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OLD "MBS 602" > Exam 3 > Flashcards

Exam 3 Flashcards

1
Q

Most fat from food comes in the form of __________

A

triglycerides

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2
Q

What class of enzyme hydrolyzes trglycerides into fatty acids?

A

lipases

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3
Q

In the fed state, where do fatty acids from food go?

A

adipose tissue

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4
Q

In the fasting state, where does the stored fatty acids go?

A

liver and muscles

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5
Q

Fatty acids are _____________ molecules because they have both a hydrophobic and hydrophilic moiety

A

amphipathic

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6
Q

In the blood fatty acids are bound to __________. Why?

A

Albumin
They are too acidic on thier own

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7
Q

What are the steps of fatty acids entering the cell—> mitochondria?

A
  1. FA transporter at plasma membrane lets FA into cell
  2. FA is bound to FBP (FA binding protein) in cytosol
  3. FA is transported into mitochondria
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8
Q

Most fatty acids are oxidized in the ______________

A

mitochondria

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9
Q

What 2 things are required for the uptake of fatty acids into the mitochondria?

A
  1. FA binds to CoA = fatty acyl CoA
  2. fatty acyl CoA binds to carnitine = fatty acyl-Carnitine
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10
Q

The uptake of fatty acids into the mitochondria is regulated by the concentration of cytoplasmic ________________

A

malonyl-CoA

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11
Q

Is carnitine derived de novo or through the diet?

A

diet

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12
Q

Does malonyl coA inhibit or promote the uptake of fatty acids in to mitochondria?

A

inhibit (represses entry)

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13
Q

Insulin (through malonyl-coA) inhibits or stimulates FA uptake into mitochondria IN THE LIVER?

A

inhibits uptake

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14
Q

AMP inhibits or stimulates FA uptake into mitochondria IN ALL TISSUES?

A

stimulates uptake

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15
Q

What is the purpose of beta-oxidation?

A

FA are broken down to generate acetyl-coA and FADH2/NADH

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16
Q

How long will the B-oxidation cycle go?

A

until only 2 carbons are left

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17
Q

Which carbon is always oxidized in B-oxidation?

A

beta carbon

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18
Q

How many carbons are removed per cycle of B-oxidation?

A

2

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19
Q

Every 2 carbons removed in the B-oxidation cycle, how many FADH2 is yielded?

A

1

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20
Q

Every 2 carbons removed in the B-oxidation cycle, how many NADH is yielded?

A

1

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21
Q

Every 2 carbons removed in the B-oxidation cycle, how many acetyl coA is yielded?

A

1

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22
Q

What does one round of B-oxidation cost?
Where does it come from?

A

1 ATP
attaching coA to FA

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23
Q

How do you find out how many cycles a certain FA will require of B-oxidation?

A

(n/2 -1) = # cycles

n = number of carbons

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24
Q

How do you find out how many acetyl-coAs are made from a certain FA undergoing B-oxidation?

A

cycles + 1

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25
Q

What is the final carbon product of B-oxidation?
Where does it go?

A

acetyl coA
Krebs cycle

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26
Q

Where does B-oxidation NOT occur?

A

brain and RBC
(no mitochondria)

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27
Q

Where does B-oxidation occur?

A

mitochondria

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28
Q

What are the two sources of acetyl coA?

A

fed: comes from pyruvate
fasting: comes from B-oxidation (much more of this)

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29
Q

Does insulin inhibit or stimulate lipolysis/B-oxidation?

A

inhibit

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30
Q

Does epinephrine inhibit or stimulate lipolysis/B-oxidation?

A

stimulate

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31
Q

When muscles need energy, FA ________ are incorporated into the plasma membrane to uptake FA from blood

A

FA transporters

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32
Q

What are the steps of lipolysis?

A
  1. triglycerides
  2. FA + glycerol
  3. fatty acyl-coA
  4. acetyl coA —> Krebs cycle
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33
Q

What is the purpose of ketone body synthesis?

A

alternative source of energy besides glucose

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34
Q

What are the 3 ketone bodies?

A

acetoacetate
B-hydroxybutyrate
acetone

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35
Q

Do ketone bodies alkalize or acidify blood?

A

acidify

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36
Q

What organ does ketone body synthesis occur?

A

liver

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37
Q

Excess _______________ built up in the mitochondria can be used to synthesize ketone bodies

A

acetyl coA

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38
Q

Is excess acetyl coA from diet or de novo used to make ketone bodies?

