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Biochemistry II > Final Exam > Flashcards

Final Exam Flashcards

1
Q

What types of tissue is GLUT1 present in?

A

most

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2
Q

What types of tissue is GLUT3 present in?

A

neuronal

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3
Q

What types of tissue is GLUT2 present in?

A

hepatocytes
pancreatic B cells

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4
Q

What types of tissue is GLUT4 present in?

A

cardio
adipo
skeletal

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5
Q

What GLUT is [glucose] sensitive?

A

GLUT2

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6
Q

What GLUT is insulin dependent?

A

GLUT4

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7
Q

What happens to GLUT4 when insulin is secreated?

A

fuses with cell membrane to access insulin in blood

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8
Q

What happens to GLUT4 when insulin is not secreated?

A

sequesters inside the cell

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9
Q

What is the commitment step of using glucose in metabolism?

A

Hexokinase

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10
Q

Is Hexokinase I-III or Hexokinase IV always at max rate making it [glucose] insensitive?

A

Hexokinase I-III

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11
Q

What inhibited Hexokinase I-III?

A

G6Pase

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12
Q

Is Hexokinase I-III or Hexokinase IV [glucose] sensitive?

A

Hexokinase IV

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13
Q

Is Hexokinase IV inhibited by G6Pase like HK I-III?

A

No

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14
Q

What cells is Hexokinase IV present in?

A

hepatocytes
pancreatic B cells

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15
Q

Is hexokinase IV inhibited or activated by insulin?

A

activated

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16
Q

What cell type is G6Pase mainly expressed in?

A

hepatocytes

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17
Q

What is positive cooperativity?

A

binding of a substrate at one active site enhances binding at another active site

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18
Q

What are the 2 conformations of the symmetry model?

A

T - tight
R - relaxed

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19
Q

In the symmetry model, how does each conformation interact with its substrate?

A

Tight - binds poorly
Relaxed - binds well

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20
Q

T/F? enyzmes can have T and R conformations

A

false (only one at a time)

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21
Q

In the symmetry model, [T]/[R] = large or small number

A

large positive

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22
Q

In the symmetry model, disassociation constant for T or R is smaller (better binding)?

A

R b/c it binds better with substrate

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23
Q

Do allosteric inhibitors or activators increase the cooperatively affect and why?

A

inhibitors; more substrate is required to overcome the bias towards the T state = increased cooperatively affect (trying to get up hill)

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24
Q

Do allosteric activators prefer the R or T state?

A

R

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25
Q

Why do allosteric activators decrease the cooperatively effect?

A

active sites don’t communicate with one another

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26
Q

In a graph, where is the allosteric inhibitor and activator located?

A

inhibitor: bottom line
activator: top line

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27
Q

Does PKA activate or inhibit PFK-2 in hepatocytes ?

A

inhibit

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28
Q

Does PPP-1 activate or inhibit FBPase-2 in hepatocytes?

A

inhibit

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29
Q

Is PKA activated or inactivated by insulin in hepatocytes?

A

inactivated

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30
Q

___________________ does not apply to cardiomyocytes

A

gluconeogenisis

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31
Q

Why does PKA activate PFK-2 in cardiomyocytes?

A

there is no phosphorylation location on PFK-2 so FBPase-2 is inhibited (phosphorylated); since epinephrine is signaled in cardiomyocytes in the f/f response there is a need for more ATP so glycolysis is kept on using the process above

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32
Q

In cardiomyocytes, PKA is not used in the well fed state since insulin is signaling not epinepherine. What is used to activate PFK-2?

A

AKT

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33
Q

In cardiomyocytes, epinephrine and insulin signaling ________ [F26BP] and ________ glycolysis

A

increase [F26BP]
increase glycolysis

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34
Q

What enzymes in glycolysis are regulated by covalent modification?

A

FBPase/PFK
pyruvate kinase

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35
Q

Does PKA activate or inhibit pyruvate kinase?

