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MCB 2000 > Final > Flashcards

Final Flashcards

1
Q

Enzymes regulated by BOTH ATP/ADP

Inhibited by High ATP

A

PFK-1, Pyruvate Kinase, PDComplex, Isocitrate Dehydrogenase

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2
Q

Enzymes only INHIBITED by high ADP

A

Pyruvate Carboxylase, PEPCK

ATP has no effect

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3
Q

Activation step for Glycogen Synthesis

A

1 UTP + G-1-P –> UDP-Glucose (During Fed State!)

By udp-glucose-pyrophosphatase

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4
Q

Activation step for FAS

A

ACC - Adds CO2 + ATP to Acetyl CoA to make Malonyl CoA (Fed State)

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5
Q

Activation step for Cholesterol Synthesis

A

(Not rate limiting step)

Making Isoprene Unit = 3 ATP + Mevalonate –> 3-Isopentenyl Pyrophosphate (Fed State)

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6
Q

Activation step for Phospholipid synthesis

A

CTP + Polar Head group or DAG (Fed State)

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7
Q

Activation step for Triglyceride synthesis

A

Sike! there is none

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8
Q

Activation steps for Gluconeogenesis

A

6 ATP/GTP, during various regulation steps - Energy Source = beta-oxidation of FAs (Fasted state)

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9
Q

Activation step for FA oxidation (Beta oxidation)

A

Fatty Acid chain + Acyl (not acetyl) CoA + ATP –> FattyAcid-CoA (Driven by pyrophosphate hydrolysis)

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10
Q

Processes during fed state

A

Glycolysis, PDC, Glycogen synthesis, FA synthesis, Cholesterol Synthesis

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11
Q

Processes during fasted state

A

Ketogenesis, Gluconeogenesis, Glycogen degradation, FA oxidation

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12
Q

Rate Limiting step for Cholesterol Synthesis

A

HMG CoA Reductase:
HMG-CoA –> Mevalonate
Requires 2 NADPH

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13
Q

Rate Limiting Step for Fatty Acid Synthesis

A

Acetyl CoA Carboxylase:

Acetyl CoA + CO2 + ATP –> Malonyl CoA

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14
Q

All Carboxylases require ______ as coenzyme

A

Biotin

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15
Q

Rate Limiting step for Glycolysis

A

PFK1

F-6-P –> F-1,6-BP

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16
Q

Rate Limiting Step for TCA Cycle

A

Isocitrate Dehydrogenase:

Isocitrate + NAD+ –> alpha-ketoglutarate + CO2

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17
Q

Rate Limiting Step for Gluconeogenesis

A

F-1,6-Bisphosphatase

F-1,6-BP –> F-6-P

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18
Q

Reactions in mitochondria

A

FA oxidation
PDC (Acetyl CoA Production)
TCA Cycle
Oxidative phosphorylation

Both mito + cytosol:
Gluconeogenesis

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19
Q

Reactions in Cytoplasm

A

Glycolysis
FA Synthesis
Cholesterol Synthesis

Both:
GNG

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20
Q

Structure of cholesterol

A

three 6 membered, one 5 membered

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21
Q

Acetone must be exhaled because ketone body production leads blood pH to ______

A

Decrease – Acidosis

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22
Q

TCA Cycle Regulated by

A

[Acetyl CoA] and [OAA], ATP utilization, O2, NAD+/NADH

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23
Q

Muscle Contraction effects:

A

TCA cycle increases, O2 consumption increases, ADP increases, H+ gradient decreases (ox. phos. increases to restore H+ Gradient)

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24
Q

Insulin receptor cascade

A

NO G Protein

Binds –> IRS-1 phos. –> PI-3-Kinase phos. –> PIP2 phos. to PIP3 –> PDK-1 phos. –> AKT phos

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25
Q

GPCR Oxytocin

A

G protein activated –> Alpha subunit activates PLC –> PIP2 cleaved to IP3 and DAG –> IP3 releases CA2+ –> Ca2+ and DAG activate PKC

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26
Q

GPCR Epi/Glucagon

A

G-alpha activates adenylate cyclase –> cAMP produced –> cAMP activates PKA

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27
Q

RTK: RAS/RAF

A

GRB2 –> Sos –> Ras –> Raf –> Mek –> Erk1/2 –> Other shit

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28
Q

Do insulin receptors dimerize?