A

de novo (liver mitochondria)

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39
Q

What state are ketone bodies made in?

A

extended fasting

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40
Q

Are ketone bodies synthesized during high or low rate of lipolysis? and why

A

High rate
lots of excess acetyl coA being made from B-oxidation

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41
Q

How many acetyl coAs are required to make 1 acetoacetate?

A

2

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42
Q

What are the reactants and products of ketone body synthesis?

A

2 acetyl coAs —> acetoacetate + acetone + B-hydroxybutryate

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43
Q

The synthesis of ketone bodies after 3 days of fasting induces a _______________ as a safety mechanism

A

feedback loop

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44
Q

The ketone body feed back loop stimulates __________ secretion to impair lipolysis

A

insulin

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45
Q

Why is the ketone body feedback loop in place?

A

prevent blood from becoming too acidic

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46
Q

If ketone bodies induce a feedback loop due to insulin the rate of lipolysis is _______ and the rate of ketogenesis is _______

A

low
low

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47
Q

What does the ketone body feedback loop prevent?

A

ketoacidosis

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48
Q

What is ketone body oxidation?

A

(ketolysis) break down of ketone bodies

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49
Q

What are ketone bodies broken down into and where do they go?

A

acetyl coA
CAC cycle

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50
Q

What tissues use ketone bodies?

A

brain
heart
muscle
kidneys

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51
Q

What tissues don’t use ketone bodies?

A

liver
RBC

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52
Q

Cells that oxidize ketone bodies have an increased or decreased need for oxidation of glucose (breakdown of glucose)

A

decreased

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53
Q

Ketolysis = increased/decreased acetyl coA = increased/decreased PDH activity = preserve glucose for brain

A

increase acetyl coA
decrease PDH

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54
Q

Does ketone body oxidation (lysis) inhibit or activate PDH and glycolysis?

A

inhibit

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55
Q

In the fed state the brain uses _____% of glucose.
In the long term fasting state the brain uses ____% ketone bodies

A

100% glucose
75% ketone bodies

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56
Q

What organ cannot oxidize ketone bodies?
Why?

A

liver
acetyl coA from ketolysis cannot be used in gluconeogensis as a carbon skeleton

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57
Q

Where does the energy for gluconeogenesis come from in the liver?

A

B-oxidation

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58
Q

What is it called when B-oxidation and ketolysis inhibits glycolysis?

A

glucose sparing (for the brain)

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59
Q

What are the two ways to slow down glycolysis via B-oxidation and ketolysis?

A
  1. ATP produced from B-oxidation and ketolysis inhibits glycolysis
  2. Acetyl coA produced from B-oxidation inhibits PDH
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60
Q

What is ketosis?

A

synthesis of ketone bodies when fasting for 2-3 days

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61
Q

What does ketosis shut off and how?

A

represses lipolysis
secretes insulin

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62
Q

What is ketoacidosis?

A

too much ketone body synthesis and too little degradation acidifies the blood

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63
Q

What kind of patients is it common for ketoacidosis to occur?

A

server insulin deficiency

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64
Q

What condition are required for diabetic ketoacidosis?
? [glucose]
? [insulin]
? [ketones]
? pH

A

[glucose] - high
[insulin] - low
[ketones] - high
pH - low

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65
Q

What are the conditions for ketotic hypoglycemia?
? [ketone bodies]
? [glucose]

A

[ketone bodies] - high
[glucose] - low

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66
Q

Ketotic hypoglycemia manifests when there is low/high insulin the the blood

A

low

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67
Q

What are the conditions for non-ketotic hypoglycemia?
? [ketone bodies]
? [glucose]

A

[ketone bodies] - low
[glucose] - low

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68
Q

non-ketotic hypoglycemia manifests when there is low/high insulin the the blood

A

high

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69
Q

Where does the ETC occur?

A

mitochondria
- inner membrane space
- inner membrane
- matrix

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70
Q

Where are the ETC complexes located?

A

inner membrane of mitochondria

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71
Q

What are the 2 mobile electron carriers of the ETC?

A

coenzyme Q
cytochtome

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72
Q

What is complex I of ETC called?

A

NADH DH

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73
Q

Complex I of ETC…
oxidizes ____ to _____
produces _____

A

NADH to NAD+
Ubiquinol

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74
Q

What is the only ETC complex that does not pump a proton?