A

inhibit

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36
Q

What is the regulatory enzyme in glycogenisis/glycogenlysis?

A

glycogen synthase

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37
Q

All the steps in glycogenlysis are ____________

A

hydrolytic

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38
Q

What is branching in glycogensis?

A

adding glucoses to a-1,4 and a-1,6 transglycosylase’s Tyr residue

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39
Q

why is glucose branched in glycogenisis?

A

fits in hepatocytes

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40
Q

What catalyzes debranching in glycogenlysis?

A

1,4-glucanotransferase
amylo-1,6-glucosidase

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41
Q

what kind of bond is broken in debranching?

A

a-1,4 glycosidic bond

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42
Q

in glycogenlysis regulation, glycogen phosphorylase b is sensitive or insensitive to the external conditions?

A

sensitive

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43
Q

in glycogenlysis regulation, glycogen phosphorylase a is sensitive or insensitive to the external conditions?

A

insensitive (gas pedal)

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44
Q

what enzyme activates glycogen phosphorylase a and b?

A

a: phosphorylase kinase
b: PPP-1

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45
Q

What inactivates glycogen synthase in glycogenisis?

A

5 kinases

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46
Q

What activates glycogen synthase in glycogenisis?

A

PPP-1

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47
Q

What are the 5 kinases that inactivate glycogen synthase in glycogenisis?

A

PKA
phosphorylase kinase
Ca2+/calmodium
glycogen synthase kinase
AMP-dependent kinase

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48
Q

What is glycogenin?

A

primes glycogen synthesis by building out chain of glucose attached to its Tyr residue

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49
Q

What 3 regulation enzymes in glycolysis?

A

hexokinase
PFK-1
pyruvate kinase

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50
Q

What is the second messenger for epinephrine (B2)?

A

cAMP

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51
Q

what is the primary kinase for epinephrine (B2)?

A

PKA

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52
Q

What type of G coupled protein does epinephrine (B2) use?

A

Gs family

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53
Q

What is the second messenger for epinephrine (a2)?

A

IP3

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54
Q

What is the primary kinase for epinephrine (a2)?

A

PKC and CAM-PK/CA2+

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55
Q

What type of G coupled protein does epinephrine (a2) use?

A

Gq family

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56
Q

What is the second messenger of insulin?

A

PIP3

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57
Q

What is the primary kinase for insulin?

A

AKT

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58
Q

What is the name of the E1 PDH subunit?

A

pyruvate dehydrogenase

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59
Q

What is the name of the E2 PDH subunit?

A

dihydrolipoamide acetyltransferase

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60
Q

What is the name of the E3 PDH subunit?

A

dihydrolipoamide dehydrogenase

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61
Q

Is cofactor CoA transient or prosthetic and for which subunit?

A

transient E1

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62
Q

Is cofactor TPP transient or prosthetic and for which subunit?

A

prosthetic E2

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63
Q

Is cofactor lipoamide transient or prosthetic and for which subunit?

A

prosthetic E2

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64
Q

Is cofactor FAD transient or prosthetic and for which subunit?

A

prosthetic E3

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65
Q

Is cofactor NAD+ transient or prosthetic and for which subunit?

A

transient E3

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66
Q

What is the point of no return in the CAC?

A

when pyruvate to acetyl CoA

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67
Q

What is the first cofactor that combines with pyruvate pre citric acid cycle?

A

TPP

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68
Q

What is the second cofactor that combines with pyruvate pre citric acid cycle?

A

lipoamide

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69
Q

What is the only positive delta G in the CAC?

A

malate

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70
Q

What 3 enzymes turn NAD into NADH in the CAC cycle?

A

isocitrate DH
a-ketogluterate
malate DH

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71
Q

What 2 enzymes release carbon in the form of CO2?

A

isocitrate DH
a-ketogluterate DH

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72
Q

what is enzyme of the commitment step during the CAC?

A

isocitrate DH

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73
Q

what is the enzyme of the regulatory step in the CAC and has the same mechanism as PDH?