A

They don’t need to, they are always dimerized

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29
Q

Substrate level phosphorylation

A

Creatine phosphate, 1,3-BPG from step 6 glycolysis, PEP from step 10 glycolysis

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30
Q

Hexokinase/Glucokinase

A

Glucokinase (high Km) = Liver
Hexokinase = brain, all other tissues
Trap Glucose within cell to commit it to glycolysis

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31
Q

TCA Cycle intermediates are used in other pathways:

A

Citrate –> FAs, sterols
Alpha-ketoglutarate –> Glutamate –> Other amino acids –> Purines
Succinyl CoA –> porphyrins/heme
Oxaloacetate –> Aspartate -> Purines/Pyrimidines
OAA –> Glucose via GNG

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32
Q

Glucokinase regulation

A

Not FBI, inducible by insulin

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33
Q

Hexokinase regulation

A

FBI by G-6-P (product)

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34
Q

PFK-1 regulation

A

No hormonal
+: AMP, F-2,6-P (Not product F-1,6-P)
-: Citrate, ATP

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35
Q

PFK-2 regulation

A

Normal hormonal fed state active (NHFedSA)

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36
Q

Pyruvate Kinase

A

High energy charge inhibition (HECI), normal hormonal fed state active (NHFedSA)

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37
Q

PDH Complex

A

Pyruvate + NAD+ + CoA –> Acetyl CoA + CO2 + NADH + H+

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38
Q

PDH Complex regulation

A

High energy charge inhibition (HECI),
+: ADP, NAD+, Pyruvate
-: ATP, NADH, Acetyl CoA
NHFedSA

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39
Q

Is there hormonal regulation in the TCA Cycle?

A

NO! There is no I/G effect on TCA Cycle

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40
Q

Isocitrate dehydrogenase regulation

A

HECI (ATP/ADP),
+: NAD+
-: NADH

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41
Q

Alpha-ketoglutarate dehydrogenase regulation

A

HECI,
+: NAD+
-: NADH, Succinyl CoA

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42
Q

Which enzymes reduce NAD+ in TCA cycle?

A

All the dehydrogenases

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43
Q

Glycogen synthase

A

UDP-Glucose to alpha-1,4 linkages

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44
Q

Glycogen synthase regulation

A

Activated by G-6-P and dephosphorylated+activated by Protein Phosphatase 1,
NHFedSA!

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45
Q

NHFSA (Normal hormonal fed state active enzymes)

A

PFK-2, Pyruvate Kinase, PDH Complex, Glycogen synthase, ACC, HMG-CoA Reductase,

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46
Q

Glycogen Phosphorylase regulation

A

Protein phosphorylase dephosphorylates and inactivates, Opposite of NHFSA, it is active when phosphorylated

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47
Q

Acetyl CoA Carboxylase regulation

A 
Citrate attaches to polymerize/activate, palmitoyl attaches to inactivate by depolymerization,
NHFSA
Inactivated by AMP-Kinases
Inhibited by ADP
HECA HECA
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48
Q

Pyruvate carboxylase

A

Pyruvate to OAA for FAS

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49
Q

Pyruvate carboxylase regulation

A

Acetyl CoA positive allosteric

Activated by High Energy Charge (HECA!)

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50
Q

PEPCK function + Regulation

A

OAA to PEP - phosphorylate and decarboxylate

Inhibited only by high ADP

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51
Q

FBPase 2 function + regulation

A

against PFK2 to break down F-2,6-P, Opposite of NHFedSA, it is active when phosphorylated
Part of 2 part enzyme, other half is PFK2

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52
Q

Glucose-6-Phosphatase location, function

A

Removes phosphate from G-6-P
Only exists in liver so glucose –> Blood!
G-6-P in muscle goes right to glycolysis

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53
Q

Lactate Dehydrogenase function and regulation

A

Anaerobic respiration.. Pyruvate + NADH –> Lactate + NAD+
More NADH = positive
Less NADH = negative
Oxygen present?