A

complex II (Succinate DH)

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75
Q

What is complex II of the ETC called?

A

Succinate DH

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76
Q

Complex II of the ETC…
oxidizes _____ to ______
produced ________

A

FAHD2 to FAD+
Ubiquinol

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77
Q

What is complex III of the ETC called?

A

cyt bc1 complex

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78
Q

Complex III of the ETC…
oxidizes ______
transfers e- to _______

A

ubiquinol
cyt C

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79
Q

What is complex IV of the ETC called?

A

cyt C oxidase

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80
Q

Complex IV of the ETC…
transfers e- to _____ generating _______

A

O2
water

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81
Q

In the ETC, where does the proton motive force (PMF) occur?

A

inner membrane space
protons are pushed into ATPase

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82
Q

The inner mitochondrial membrane is permeable or impermeable?

A

impermeable

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83
Q

What is complex V of the ETC called?

A

F0F1 ATP synthase

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84
Q

What is the chemisomotic-coupling hypothesis?

A

oxidation of NADH and FADH2 is couple with the transport of H+ out of the matrix into the inner membrane space and that gradient drive H+ into ATPase

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85
Q

What is the net ATP product of the ETC?
#1 oxidation of 1 NADH = ____ ATP
#2 oxidation of 1 FADH2 = _____ ATP

A

NADH – 3 ATP
FADH2 – 2 ATP

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86
Q

ATP production is larger from break down of carbs (glucose) or fats?

A

fats

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87
Q

_____ is the most important factor controlling the rate of oxidative phosphorylation

A

ADP

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88
Q

ATP consumption is high or low when…
ETC doesn’t pump H+
NADH grows slowing CAC
ATP synthase makes low ATP

A

low consumption

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89
Q

ATP consumption is high or low when…
ADP increases
ATP synthase makes ATP
CAC increases

A

high consumption

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90
Q

What are the 2 families of ETC inhibitors?

A
  1. targets complex I (NADH DH)
  2. targets complex IV (cyt c oxidase)
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91
Q

ETC inhibitors make the body hot or cold?

A

cold

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92
Q

What is an example of complex I inhibitor of ETC?

A

metformin

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93
Q

Metformin lowers ________ in the blood

A

glucose

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94
Q

Metformin can cause ___________ because of the increase in anaerobic glycolysis

A

lactic acidosis

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95
Q

How do complex IV (cyt c oxidase) inhibitors work?

A

bind to heme

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96
Q

How do uncouplers of the ETC work?

A

collapse the pH gradient causing H+ to cross back making complexes go faster

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97
Q

ETC uncouplers cause the body to become hot or cold?

A

hot

98
Q

How do you interpret this fatty acid to be?
16:2

A

16 carbons
2 double bonds

99
Q

How do you name carbons with the alternative method?

A

start number carbons at the CH3 end of the chain

99
Q

How do you name fatty acids using the standard method?

A

start number carbons at the carbonyl carbon

100
Q

Do saturated FA have a double bond?

A

no

101
Q

Do unsaturated FA have a double bond?

A

yes

102
Q

Saturated fats tend to be solid or liquid at room temperature?

A

solid (animal products)

103
Q

Unsaturated fats tend to be solid or liquid at room temperature?

A

liquid (plant products)

104
Q

Do saturated or unsaturated FA can come in trans and cis?

A

unsaturated

105
Q

The human body can only synthesize cis or trans unsaturated FA but can degrade both?

A

cis

106
Q

Cis FA tend to be liquid or solid?

A

liquid

107
Q

Trans FA tend to be liquid or solid?

A

solid

108
Q

In the standard method of naming fats, what does the delta mean?

A

double bond position

109
Q

What are the 3 essential fatty acids?

A
  1. linoleate (w-6)
  2. linolenate (w-3)
  3. arachidonate
110
Q

What 2 fatty acids are used as supplements?

A

EPA (w-3)
DHA (w-3)

111
Q

Free fatty acids are toxin in high concentrations because they are so acidic. What are they bound to to neutralize them?

A

albumin

112
Q

Inside of cells fatty acids are bound to ________ instead of albumin to neutralize them

A

FABPs

113
Q

What are the 4 general steps of FA synthesis?

A
  1. citrate movement from mitochondria (CAC) to cytoplasm of hepatocytes (liver cells)
  2. production of cytoplasmic acetyl coA (from citrate)
  3. production of malonyl coA
  4. FA synthesis via FA synthase
114
Q

Where does FA synthesis occur?