A

a-ketogluterate DH

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74
Q

What is the only membrane bound enzyme in the CAC?

A

succinate DH

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75
Q

What is the acronym for the name of the molecules in the CAC?

A

Can
I
Keep
Sell
Sex
For
Money
Officer?

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76
Q

what is the acronym for the type of enzyme used in each step of the CAC?

A

So
At
Disco
Devil
Sucked
Down
Five
Drinks

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77
Q

what enzyme in the CAC is referred to as catalytic perfection?

A

fumarase

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78
Q

increased cAMP production = increase/decrease of adenylyl cyclase?

A

increase

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79
Q

How many CO2 is made in one turn of the CAC?

A

2

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80
Q

How many NADH is made in one turn of the CAC?

A

3

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81
Q

How many FADH2 is made in one turn of the CAC?

A

1

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82
Q

How many ATP is made in one turn of the CAC?

A

1

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83
Q

How many GTP is made in one turn of the CAC?

A

1

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84
Q

does increased levels of ATP increase/decrease the level of PDH/CAC?

A

decrease

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85
Q

does increased levels of ADP/AMP increase/decrease the level of PDH/CAC?

A

increase

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86
Q

does increased levels of NAD increase/decrease the level of PDH/CAC?

A

increase

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87
Q

What are 3 inhibitors of CAC?

A
  1. NADH
  2. acetyl coA
  3. ATP
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88
Q

Why is NADH an inhibitor of CAC?

A

inhibits E3 (lipoamide cannot reoxidized)

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89
Q

why is acetyl coA an inhibitor of CAC?

A

inhibits E2 (competes with free floating CoA-SH)

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90
Q

Is PDH regulated by covalent modification?

A

yes

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91
Q

what enzyme of the CAC catalyzes hydrolysis of thioester?

A

citrate synthase

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92
Q

what enzyme is inhibited by succinyl-coA?

A

a-ketogluterate DH

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93
Q

what enzyme uses Fe clusters in the CAC?

A

acontiase

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94
Q

Increased PPP means that adenylyl cyclase is active or inactive?

A

inactive

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95
Q

increased glycogen synthease means adenylyl cyclase is active or inactive?

A

inactive

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96
Q

T/F: Under standard conditions, malate oxidation by NAD+ is energentically favored

A

false

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97
Q

T/F: insulin signaling decreases PDH phosphatase activity

A

false

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98
Q

T/F: reaction catalyzed by aconitase requires a 180 flip

A

true

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99
Q

T/F: PDH is found in the cytosol

A

false

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100
Q

T/F: can oxaloacetate be viewed as a catalyst

A

true

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101
Q

is PDH activated or inactivated when phosphorylated?

A

inactivated

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102
Q

what does pyruvate dehydrogenase kinase do?

A

phosphorylates PDH and makes it inactive

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103
Q

PDK 1 is present in what kind of cells?

A

panceratic beta cells
cardiomyocytes

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104
Q

PDK 2 is present in what kind of cells?

A

cardiomyocytes
hepatocytes

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105
Q

PDK 4 increases expression in the fasting or well fed state?

A

fasting

106
Q

what does pyruvate dehydrogenase phosphatase do?

A

dephosphorylates PDH

107
Q

what cells is PDP 1 located in?

A

skeletal muscle cells

108
Q

what is name of the intermediate for oxaloacetate to citrate called in the CAC?

A

s-citryl coA

109
Q

what is name of the intermediate for citrate to isocitrate called in the CAC?

A

cis-acontiase

110
Q

what is the most important anapleurotic reaction?

A

pyruvate –> oxaloacetate

111
Q

what enzyme catalyzes the most important anapleurotic reaction?

A

pyruvate carboxylase

112
Q

what cofactor is involved in the most important anapleurotic reaction?

A

biotin

113
Q

What molecule activates the most important anapleurotic reaction?

A

acetyl coA

114
Q

what is the P/O ratio for NADH?