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54
Q

Cholesterol made where?

A

Liver

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55
Q

Requirements for cholesterol synthesis

A

Acetyl CoA - thioester bonds
ATP
NADPH
O2

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56
Q

Mnemonic for Cholesterol

A

Alcoholic’s Anonymous Has Me Insane and Dying, I’D Go For Some Sweet PinaColada Laced Cocaine

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57
Q

LDL receptors undergo ___

A

Receptor mediated endocytosis

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58
Q

LDL receptors if mutated

A

LDL production will increase abnormally

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59
Q

Statin Drugs which step interfers

A

HMG-CoA Reductase

Competitive inhibitors!

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60
Q

HMG-CoA Reductase regulation

A

Phosphorylation by AMPKinases, HECA
Degradation - half life is 3 hrs - if Cholesterol is HIGH
Transcription/Translation by SCAP, SREBP, SRE - ONLY IF Cholesterol is LOW

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61
Q

SCAP SREBP SRE mechanism

A

SCAP and SREBP on membrane, if low cholesterol detected, they go into a golgi and go to nucleus where SREBP binds to SRE on chromosome and activates production of HMG-CoA

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62
Q

HDL

A

Reverse cholesterol transport- brings back cholesterol from vascular tissue to return to lver

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63
Q

Trans fat vs Saturated fat

A

Trans fat lowers HDL and raises LDL. Saturated Fat raises LDL but ignores HDL

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64
Q

Are there glucagon receptors in muscle?

A

No, only the liver responds to I/G ratio

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65
Q

Glycogen phosphorylase cleaves glycogen at the _________ ends

A

non-reducing ends

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66
Q

Transferase in glycogen degradation

A

transfers 3 glucoses before a branch point to the non-reducing end of a 1,4 linkage

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67
Q

Alpha-1,6-Glucosidase

A

for branch point cleavage

68
Q

Phosphoglucomutase

A

Converts G-1-P from glycogen degradation to G-6-P using serine to hold the phosphate

69
Q

Glycogen phosphorylase a and b, T and R forms in muscle and liver

A

aR=most active + phosphorylated
bT form in muscle, can become bR form with AMP
aR form in liver, can become aT form (less active) with increased glucose

70
Q

Why allosteric and hormonal regulation of glycogen degradation

A

allosteric is faster than hormonal, so can respond to smaller and quicker changes in glucose homeostasis

71
Q

Precursors for GNG

A

Lactate, AAs (muscle), Glycerol from TAG breakdown, TCA cycle intermediates (OAA)

72
Q

Cori Cycle main idea

A

Lactate from muscle moved to liver to be remade into pyruvate for glucose production
Lactate recycling

73
Q

Alanine aminotransferase

A

Converts alanine to pyruvate by removing an amino group

74
Q

Glycerol processed into GNG how?

A

Glycerol kinase then glycerol phosphate dehydrogenase to DHAP –> enters as intermediate

75
Q

Can Fatty acids be used as substrates for gluconeogenesis?

A

NO! They yield acetyl-CoA

No reverse for pyruvate dehydrogenase, kinetically or themodynamically

76
Q

GNG big picture:

A

Pyruvate to OAA
OAA leaves mitochondria as aspartic acid or malate
OAA to PEP by PEPCK
PEP to glucose
ATP comes from oxidation of fatty acids or ketone bodies

77
Q

Pyruvate carboxylase

A

Biotin for any carboxylase!

Pyruvate + ATP + CO2 –> OAA + ADP + Pi + 2H+

78
Q

PEPCK (Carboxykinase)

A

OAA + GTP –> PEP + GDP + CO2

Opposite Pyruvate kinase

79
Q

F-1,6-Bisphosphatase

A

Hydrolysis of F-1,6-bisphosphate to F-6-P
Opposite PFK1
Inhibited by F-2,6-Bisphosphate
RATE LIMITING POINT in GNG

80
Q

Glucose-6-Phosphatase in GNG, not Glycogen deg.

A

Not in muscle, only liver

Converts G-6-P to Glucose, released to bloodstream

81
Q

When does FA oxidation happen?

