Final Exam Flashcards
1
Q
What types of tissue is GLUT1 present in?
A
most
2
Q
What types of tissue is GLUT3 present in?
A
neuronal
3
Q
What types of tissue is GLUT2 present in?
A
hepatocytes
pancreatic B cells
4
Q
What types of tissue is GLUT4 present in?
A
cardio
adipo
skeletal
5
Q
What GLUT is [glucose] sensitive?
A
GLUT2
6
Q
What GLUT is insulin dependent?
A
GLUT4
7
Q
What happens to GLUT4 when insulin is secreated?
A
fuses with cell membrane to access insulin in blood
8
Q
What happens to GLUT4 when insulin is not secreated?
A
sequesters inside the cell
9
Q
What is the commitment step of using glucose in metabolism?
A
Hexokinase
10
Q
Is Hexokinase I-III or Hexokinase IV always at max rate making it [glucose] insensitive?
A
Hexokinase I-III
11
Q
What inhibited Hexokinase I-III?
A
G6Pase
12
Q
Is Hexokinase I-III or Hexokinase IV [glucose] sensitive?
A
Hexokinase IV
13
Q
Is Hexokinase IV inhibited by G6Pase like HK I-III?
A
No
14
Q
What cells is Hexokinase IV present in?
A
hepatocytes
pancreatic B cells
15
Q
Is hexokinase IV inhibited or activated by insulin?
A
activated
16
Q
What cell type is G6Pase mainly expressed in?
A
hepatocytes
17
Q
What is positive cooperativity?
A
binding of a substrate at one active site enhances binding at another active site
18
Q
What are the 2 conformations of the symmetry model?
A
T - tight
R - relaxed
19
Q
In the symmetry model, how does each conformation interact with its substrate?
A
Tight - binds poorly
Relaxed - binds well
20
Q
T/F? enyzmes can have T and R conformations
A
false (only one at a time)
21
Q
In the symmetry model, [T]/[R] = large or small number
A
large positive
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
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)
24
Q
Do allosteric activators prefer the R or T state?
A
R
25
Why do allosteric activators decrease the cooperatively effect?
active sites don't communicate with one another
26
In a graph, where is the allosteric inhibitor and activator located?
inhibitor: bottom line
activator: top line
27
Does PKA activate or inhibit PFK-2 in hepatocytes ?
inhibit
28
Does PPP-1 activate or inhibit FBPase-2 in hepatocytes?
inhibit
29
Is PKA activated or inactivated by insulin in hepatocytes?
inactivated
30
___________________ does not apply to cardiomyocytes
gluconeogenisis
31
Why does PKA activate PFK-2 in cardiomyocytes?
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
32
In cardiomyocytes, PKA is not used in the well fed state since insulin is signaling not epinepherine. What is used to activate PFK-2?
AKT
33
In cardiomyocytes, epinephrine and insulin signaling ________ [F26BP] and ________ glycolysis
increase [F26BP]
increase glycolysis
34
What enzymes in glycolysis are regulated by covalent modification?
FBPase/PFK
pyruvate kinase
35
Does PKA activate or inhibit pyruvate kinase?
inhibit
36
What is the regulatory enzyme in glycogenisis/glycogenlysis?
glycogen synthase
37
All the steps in glycogenlysis are ____________
hydrolytic
38
What is branching in glycogensis?
adding glucoses to a-1,4 and a-1,6 transglycosylase's Tyr residue
39
why is glucose branched in glycogenisis?
fits in hepatocytes
40
What catalyzes debranching in glycogenlysis?
1,4-glucanotransferase
amylo-1,6-glucosidase
41
what kind of bond is broken in debranching?
a-1,4 glycosidic bond
42
in glycogenlysis regulation, glycogen phosphorylase b is sensitive or insensitive to the external conditions?
sensitive
43
in glycogenlysis regulation, glycogen phosphorylase a is sensitive or insensitive to the external conditions?
insensitive (gas pedal)
44
what enzyme activates glycogen phosphorylase a and b?
a: phosphorylase kinase
b: PPP-1
45
What inactivates glycogen synthase in glycogenisis?
5 kinases
46
What activates glycogen synthase in glycogenisis?
PPP-1
47
What are the 5 kinases that inactivate glycogen synthase in glycogenisis?
PKA
phosphorylase kinase
Ca2+/calmodium
glycogen synthase kinase
AMP-dependent kinase
48
What is glycogenin?
primes glycogen synthesis by building out chain of glucose attached to its Tyr residue
49
What 3 regulation enzymes in glycolysis?
hexokinase
PFK-1
pyruvate kinase
50
What is the second messenger for epinephrine (B2)?
cAMP
51
what is the primary kinase for epinephrine (B2)?