A

2.5 (NADH comes from matrix)
1.5 (using G3P pathway)

115
Q

Which Complex is NOT involved in succinate oxidation?

A

Complex I

116
Q

What is the P/O ratio fro NADH generated in the cytosol?

A

1.5 (FAD dependent)
2.5 (malate/aspartate)

117
Q

Why are the 2 issues involving NADH in the cytosol?

A
  1. cannot cross the inner membrane
  2. can only enter the RETC via Complex I which is on the matrix side
118
Q

How many ATP are generated and H+ translocated using the FADH dependent method?

A

1.5 ATP
6 H+

119
Q

How many ATP a generated and H+ translocated using the malate/aspartate dependent method?

A

2.5 ATP
10 H+

120
Q

Including the actions of respiratory electron transport and F1F0 ATPase, how many ATPs will be generated as a result of converting one pyruvate to an acetyl coA

A

2.5

121
Q

T/F almost all oxidoreductases require a cofactor to function

A

true

122
Q

NADH is an obligate _______ donor

A

hydride (2e-)

123
Q

What is the only Complex involving NADH?

A

Complex I

124
Q

Flavins are __e- acceptors and ___e- donors

A

2e- acceptors
1e- donor

125
Q

What are the 4 obligate 2e- (hydride) donors?

A
  1. NADH (Complex I)
  2. succinate (Complex II)
  3. glycerol-3-P
  4. fatty acetyl coA
126
Q

What allows flavins to be obligate 1e- donors?

A

semiquinone intermediate

127
Q

Fe/S clusters are obligate ___e- donors/acceptors

A

1e-

128
Q

What are the 2 oxidative states of 2Fe/2S and 4Fe/4S?
Ferric/ferrous?

A

Fe II (ferrous)
Fe III (ferric)

129
Q

Rieske Fe/S clusters are ________ to reduce and ________ to oxidize

A

easier
harder

130
Q

Does 2Fe/2S or 4Fe/4S comes first reducation wise?

A

2Fe/2S easier to reduce again

131
Q

UQ is a obligate ___e- donor/acceptor?

A

1e-

132
Q

What coenzyme shuttles e- between donors/acceptors?

A

UQ

133
Q

What is the Q-cycle?

A

as UQ is reduced H+ is pumped into the IMS

134
Q

Hemes are prosthetic groups for __________

A

cytochromes

135
Q

Hemes are obligate ___e- donor/acceptor

A

1e-

136
Q

What is special about cytochrome a3?

A

it is penta so the 6th spot is open for O2 binding

137
Q

What is the only complex with Cu?

A

Complex IV

138
Q

What are the 2 types of Cu and what do they do?

A

CuA: electron transfer
CuB: assists cytochrome a3 in O2 reduction

139
Q

Rieske 4Fe/4S is easier to reduce, what is its delta G?

A

positive (easier to reduce)

140
Q

How is partial reduction of O2 prevented?

A

keeping cofactors near each other

141
Q

What is another name from Complex I?

A

NADH ubiquinone oxidoreductase

142
Q

What is another name for Complex II?

A

succinate ubiquinone oxidoreductase

143
Q

What is another name for Complex III?

A

ubiquinol cytochrome c oxidoreductase

144
Q

What is another name for Complex IV?

A

cytochrome c oxidase

145
Q

What is the largest Complex?

A

Complex I

146
Q

How many H+ are translocated from Complex I?

A

4

147
Q

What are 2 inhibitors of Complex I?

A

Rotenone
Amytal

148
Q

What happens to the RETC when Complex I inhibitors are present?

A

NADH accumulates = lactate accumulation (lactate DH) = CAC inhibited

149
Q

Exposure to rotenone will lead to an increase in __________ production

A

lactate

150
Q

What cofactor does Complex II have that doesn’t participate in e- transfer and we are not sure why its there

A

heme b

151
Q

How many H+ are translocated at Complex II?

A

none

152
Q

What is an inhibitor of Complex II?