A

Fasted state, low I/G

82
Q

3 lipases in FA Oxidation

A 
Adipose Triglyceride lipase
Hormone Sensitive lipase
Monoacylglyceride Lipase
Each cleaves a single FA
AHM
83
Q

Activation of lipases in FA Oxidation

A

Phosphorylated perilipin activates ATGL
HS Lipase phosphorylated by Protein Kinase A
Protein Kinase A
Protein Kinase A

84
Q

Albumin role in FA oxidation

A

Serum protein
Binds multiple fatty acids
Transports FAs to tissues since FAs are hydrophobic

85
Q

Carnitine Acyltransferase I and II

A

1 attaches carnitine to activated FA - CoA removed

2 removes carnitine - adds CoA back

86
Q

Translocase of FA-carnitine

A

Moves FA-Carnitine into matrix of mitochondria

87
Q

Beta oxidation process:

A
  1. Oxidation = double bond formation, FAD reduced
  2. Hydration = alcohol formation
  3. Oxidation to yield ketone, NAD+ reduced
  4. Add SH to make Acetyl CoA and a Fatty acid CoA to continue oxidation
88
Q

How many ATP does 1 palmitic acid yield

A

106, not 108, since 2 ATP are required for activation

89
Q

Carnitine Acyltransferase regulation

A

Inhibited by Malonyl CoA - Cannot make and break down FA’s at the same time…

90
Q

FA Oxidation regulation

A

High [FA] = stimulates

ATP utilization controls rate of ETC - regulates oxidative enzymes of TCA cycle and beta-oxidation (NAD+ and FAD)

91
Q

Ketone body formation process:

A

2 Acetyl CoA –> Acetoacetyl CoA –> HMG-CoA –> Acetoacetate –> Acetone and D-3-hydroxybutyrate
Acetone is exhaled

92
Q

Advantages of ketone bodies

A

Water soluble
fuel source during prolonged fasting - for brain
Muscle sparing during fasting

93
Q

Conditions for Ketosis

A

Low insulin, low carb diets, Type 1 diabetes, Chronic alcoholism

94
Q

Oxidation of ketone bodies

A

Ketone body –> acetoacetate –> Acetoacetyl CoA –> 2 Acetyl CoA
Succinyl CoA used

95
Q

Can liver use ketone bodies?

A

Liver produces ketone bodies but CANNOT oxidize them!!

96
Q

Cholera toxin

A

cAMP continuously produced - dehydration - diarrhea

97
Q

Energy charge equilibrium maintained by enzyme:

A

Adenylate Kinase

2 ADP ATP + AMP

98
Q

Step 6 of Glycolysis

A

Redox reaction with NAD+ to form 1,3-BPG and NADH

1,3-BPG has high phosphoryl transfer potential (substrate level phosphorylation)

99
Q

Fructose-2,6-Bisphosphate effect on PFK1

A

Can override the inhibition of high ATP!

100
Q

Pyruvate dehydrogenase complex reaction

A

2 Pyruvate + NAD+–> CO2 + Acetyl CoA + NADH

101
Q

Vitamin coenzymes of PDC

A

Thiamine PPi - decarboxylation - releases CO2
Lipoamide - binds acetyl group, attaches CoA group
FAD – oxidizes Lipoamide

102
Q

Can I keep selling sex for money officer?

A

Citrate, Isocitrate, a-ketoglutarate, succinyl CoA, Succinate, Fumarate, malate, oxaloacetate!

103
Q

Citrate Synthase

A

Condensation reaction between OAA and Acetyl CoA - ORDERED BINDING
OAA binds 1st to create site for Acetyl CoA!

104
Q

What drives citrate synthase reaction?