A

liver

115
Q

Metabolic conditions that allow citrate to leave CAC (mitochondria) for FA synthesis are…
_____ insulin
_____ PFK1
glucose —–> ______
pyruvate into _______

A

increased insulin
increased PFK1 activity
glucose —–> pyruvate
pyruvate —-> CAC

116
Q

Does insulin stimulate or inhibit FA synthesis?

A

stimualte

117
Q

In FA synthesis, citrate leaves the mitochondria and turns into ___________

A

acetyl coA

118
Q

In FA synthese, after citrate is turned into acetyl coA, what does it become next?

A

malonyl coA

119
Q

What enzyme turns acetyl coA into malonyl coA in FA synthesis?

A

acetyl coA carboxylase

120
Q

Does insulin inhibit or activate acetyl-coA carboxylase?

A

activates (promotes FA synthesis)

121
Q

Where do the first 2 carbons needed for FA synthesis come from?

A

acetyl CoA

122
Q

Each 2 carbon addition during FA synthesis costs ____ NADPH and ____ ATP

A

2 NADPH
1 ATP

123
Q

How many NADPHs are required for synthesizing a C16?

A

14
2x7rounds

124
Q

How many ATP are needed to synthesize C16?

A

7
(acetyl coA –> malonyl CoA)

125
Q

How many acetyl coA are needed to synthesize a C16?

A

8
(1 primer + 7 malonyl coA)

126
Q

What are the two sources of NADPH for FA synthesis in the liver?

A
  1. PPP (2 NADPH per glucose)
  2. Malate DH (1 NADPH per malate)
127
Q

Regular FA synthesis goes only up to C___, anything longer than that has to be syntheized by ______________

A

16
elongation

128
Q

What are the 2 steps of FA elongation?

A
  1. activation via esterification
  2. elongation
129
Q

What is desaturation of FAs?

A

addition of double bonds

130
Q

What 2 molecules are required for FA desaturation?

A

O2
NADH

131
Q

What is the limitation of desaturation of FA in humans?

A

desaturase can only introduce double bonds between carbon atoms 1-9

132
Q

FAs that contain 2 or more double bonds after carbon 9 come from diet making them ______________

A

essential

133
Q

What are the two types of essential fatty acids?

A
  1. Linoleate (w-6)
  2. Linolenate (w-3)
134
Q

The body converts ___________ to EPA and DHA (supplements)

A

linolenate (w-3)

135
Q

The body converts _________ to arachidonate

A

linoleate (w-6)

136
Q

What is the supplement DHA important for?

A

brain and retina

137
Q

What are eicosanoids?

A

stores arachidonic acid

137
Q
A
138
Q

What is the purpose of prostaglandins?

A

inflammation

139
Q

NSAIDs like aspirin inhibit ___________ enzyme

A

COX 1 & 2

140
Q

What are the 2 functions of inhibition of aspirin?

A
  1. inhibits prostaglandin (reduce inflammation)
  2. inhibits thromboxane (anticoagulant)
141
Q

What are the major sources of trans fats?

A

animal meat
heated cis fats
chemically hydrogenated fats

142
Q

What are lipoproteins?

A

large assembly of molecules made of proteins and lipids that transport lipids

143
Q

What are the 4 major lipid classes?

A
  1. triglycerides
  2. cholesteryl esters
  3. cholesterol
  4. free FAs
144
Q

What are the 5 major groups of plasma lipoproteins?

A
  1. chylomicrons
  2. VLDL
  3. IDL
  4. LDL
  5. HDL
145
Q

What are the 2 “bad” lipoproteins?

A

IDL
LDL

146
Q

Chylomicrons and VLDL are mainly made of ___________

A

lipids

147
Q

Cholestrol and phospholipids (IDL, LDL, and HDL) are mainly made of _____________

A

proteins

148
Q

What are the 2 chemical properties of lipoproteins?

A
  1. density
  2. size
149
Q

Are chylomicrons or HDL lighter?

A

chylomicrons

150
Q

What’s the heaviest lipoprotein?

A

HDL

151
Q

What are the proteins present in lipoproteins called?

A

Apo

152
Q

Why is ApoB-100 important?

A

marker for bad cholesterol (LDL)

152
Q

What kind of Apo is ApoB-100?
exchangeable or non-exchangeable?