A

thenoyl trifluoroacetone carboxin
TTC

153
Q

Complex III has 2 sets of 11 subunits, the side oriented towards the IMS is Q__ and the side oriented near the matrix is Q____

A

Q P (IMS) (positive)
Q N (Matrix) (negative)

154
Q

How many H+ are translocated at Complex III?

A

4

155
Q

What cycle is used also in Complex III to translocated H+?

A

Q cycle

156
Q

What are 3 inhibitors of Complex III?

A
  1. myxothiazol
  2. antimycin A
  3. stigmatellin
157
Q

In Complex IV, what does subunit I do?

A

O2 reduction

158
Q

What cofactors are in Complex IV’s subunit I?

A

Cyt. a
Cyt. a3
Cu B

159
Q

In Complex IV, what does subunit II do?

A

site of Cyt. c binding

160
Q

What cofactor is in Complex IV’s subunit II?

A

CuA

161
Q

In Complex IV, what does subunit III do?

A

hydrophobic channels to direct O2 to subunit I

162
Q

What cofactor is in Complex IV’s subunit III?

A

none

163
Q

How many H+ are translocated across Complex IV?

A

2 (per e- pair)

164
Q

What are the 3 channels of Complex IV?

A

K channel
D channel
H channel

165
Q

Complex IV’s K channel’s H+ comes from _______

A

Cu B

166
Q

Complex IV’s D channel’s H+ comes from _______

A

Cyt. a3

167
Q

Complex IV’s H channel’s H+ comes from _______

A

matrix

168
Q

Which Complex IV channel is vectoral?

A

H channel (matrix to IMS physically)

169
Q

I am an electron transport complex, I have no Rieske Fe/S, no hemes and no FAD.

A

Complex I

170
Q

I am an electron transport complex, I have Fe/S and hemes but no flavins.

A

Complex III

171
Q

There is a __________ gradient and a ___________ gradient across the inner membrane

A

concentration
charge

172
Q

RETC’s goal is to pump H+ into ________ for ATPase to make ATP

A

IMS

173
Q

The pH in the IMS is _______ than the pH in the matrix

A

lower (more H+)

174
Q

The delta G pushing against the gradient is POSITIVE OR NEGATIVE?

A

positive

175
Q

The delta G at the end of RETC is POSITIVE OR NEGATIVE?

A

negative

176
Q

What is the chemiosmotic hypotheisis?

A

Free E (-G) delivered from H+ passage across the membrane with the gradient provides the driving force for ADP phosphorylation

177
Q

What is an uncoupling agent?

A

able to cross the mitochondrial inner membrane (in protonated state), the deprotonates once across (INCREASE PERMIABILITY)

178
Q

What are 4 examples of uncoupling agents?

A
  1. 2,4-dinitrophenol
  2. Fluorocarbonyl cyanide phenylhydrazine
  3. Dicoumarol
  4. Thermogenin
179
Q

The coupling agent, ___________, is expressed in brown fat of mitochondria

A

Thermogenin

180
Q

What is brown fat?

A

uses proton gradient to generate heat to protect CNS and organs (babies)

181
Q

T/F Introduction of a K+ channel in the mitochondria inner membrane will disrupt ATP synthesis by F1F0.

A

true

182
Q

T/F introduction of a K+ channel in the mitochondria inner membrane will result in lactate accumulation.

A

False (uncoupling agents are not inhibitors so they are no inhibiting the e- flow they are only affecting “downstream” ATP synthesis)

183
Q

What couples the H+ generated by RET and ADP phosphorylation?

A

F1F0 ATPase

184
Q

Where is F1F0 ATPase located?

A

F0 - inner membrane
F1 - matrix

185
Q

What are the subunits of F1?

A

3 alpha
3 beta
1 gamma
1 delta
1 epsilon

186
Q

What does the alpha subunit do of F1?

A

binds ATP but DOES NOT catalyze

187
Q

the alpha subunit of F1 provides an ______ residue to the beta subunit

A

Arginine

188
Q

What are the 3 binding options for the beta subunit of F1?