PKA
52
What type of G coupled protein does epinephrine (B2) use?
Gs family
53
What is the second messenger for epinephrine (a2)?
IP3
54
What is the primary kinase for epinephrine (a2)?
PKC and CAM-PK/CA2+
55
What type of G coupled protein does epinephrine (a2) use?
Gq family
56
What is the second messenger of insulin?
PIP3
57
What is the primary kinase for insulin?
AKT
58
What is the name of the E1 PDH subunit?
pyruvate dehydrogenase
59
What is the name of the E2 PDH subunit?
dihydrolipoamide acetyltransferase
60
What is the name of the E3 PDH subunit?
dihydrolipoamide dehydrogenase
61
Is cofactor CoA transient or prosthetic and for which subunit?
transient E1
62
Is cofactor TPP transient or prosthetic and for which subunit?
prosthetic E2
63
Is cofactor lipoamide transient or prosthetic and for which subunit?
prosthetic E2
64
Is cofactor FAD transient or prosthetic and for which subunit?
prosthetic E3
65
Is cofactor NAD+ transient or prosthetic and for which subunit?
transient E3
66
What is the point of no return in the CAC?
when pyruvate to acetyl CoA
67
What is the first cofactor that combines with pyruvate pre citric acid cycle?
TPP
68
What is the second cofactor that combines with pyruvate pre citric acid cycle?
lipoamide
69
What is the only positive delta G in the CAC?
malate
70
What 3 enzymes turn NAD into NADH in the CAC cycle?
isocitrate DH
a-ketogluterate
malate DH
71
What 2 enzymes release carbon in the form of CO2?
isocitrate DH
a-ketogluterate DH
72
what is enzyme of the commitment step during the CAC?
isocitrate DH
73
what is the enzyme of the regulatory step in the CAC and has the same mechanism as PDH?
a-ketogluterate DH
74
What is the only membrane bound enzyme in the CAC?
succinate DH
75
What is the acronym for the name of the molecules in the CAC?
Can
I
Keep
Sell
Sex
For
Money
Officer?
76
what is the acronym for the type of enzyme used in each step of the CAC?
So
At
Disco
Devil
Sucked
Down
Five
Drinks
77
what enzyme in the CAC is referred to as catalytic perfection?
fumarase
78
increased cAMP production = increase/decrease of adenylyl cyclase?
increase
79
How many CO2 is made in one turn of the CAC?
2
80
How many NADH is made in one turn of the CAC?
3
81
How many FADH2 is made in one turn of the CAC?
1
82
How many ATP is made in one turn of the CAC?
1
83
How many GTP is made in one turn of the CAC?
1
84
does increased levels of ATP increase/decrease the level of PDH/CAC?
decrease
85
does increased levels of ADP/AMP increase/decrease the level of PDH/CAC?
increase
86
does increased levels of NAD increase/decrease the level of PDH/CAC?
increase
87
What are 3 inhibitors of CAC?
1. NADH
2. acetyl coA
3. ATP
88
Why is NADH an inhibitor of CAC?
inhibits E3 (lipoamide cannot reoxidized)
89
why is acetyl coA an inhibitor of CAC?
inhibits E2 (competes with free floating CoA-SH)
90
Is PDH regulated by covalent modification?
yes
91
what enzyme of the CAC catalyzes hydrolysis of thioester?
citrate synthase
92
what enzyme is inhibited by succinyl-coA?
a-ketogluterate DH
93
what enzyme uses Fe clusters in the CAC?
acontiase
94
Increased PPP means that adenylyl cyclase is active or inactive?
inactive
95
increased glycogen synthease means adenylyl cyclase is active or inactive?
inactive
96
T/F: Under standard conditions, malate oxidation by NAD+ is energentically favored
false
97
T/F: insulin signaling decreases PDH phosphatase activity
false
98
T/F: reaction catalyzed by aconitase requires a 180 flip
true
99
T/F: PDH is found in the cytosol
false
100
T/F: can oxaloacetate be viewed as a catalyst
true
101
is PDH activated or inactivated when phosphorylated?
inactivated
102
what does pyruvate dehydrogenase kinase do?
phosphorylates PDH and makes it inactive
103
PDK 1 is present in what kind of cells?
panceratic beta cells
cardiomyocytes
104
PDK 2 is present in what kind of cells?