A

Hydrolysis of high energy thioester bond of acetyl CoA

105
Q

Why is isocitrate dehydrogenase the rate limiting enzyme of TCA

A

1st step to produce NADH, depends on ETC to return NAD+

CO2 is removed

106
Q

Regulation within the TCA Cycle

A

Generally HECI, no hormonal control!
Citrate synthase controlled by small [OAA]
Inhibited by high NADH, low NAD+

107
Q

Anapleurotic reaction

A

Filling up / Refilling reactions

108
Q

E0 is positive when

A

The thing will accept electrons, like Oxygen

109
Q

Complex 1

A

Proton pumps

NADH –> FMN, 4 H+ pumped per 2 e- passed to CoQ

110
Q

Complex 2

A

Accepts from FAD

No proton pumping

111
Q

Isoprene units also appear in ____

A

not only cholesterol but also CoQ in ETC

112
Q

Complex 3

A

Transfers from CoQ to oxidized cytochrome c

pumps 2H+

113
Q

Complex 4

A

transfers from cytochrome c to oxygen to make water

Pumps 4 H+

114
Q

Cyanide, Azide, CO inhibit which complex

A

Complex 4
CN and N3 with Fe 3+ of heme a3
CO with Fe2+ of heme a3

115
Q

Reactive O2 species

A

OH radical most reactive

When O2 accepts a single electron to form superoxide

116
Q

Superoxide dismutase

A

Superoxide dismutase turns superoxide to H2O2

117
Q

Catalase (peroxisomes)

A

Turn H2O2 to H2O and O2

118
Q

GSH (glutathione) peroxidase and reductase

A

SH groups act as nucleophiles
React with peroxide to give GSSG
Reductase breaks GSSG back to GSH using NADPH

119
Q

Nonenzymatic antioxidants

A

Vitamin E - Protects against lipid peroxides

Vitamin C - supports reduced form of Vitamin E

120
Q

Number of ATP for NADH and FAD

A
  1. 5 ATP for NADH

1. 5 ATP for FAD

121
Q

Subunit a vs. alpha

A

Subunit a has 2 half channels, alpha subunits are just spacers between beta subunits

122
Q

Conformations of beta subunits

A

L - Loose - binds ADP and Pi
T - Tight - turns ADP + Pi To ATP, but holds it
O - open - releases ATP

123
Q

Amino acid on C subunits in c ring

A

Aspartic acid

124
Q

ATP yield per glucose from complete oxidation

A

Invest 2, get out 32, net yield is +30 ATP

125
Q

Glycerol-3-phosphate shuttle

A

Located in muscle, brings electrons from cytosol to ETC

Yields 1.5 ATP per NADH instead of 2.5 since it uses FAD

126
Q

Malate Aspartate shuttle

A

Located in liver/heart

Still uses NADH so 2.5 ATP are yielded still per NADH

127
Q

Respiratory control

A

ADP concentration controls rate of O2 consumption

128
Q

As ATP is used…

A

O2 consumption increases, pmf can be sensed and must be maintained, everything speeds up

129
Q

ATP-ADP translocase

A

Most ATP to cytoplasm, ADP to mitochondria

130
Q

Respiratory inhibitors

A 
Rotenone + Amytal - C1
Antimycin A - C3
CN-, N3-, Fe3+ heme a3 on C4
CO - Fe2+ on heme a3 on C4
Buildup of NADH
131
Q

ATP Synthase inhibitors

A

Oligomycin
DCCD
Same thing happens as respiratory inhibitors, whole process of ETC slows
Buildup of NADH

132
Q

Uncouplers

A

p-nitro phenol
If stuff is still running, then this is probably it
Buildup of NAD+ but no ATP generated

133
Q

UCP-1 found in…

A

Brown Adipose tissue only

134
Q

Why use glycogen, in terms of osmotic pressure

A

Glycogen has a fraction of osmotic pressure vs. equivalent #glucose molecules

135
Q

Alpha vs. beta linkages

A 
Alpha = trans - Glycogen
Beta = Cis - Cellulose
136
Q

Ketone + Alcohol =

A

Hemiketal

137
Q

Glycogenin is a protein that…

A

Synthesizes the primer of glycogen synthesis - a short oligosaccharide of glucose

138
Q

Activation step of glycogen synthesis driven by:

A

Cleavage of pyrophosphate

UTP + G-1-P –> UDP-Glucose + PPi

139
Q

AKT effect on glycogen

A

AKT from insulin signalling

AKT deactivates glycogen synthase KINASE, which allows glycogen synthase to be active in dephosphorylated form

140
Q

Fatty acid synthesis location

A

Liver, also adipose tissue to lesser extent

141
Q

What happens without insulin to Acetyl CoA

A

Ketone bodies are made instead of fatty acids

142
Q

Sources of NADPH

A

PPP - Glucose to Ribulose 5-c Sugar, gives 2 NADPH

Malic Enzyme - Malate to pyruvate - gives 1 NADPH

143
Q

What breaks down citrate in cytosol?