A

AMP PNP (ATP)
ADP + Pi
empty

189
Q

When (AMP PNP) ATP is bound to the beta subunit of F1, is the KD high or low?

A

low (high association)

190
Q

The center of the alpha/beta orange of F1 is very _________ made of ___________

A

hydrophobic
3 alpha helices

191
Q

In the presence of ATP and the absence of F0, the gamma subunit rotates in the ____________ direction

A

counter clockwise

192
Q

Which subunit of F1F0 ATPase is in the matrix? F1 or F0?

A

F1

193
Q

How many alpha helices is the c ring of F0 made of?

A

12

194
Q

c ring of F0 has Asp61 on each subunit, what is special about the last one?

A

It is partially off the subunit because of helical unwinding which allows H+ to bind and be dropped off in the matrix

195
Q

subunit a of F0 has a _______ residue

A

Arg 210

196
Q

What subunit of F0 has a half channel for H+?

A

a

197
Q

Which complex does dicoumarol bind to?

A

none

198
Q

Which complexes activity is inhibited by dicoumarol?

A

F1F0 ATPase

199
Q

Consider an F1F0 ATPase who has 9 c subunits, how many H+ across the mitochondria inner membrane will result in one full revolution of the c ring?

A

9

200
Q

Consider a F1F0 ATPase who has 9 c subunits. Passage of how many H+ across the mitochondria inner membrane will result in one full revolution of the gamma subunit?

A

9

201
Q

How many ATP are made for every gamma revolution?

A

3

202
Q

What is the purpose of the Complexes in the RETC?

A

build a high concentration of H+ in the IMS

203
Q

H+ in the IMS enters ATPase where?

A

F0 (a subunit)

204
Q

What structurally distinguishes heme a, b, and c

A

a: long tail
b: normal
c: S-protein

205
Q

T/F: under standard conditions, malate oxidation by NAD+ is energetically favored

A

false

206
Q

T/F: almost all hemes found in the ETC are hexacoordinate

A

true

207
Q

T/F: In the context of the citric acid cycle, oxaloacetate can be viewed as a catalyst

A

true

208
Q

What electron transport complex contains a Reiske Fe/S center?

A

complex III

209
Q

What electron transport complexes do not contain hemes?

A

complex I

210
Q

Which about stigmatellin is true?
a. It binds to QP site
b. Interrupts Q cycle
c. Prevents conformational change in Complex III
d. All are true

A

d. All are true

211
Q

What is the order of electron transfer in Complex I?

A

NADH, FMN, Fe/S, UQ

212
Q

In Complex I, what would happen if conformational change is not possible?

A

no H+ transfer but e- would still happen

213
Q

What would happen if UQ binding is affected in Complex I?

A

no e- transfer and no H+ transfer stopping all other complexes after I

214
Q

Would someone with no e- transfer or with e- would have more pyruvate DH kinase activity/lactate accumulation?

A

the one with NO e- transfer because NADH would accumulate and Pyruvate DH would have to deal with it ramping up glycolysis

PDK is activates by NADH

215
Q

Why are the cofactors in the specific orders they’re in in the RETC?

A

reduction potential and obligate donor/acceptors

216
Q

How does CN affect succinate DH (complex II)?

A

decreases succinate DH (COMPLEX II) activity b/c it affects O2 ability to be a final e- acceptor which will back up the cycle

217
Q

T/F: in the absence of F0, F1 catalyzes ATP synthesis

A

false (catalyzes ATP hydrolysis)

218
Q

T/F: The identity of the fatty acyl-CoA dehydrogenase used in -oxidation depends upon the carbon chain length of the fatty acyl-CoA substrate.

A

true

219
Q

Carboxin is an inhibitor for which complex?

A

Complex II (inhibits succinate)

220
Q

What is the visual difference between NADH and FAD?

A

NADH has 1 N ring
FAD has 2 N rings

221
Q

What is the visual difference between FAD and FMN?