A

non-exchangeable

153
Q

Where are chylomicrons originated and VLDL?

A
  1. dietary lipids (chylomicrons)
  2. lipid synthesis (VLDL)
154
Q

What makes VLDL different from chylomicrons composition?

A

VLDL has much more cholesterol esters

155
Q

Chylomicrons and VLDL are hydrolyzed of thier triacylglycerol by ______________

A

lipoprotein lipase

156
Q

What are the 5 steps of the fate of chylomicrons?

A
  1. fat uptake from diet
  2. chylomicron synthesis
  3. removal of FAs
  4. enrichment in cholestrol/loss of triacylglycerol
  5. liver uptakes remnants via LDL receptor-related protein
157
Q

What are the 5 steps of the fate of VLDL?

A
  1. Fat synthesis in liver
  2. VLDL synthesis
  3. removal of FAs
    4.enrichment in cholestrol/loss of triacylglycerol
  4. liver uptakes remnant (LDL)
158
Q

Is chylomicron remnants or LDL richer in cholesterol?

A

LDL

159
Q

Lipoprotein lipase deficiency leads to ________- triglyceridemia

A

hyper (elevated triglycerides in blood)

160
Q

What 2 things does HTGL (hepatic lipase) do?

A

converts VLDL into IDL
remodels large HDLs into smaller ones

161
Q

What hormone controls lipoprotein lipase and how?

A

insulin
stimulates LPL activity in ADIPOCYTES
inhibits LPL in MUSCLES

162
Q

What happens to chylomicrons after lipolysis?

A

remnants taken up by liver (endocytosis)

163
Q

What happens to VLDL after lipolysis?

A

degraded to IDL and LDL and taken up by liver

164
Q

How is LDL metabolized into the liver?

A

LDL receptor

165
Q

Recognition of LDL via LDL-r is mediated by _______

A

B-100

166
Q

What is reverse cholesterol transport?

A

HDL removes fat molecules form cells because they cannot do it themselves

167
Q

What 2 things are HDL very important for?

A
  1. HDL removes cholesterol from arterial walls
  2. high levels of HDL protect against atherosclerosis
168
Q

What does LCAT do in HDL metabolism?

A

converts free cholestrol into cholesteryl esters which is taken up by HDL

169
Q

What is CETP important for in HDL metabolism?

A

collects triglerides from VLDL/LDL and exchanges them for cholesteryl esters from HDL

170
Q

What is PLTP important for in HDL metabolism?

A

transfers phospholipids from lipoproteins to HDL

171
Q

LCAT is bound to ____ and _____ in the blood

A

LDL and HDL

172
Q

What molecule does cholesterol look like?

A

steroids

173
Q

What are the 2 important carbons on cholesterol?

A

C3 - hydroxyl group (site of esterfication)
C17 - aliphatic chain

174
Q

where does cholesterol come from?

A

de novo
diet

175
Q

Where do all the carbon atoms of cholesterol come from?

A

acetyl coA

176
Q

It costs ______ acetyl coA and ____ ATP per 1 cholesterol?

A

18 acetyl coA
36 ATP

177
Q

Where does the acetyl coA that goes into cholesterol come from?

A

mitochondrion citrate

178
Q

Where in the cell does cholestrol synthesis take place?

A

cytoplasm and ER

179
Q

What organ does most of cholesterol synthesis take place in?

A

liver

180
Q

Whats the difference between cholesterol and cholesterol esters?

A

esters have a FA side on the C3

181
Q

What is the main purpose of cholesterol esters?

A

storage and transport of cholestrol

182
Q

What are the two pathways of cholesterol ester synthesis and the enzyme used?

A
  1. in tissues (ACAT)
  2. in plasma *LCAT)
183
Q

Break down of cholesterol esters make what and is done by what enzyme?

A

cholesterol and FA
esterases

184
Q

What are the 3 types of esterases?

A
  1. pancreatic cholesterol easterases
  2. lysosomal acid cholesteryl hydrolase
  3. NCEH
185
Q

What is the purpose of cholesterol?

A

changes membrane fluidity

186
Q
A
187
Q

What are the 4 types of membranes containing cholesterol and rank them from least to most cholesterol.

A
  1. ER, Golgi, mitochondria (most fluid)
  2. plasma membrane
  3. RBC membrane and nerve cells
  4. cell membrane of eye lens (stiff)
188
Q

What are 3 important derivatives of cholesterol?

