

175
Q

which is active primarily in muscle, glycogen phosphorylase a or b?

A

b

176
Q

which is active primarily in liver, glycogen phosphorylase a or b?

A

a

177
Q

which indicates active state of glycogen phosphorylase, T or R?

A

R (relaxed) state. T = tight state.

178
Q

what does glycogen phosphorylase kinase do?

A

phosphorylases glycogen phosphorylase using ATP as a source of phosphate. b = unphos, a = phos. think b = bare.

179
Q

in muscle, glycogen phosphorylase b is activated by what?

A

AMP

180
Q

in muscle, glycogen phosphorylase b is inhibited by what?

A

ATP, glucose-6P

181
Q

in liver, glycogen phosphorylase a is activated by what?

A

not sure

182
Q

in liver, glycogen phosphorylase a is inhibited by what?

A

glucose (transforms it to the T state)

183
Q

even in the presence of oxygen, do cancer cells do glycolysis?

A

yes, this is termed aerobic glycolysis. produces large amounts of lactate

184
Q

how can we see whether tumors are taking up large amounts of glucose?

A

via PET scanning: basically labeled glucose that is detected (18-F-fluorodeoxyglucose)

185
Q

how do cancer cells gain growth advantage by relying on glycolysis?

A
  1. ability to grow in hypoxic environments

2. good rates of synthesis of key metabolic intermediates for biosynthesis and growth regulation

186
Q

what is PKM2?

A

isozyme of pyruvate kinase in cancer cells. slows rate of glycolysis, allowing the accumulation of metabolic intermediates that are used for cell growth

187
Q

what is IDH1?

A

isocitrate dehydrogenase isozyme in CYTOPLASM (usually part of the citric acid cycle in mito). MUTATED IDH1 produces 2HG, which may affect tumor growth (not sure exactly, but measuring this is a useful way to detect cancer).

188
Q

how many ATP from glucose are obtained via glycolysis?

A

net 2/glucose

189
Q

what might be the advantages of using glycolysis to lactate (and not CAC) for cancer cells?

A
  1. simple pathway
  2. ATP needed for cell division/growth is less than that for cell maintenance
  3. the malate-aspartate shuttle might be saturated at higher rates of CAC?, so pyruvate -> lactate ensures steady rate of NAD regeneration.
  4. ability to grow in hypoxic environments and provide lactate to non-hypoxic cells
190
Q

what is LDH-A?

A

LDH isozyme that favors pyruvate -> lactate

191
Q

what happens to the activity of pyruvate dehydrogenase in cancer cells?

A

decreased activity, due to phosphorylation by a protein kinase (PDK)

192
Q

what controls the expression of LDH-A and PDK genes (cancer cells)?

A

transcription factor called HIF-1alpha. upregulated in cancer cells

193
Q

what is VHL?

A

tumor suppressor gene. normally binds to HIF-1alpha and leads to proteosomal destruction of HIF-1alpha. but VHL is inactivated in cancer phenotpyes leading to increased HIF-1alpha expr.

194
Q

increased HIF-1alpha expr leads to what?

A

upregulated LDH-A and PDK

195
Q

what is PKM2?

A

isozyme of pyruvate kinase. prevalent in cancer phenotypes. relatively slow isozyme: effect = slow glycolysis overall (slow PEP -> pyruvate) to allow accumulation of upstream intermediates needed for growth

196
Q

What is VHL?

A

Von Hippel-Lindau, a tumor suppressor gene. If mutated, will allow HIF-1a to proliferate. HIF-1a upregulates PDK and LDH-A

197
Q

what determines the fate of pyruvate?

A

NADH/NAD ratio

x M1 Biochem Quiz 1 (2 decks)

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