A

FAD has a bunch of stuff at the bottom
FMN looks just like it without the clutter at the bottom

222
Q

What is visual difference between CuA and CuB?

A

CuA is more complicated looking (makes a square)

223
Q

How does stigmatellin affect Rieske Fe/S clusters?

A

affects the reduction potential

224
Q

what are 2 reasons fat is good for storage?

A
  1. carbon reduces easily
  2. little water
225
Q

what catalyzes the hydrolysis of TAGs to glycerol and fatty acids?

A

pancreatic lipase

226
Q

What is the cascade of lipolysis?

A
  1. TAG
  2. DAG
  3. MAG
  4. glycerol
227
Q

What enzyme catalyzes TAG to DAG?

A

TAG lipase

228
Q

What enzyme catalyzes DAG to MAG?

A

DAG lipase

229
Q

What enzyme catalyzes MAG to glycerol?

A

MAG lipase

230
Q

What is fatty acid activation?

A

fatty acid has AMP attached to it then turns into acyl coA

231
Q

What catalyzes fatty acid activation?

A

acyl CoA ligase

232
Q

What transports fatty acids to the matrix?

A

L-carnitine (CAT)

233
Q

What is the order of enzymes in B oxidation?

A
  1. acyl-coA DH
  2. enoyl-coA hydratase
  3. L-hydroxyacyl CoA DH
  4. thiolase
234
Q

_________ inhibits carnitine (CAT) transport system

A

malonyl coA

235
Q

What makes ketone bodies?

A

hepatocytes

236
Q

_________ [acetyl coA] favors ketone body formation

A

increasing

237
Q

ketone levels increase in the fasting or well feed state

A

fasting

238
Q

What is the purpose of ketone bodies?

A

alternative fuel source so CNS can use glucose

239
Q

What molecule does ketone body formation start with?

A

acetyl coA from B oxidation

240
Q

How is acetyl CoA moved to the cytosol for FA synthesis?

A

as citrate

241
Q

What are the 2 sources of NADPH for FA synthesis?

A

Malic enzyme
PPPathway

242
Q

what transports fatty acyl CoA into the marix for B oxidation?

A

L-carnitine (CAT)

243
Q

what is the name of the 12 c fatty acid?

A

lauric acid

244
Q

what is the name of the 14 c fatty acid?

A

myristic acid

245
Q

what is the name of the 16 c fatty acid?

A

palmitic acid

246
Q

what is the name of the 18 c fatty acid?

A

stearic acid

247
Q

what are the 2 possible fates of pyruvate?

A

turn into oxaloacetate via pyruvate carboxylase
turn into acetyl coA via pyruvate DH (plus cofactors)

248
Q

increased acetyl coA = increased or decreased PDH

A

decreased

249
Q

increased acetyl coA = increased or decreased pyruvate carboxylase

A

increased

250
Q

In order for B oxidation to occur, what is needed?

A

inactivated fatty acyl CoA

251
Q

What is the fate of acetly coA generated by B oxidation?

A

CAC

252
Q

What is the important enzyme for ketone bodies?

A

HMG CoA lyasee

253
Q

what cofactor creates trans double bonds?

A

FAD

254
Q

What cofactor had H2O involved?

A

NAD

255
Q

What cofactor uses SH-CoA?

A

lipoamide

256
Q

What enzyme is the largest player in fatty acid synthase?

A

ACP

257
Q

What is the order of enzymes in fatty acid synthase?

A

KS
MAT
KS
KR
DH
ER

258
Q

Why is glycogen synthesis better in hepatocytes than skeletal myocytes?

A

G6P can be broken down into something useable and transported out of cell

259
Q

is glycogen phosphorylase favored in fasting or well fed?

A

fasting/fight or flight

260
Q

TAG lipase is activated or inhibited by phosphorylation?

A

activated

261
Q

perilipin is activated or inhibited by phosphorylation?

A

activated

Biochemistry II (6 decks)

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