cardiomyocytes
hepatocytes
105
PDK 4 increases expression in the fasting or well fed state?
fasting
106
what does pyruvate dehydrogenase phosphatase do?
dephosphorylates PDH
107
what cells is PDP 1 located in?
skeletal muscle cells
108
what is name of the intermediate for oxaloacetate to citrate called in the CAC?
s-citryl coA
109
what is name of the intermediate for citrate to isocitrate called in the CAC?
cis-acontiase
110
what is the most important anapleurotic reaction?
pyruvate –> oxaloacetate
111
what enzyme catalyzes the most important anapleurotic reaction?
pyruvate carboxylase
112
what cofactor is involved in the most important anapleurotic reaction?
biotin
113
What molecule activates the most important anapleurotic reaction?
acetyl coA
114
what is the P/O ratio for NADH?
2.5 (NADH comes from matrix)
1.5 (using G3P pathway)
115
Which Complex is NOT involved in succinate oxidation?
Complex I
116
What is the P/O ratio fro NADH generated in the cytosol?
1.5 (FAD dependent)
2.5 (malate/aspartate)
117
Why are the 2 issues involving NADH in the cytosol?
1. cannot cross the inner membrane
2. can only enter the RETC via Complex I which is on the matrix side
118
How many ATP are generated and H+ translocated using the FADH dependent method?
1.5 ATP
6 H+
119
How many ATP a generated and H+ translocated using the malate/aspartate dependent method?
2.5 ATP
10 H+
120
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
2.5
121
T/F almost all oxidoreductases require a cofactor to function
true
122
NADH is an obligate _______ donor
hydride (2e-)
123
What is the only Complex involving NADH?
Complex I
124
Flavins are __e- acceptors and ___e- donors
2e- acceptors
1e- donor
125
What are the 4 obligate 2e- (hydride) donors?
1. NADH (Complex I)
2. succinate (Complex II)
3. glycerol-3-P
4. fatty acetyl coA
126
What allows flavins to be obligate 1e- donors?
semiquinone intermediate
127
Fe/S clusters are obligate ___e- donors/acceptors
1e-
128
What are the 2 oxidative states of 2Fe/2S and 4Fe/4S?
Ferric/ferrous?
Fe II (ferrous)
Fe III (ferric)
129
Rieske Fe/S clusters are ________ to reduce and ________ to oxidize
easier
harder
130
Does 2Fe/2S or 4Fe/4S comes first reducation wise?
2Fe/2S easier to reduce again
131
UQ is a obligate ___e- donor/acceptor?
1e-
132
What coenzyme shuttles e- between donors/acceptors?
UQ
133
What is the Q-cycle?
as UQ is reduced H+ is pumped into the IMS
134
Hemes are prosthetic groups for __________
cytochromes
135
Hemes are obligate ___e- donor/acceptor
1e-
136
What is special about cytochrome a3?
it is penta so the 6th spot is open for O2 binding
137
What is the only complex with Cu?
Complex IV
138
What are the 2 types of Cu and what do they do?
CuA: electron transfer
CuB: assists cytochrome a3 in O2 reduction
139
Rieske 4Fe/4S is easier to reduce, what is its delta G?
positive (easier to reduce)
140
How is partial reduction of O2 prevented?
keeping cofactors near each other
141
What is another name from Complex I?
NADH ubiquinone oxidoreductase
142
What is another name for Complex II?
succinate ubiquinone oxidoreductase
143
What is another name for Complex III?
ubiquinol cytochrome c oxidoreductase
144
What is another name for Complex IV?
cytochrome c oxidase
145
What is the largest Complex?
Complex I
146
How many H+ are translocated from Complex I?
4
147
What are 2 inhibitors of Complex I?
Rotenone
Amytal
148
What happens to the RETC when Complex I inhibitors are present?
NADH accumulates = lactate accumulation (lactate DH) = CAC inhibited
149
Exposure to rotenone will lead to an increase in __________ production
lactate
150
What cofactor does Complex II have that doesn't participate in e- transfer and we are not sure why its there
heme b
151
How many H+ are translocated at Complex II?
none
152
What is an inhibitor of Complex II?
thenoyl trifluoroacetone carboxin
TTC
153
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____
Q P (IMS) (positive)
Q N (Matrix) (negative)
154
How many H+ are translocated at Complex III?
4
155
What cycle is used also in Complex III to translocated H+?
Q cycle
156
What are 3 inhibitors of Complex III?
1. myxothiazol
2. antimycin A
3. stigmatellin
157
In Complex IV, what does subunit I do?