A

ATP Citrate lyase

144
Q

AMP kinases

A

Phosphorylate and deactivate carboxylases and HMG CoA Reductase
Activated by AMP
Inhibited by ATP

145
Q

Fatty Acid Synthesis Process:

A
  1. Condensation to release CO2
  2. Reduction of Carbonyl to get alcohol
  3. Dehydration to yield water
  4. Reduction of Double bond
  5. Pass to condensing enzyme to continue
146
Q

Source of carbons for FAS

A

Carbon from DIET

147
Q

Where does saturated–>unsaturated bond happen?

A

Endoplasmic reticulum

148
Q

Glucose-6-Phosphate Dehydrogenase

A

G-6-P –> some intermediate

Rate controlling step of PPP, generates 1 NADPH

149
Q

Triacylglycerols - Why make them?

A

Hydrophobic, efficient storage, energy WITHOUT NITROGEN

150
Q

Sources of glycerol

A

Adipose tissue depends on DHAP from glycolysis ONLY

Liver gets it from glycerol kinase

151
Q

Common intermediate between Phospholipid vs. TAG biosynthesis

A

Phosphotidate

152
Q

Lipoprotein Lipase

A

During FED state, activated by insulin

153
Q

LDL, HDL, VLDL, Chylomicrons Relative densities and protein concentrations

A

Density and [TAG] = Chylomicrons>VLDL>LDL>HDL

Protein Content = HDL>LDL>VLDL>Chylomicrons

154
Q

Thiolase

A

condenses acetyl coa + acetyl coa to acetoacetyl coA

155
Q

How many ATP from palmitic acid

A 
10 for each acetyl coA through TCA
8*10 = 80
split it 7 times in beta oxidation - 4 ATP each
7*4 = 28
Invested 2 carbons
108-2 = 106 ATP
156
Q

What do you need for Cholesterol synthesis

A

ATP for Isoprene unit formation
NADPH for Mevalonate formation and Cyclization and hydroxylation
O2 for Cyclization and hydroxylation

157
Q

Where does cyclization of Cholesterol occur?

A

Smooth ER

158
Q

Only 5 enzymes that are activated by phosphorylation

A 
FBPase-2
Glycogen phosphorylase
Perilipin
HS Lipase 
AMPKinase
159
Q

Fatty Acid Oxidation regulated by:

A

Rate of oxidation of NADH and FADH2 in TCA cycle
ATP/ADP ratio - BECAUSE TCA CYCLE DEPENDS ON IT TOO
Malonyl CoA inhibits
High fatty acids activates

160
Q

Rate limiting enzyme of TAG degradation

A

HS lipase- phosphorylated and activated by PKA

161
Q

Rate Limiting enzyme in FA Oxidation

A

Carnitine palmitoyl transferase 1

Inhibited by malonyl CoA

162
Q

Glyceraldehyde 3-phosphate dehydrogenase

A

Step 6 Glycolysis, makes 1,3-BPG
NAD+ –> NADH
Thioester intermediate!
NOT FBI by ATP!

163
Q

What type of reaction does PDH Complex catalyze?

A

Oxidative decarboxylation

Pyruvate –> CO2 + Acetyl CoA

164
Q

Citrate synthase binding, be specific

A

Independently is NOT equal to “induced fit”
ORDERED BINDING..
Also FBI by Citrate!

165
Q

Pantothenic Acid is a coenzyme for

A

Acyl Carrier Protein in FAS

166
Q

What drives condensation reactions in Lipogenesis?

A

Decarboxylation, not NADPH

167
Q

Fatty acids produced from ______ end to _______ end

A

Omega (reducing) to Carboxylic acid end (non-reducing)

MCB 2000 (3 decks)

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