O2 reduction
158
What cofactors are in Complex IV's subunit I?
Cyt. a
Cyt. a3
Cu B
159
In Complex IV, what does subunit II do?
site of Cyt. c binding
160
What cofactor is in Complex IV's subunit II?
CuA
161
In Complex IV, what does subunit III do?
hydrophobic channels to direct O2 to subunit I
162
What cofactor is in Complex IV's subunit III?
none
163
How many H+ are translocated across Complex IV?
2 (per e- pair)
164
What are the 3 channels of Complex IV?
K channel
D channel
H channel
165
Complex IV's K channel's H+ comes from _______
Cu B
166
Complex IV's D channel's H+ comes from _______
Cyt. a3
167
Complex IV's H channel's H+ comes from _______
matrix
168
Which Complex IV channel is vectoral?
H channel (matrix to IMS physically)
169
I am an electron transport complex, I have no Rieske Fe/S, no hemes and no FAD.
Complex I
170
I am an electron transport complex, I have Fe/S and hemes but no flavins.
Complex III
171
There is a __________ gradient and a ___________ gradient across the inner membrane
concentration
charge
172
RETC's goal is to pump H+ into ________ for ATPase to make ATP
IMS
173
The pH in the IMS is _______ than the pH in the matrix
lower (more H+)
174
The delta G pushing against the gradient is POSITIVE OR NEGATIVE?
positive
175
The delta G at the end of RETC is POSITIVE OR NEGATIVE?
negative
176
What is the chemiosmotic hypotheisis?
Free E (-G) delivered from H+ passage across the membrane with the gradient provides the driving force for ADP phosphorylation
177
What is an uncoupling agent?
able to cross the mitochondrial inner membrane (in protonated state), the deprotonates once across (INCREASE PERMIABILITY)
178
What are 4 examples of uncoupling agents?
1. 2,4-dinitrophenol
2. Fluorocarbonyl cyanide phenylhydrazine
3. Dicoumarol
4. Thermogenin
179
The coupling agent, ___________, is expressed in brown fat of mitochondria
Thermogenin
180
What is brown fat?
uses proton gradient to generate heat to protect CNS and organs (babies)
181
T/F Introduction of a K+ channel in the mitochondria inner membrane will disrupt ATP synthesis by F1F0.
true
182
T/F introduction of a K+ channel in the mitochondria inner membrane will result in lactate accumulation.
False (uncoupling agents are not inhibitors so they are no inhibiting the e- flow they are only affecting "downstream" ATP synthesis)
183
What couples the H+ generated by RET and ADP phosphorylation?
F1F0 ATPase
184
Where is F1F0 ATPase located?
F0 - inner membrane
F1 - matrix
185
What are the subunits of F1?
3 alpha
3 beta
1 gamma
1 delta
1 epsilon
186
What does the alpha subunit do of F1?
binds ATP but DOES NOT catalyze
187
the alpha subunit of F1 provides an ______ residue to the beta subunit
Arginine
188
What are the 3 binding options for the beta subunit of F1?
AMP PNP (ATP)
ADP + Pi
empty
189
When (AMP PNP) ATP is bound to the beta subunit of F1, is the KD high or low?
low (high association)
190
The center of the alpha/beta orange of F1 is very _________ made of ___________
hydrophobic
3 alpha helices
191
In the presence of ATP and the absence of F0, the gamma subunit rotates in the ____________ direction
counter clockwise
192
Which subunit of F1F0 ATPase is in the matrix? F1 or F0?
F1
193
How many alpha helices is the c ring of F0 made of?
12
194
c ring of F0 has Asp61 on each subunit, what is special about the last one?
It is partially off the subunit because of helical unwinding which allows H+ to bind and be dropped off in the matrix
195
subunit a of F0 has a _______ residue
Arg 210
196
What subunit of F0 has a half channel for H+?
a
197
Which complex does dicoumarol bind to?
none
198
Which complexes activity is inhibited by dicoumarol?
F1F0 ATPase
199
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?
9
200
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?
9
201
How many ATP are made for every gamma revolution?
3
202
What is the purpose of the Complexes in the RETC?
build a high concentration of H+ in the IMS
203
H+ in the IMS enters ATPase where?
F0 (a subunit)
204
What structurally distinguishes heme a, b, and c
a: long tail
b: normal
c: S-protein
205
T/F: under standard conditions, malate oxidation by NAD+ is energetically favored
false
206
T/F: almost all hemes found in the ETC are hexacoordinate
true
207
T/F: In the context of the citric acid cycle, oxaloacetate can be viewed as a catalyst
true
208
What electron transport complex contains a Reiske Fe/S center?
complex III
209
What electron transport complexes do not contain hemes?
complex I
210
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
d. All are true
211
What is the order of electron transfer in Complex I?
NADH, FMN, Fe/S, UQ
212
In Complex I, what would happen if conformational change is not possible?
no H+ transfer but e- would still happen
213
What would happen if UQ binding is affected in Complex I?
no e- transfer and no H+ transfer stopping all other complexes after I
214
Would someone with no e- transfer or with e- would have more pyruvate DH kinase activity/lactate accumulation?
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
Why are the cofactors in the specific orders they’re in in the RETC?
reduction potential and obligate donor/acceptors
216
How does CN affect succinate DH (complex II)?
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
T/F: in the absence of F0, F1 catalyzes ATP synthesis
false (catalyzes ATP hydrolysis)
218
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.
true
219
Carboxin is an inhibitor for which complex?
Complex II (inhibits succinate)
220
What is the visual difference between NADH and FAD?
NADH has 1 N ring
FAD has 2 N rings
221
What is the visual difference between FAD and FMN?
FAD has a bunch of stuff at the bottom
FMN looks just like it without the clutter at the bottom
222
What is visual difference between CuA and CuB?
CuA is more complicated looking (makes a square)
223
How does stigmatellin affect Rieske Fe/S clusters?
affects the reduction potential
224
what are 2 reasons fat is good for storage?
1. carbon reduces easily
2. little water
225
what catalyzes the hydrolysis of TAGs to glycerol and fatty acids?
pancreatic lipase
226
What is the cascade of lipolysis?
1. TAG
2. DAG
3. MAG
4. glycerol
227
What enzyme catalyzes TAG to DAG?
TAG lipase
228
What enzyme catalyzes DAG to MAG?
DAG lipase
229
What enzyme catalyzes MAG to glycerol?
MAG lipase
230
What is fatty acid activation?
fatty acid has AMP attached to it then turns into acyl coA
231
What catalyzes fatty acid activation?
acyl CoA ligase
232
What transports fatty acids to the matrix?
L-carnitine (CAT)
233
What is the order of enzymes in B oxidation?
1. acyl-coA DH
2. enoyl-coA hydratase
3. L-hydroxyacyl CoA DH
4. thiolase
234
_________ inhibits carnitine (CAT) transport system
malonyl coA
235
What makes ketone bodies?
hepatocytes
236
_________ [acetyl coA] favors ketone body formation
increasing
237
ketone levels increase in the fasting or well feed state
fasting
238
What is the purpose of ketone bodies?
alternative fuel source so CNS can use glucose
239
What molecule does ketone body formation start with?
acetyl coA from B oxidation
240
How is acetyl CoA moved to the cytosol for FA synthesis?
as citrate
241
What are the 2 sources of NADPH for FA synthesis?
Malic enzyme
PPPathway
242
what transports fatty acyl CoA into the marix for B oxidation?
L-carnitine (CAT)
243
what is the name of the 12 c fatty acid?
lauric acid
244
what is the name of the 14 c fatty acid?
myristic acid
245
what is the name of the 16 c fatty acid?
palmitic acid
246
what is the name of the 18 c fatty acid?
stearic acid
247
what are the 2 possible fates of pyruvate?
turn into oxaloacetate via pyruvate carboxylase
turn into acetyl coA via pyruvate DH (plus cofactors)
248
increased acetyl coA = increased or decreased PDH
decreased
249
increased acetyl coA = increased or decreased pyruvate carboxylase
increased
250
In order for B oxidation to occur, what is needed?
inactivated fatty acyl CoA
251
What is the fate of acetly coA generated by B oxidation?
CAC
252
What is the important enzyme for ketone bodies?
HMG CoA lyasee
253
what cofactor creates trans double bonds?
FAD
254
What cofactor had H2O involved?
NAD
255
What cofactor uses SH-CoA?
lipoamide
256
What enzyme is the largest player in fatty acid synthase?
ACP
257
What is the order of enzymes in fatty acid synthase?
KS
MAT
KS
KR
DH
ER
258
Why is glycogen synthesis better in hepatocytes than skeletal myocytes?
G6P can be broken down into something useable and transported out of cell
259
is glycogen phosphorylase favored in fasting or well fed?
fasting/fight or flight
260
TAG lipase is activated or inhibited by phosphorylation?
activated
261
perilipin is activated or inhibited by phosphorylation?
activated