A
  1. bile acid
  2. vitamin D1
  3. steroids
189
Q

What is the equation for [LDL]?

A

total - HDL - TG/5

190
Q

What are 3 ways to reduce cholesterol uptake?

A
  1. diet
  2. additives
  3. weight loss/exercise
  4. statins
191
Q

Statins are competitive inhibitors of __________________

A

HMG coA reductase

192
Q

________ must be ingested for the synthesis of AAs, proteins, neurotransmitters, nucleotides and ATP

A

nitrogen

193
Q

What is the limitation of nitrogen?

A

it cannot be stored in the body

194
Q

What are the 2 reactions that convert ammonium (NH4+) into organic nitrogen?

A
  1. a-ketogluterate + NH4+ ——> glutamate
  2. glutamate + NH4+ —–> glutamine
195
Q

What enzyme catalyzes a-ketogluterate + NH4+ ——> glutamate?

A

glutamate DH

196
Q

What enzyme catalyzes glutamate + NH4+ —–> glutamine?

A

glutamine synthetase

197
Q

Is glutamine or glutmate toxic?

A

glutamate

198
Q

What are the 3 roles of amino acids in metabolism?

A
  1. protein synthesis
  2. fuel source
  3. precursor for biosynthesis
199
Q

What are the 3 sources of amino acids?

A
  1. breakdown of body protein
  2. AA from diet
  3. biosynthesis from other metabolites
200
Q

What are the 3 classifications of amino acids?

A
  1. glucogenic
  2. ketogenic
  3. amphibolic
201
Q

What does it mean if an amino acid is classified as glucogenic?

A

gives rise to glucose via conversion of pyruvate/TCA intermediate

202
Q

What does it mean if an amino acids is classified as ketogenic?

A

gives rise to acetyl coA

203
Q

What are the 9 essential amino acids?

A

Arg
His
Ile
Leu
Thr
Lys
Met
Phe
Trp
Val
(Any Help In Learning These Little Molecules Proves Truly Valuable)

204
Q

What are non-essential amino acids?

A

can be synthesized in the body

205
Q

What is nitrogen balance?

A

the uptake and degradation of nitrogen must be equal

206
Q

What is positive nitrogen balance? What are 3 scenarios?

A

taking up more than you can degrade
1. growing children
2. pregnancy
3. tissue repair

207
Q

What is negative nitrogen balance?

A

more degradation that uptake

208
Q

What are 3 examples of negative nitrogen balance?

A
  1. trauma/stress
  2. marasmus
  3. kwashiorkor
209
Q

In negative nitrogen balance, Marasmus has prolonged deficiency in ______ and _______

A

protein
caloric intake

210
Q

In negative nitrogen balance, Kwashiorkor has prolonged deficiency in ______ but not _______

A

protein
caloric intake

211
Q

What are 2 ways proteins can be degraded by cells?

A

lysosomes (cytoplasm)
proteasomes (cytoplasm/nucleus)

212
Q

How are proteins targeted to proteasomes for degradation?

A

marked with poly-ubiquitin tag

213
Q

Where does protein degradation start and continue?

A

stomach via juices and proteases

pancreas and small intestines

214
Q

What 2 ways do digested proteins enter the blood stream as amino acids/small peptides?

A
  1. Na+ dependent transport
  2. just cross the lining
215
Q

What are the 2 steps in the 1st step of amino acid catabolism?

A
  1. transamination
  2. oxidative deamination
216
Q

Where are amino acids degraded?

A

muscle and liver

217
Q

What is the first step of amino acids catabolism?

A

removal of alpha-amino group (transamination then ox. deamination)

218
Q

What occurs in the transamination step of amino acid catabolism?

A

alpha-amino group of AA is transferred to a-keto acid to form glutamate

219
Q

What occurs in the oxidative deamination step of amino acid catabolism?

A

glutamate is deaminated to yield NH4+

220
Q

why does glutamate play a central role in amino acid catabolism?

A

controls the nitrogen levels

221
Q

Transamination and oxidative deamination of AAs is a ___________ reaction

A

coupled

222
Q

What enzyme catalyzes transamination/oxidative deamination?

A

glutamate DH

223
Q

What 2 molecules inhibit glutamate DH?

A

GTP and ATP

224
Q

Where does the urea cycle occur?

A

cytoplasm and mitochondria

225
Q

Where do the 2 nitrogens and the carbon from urea come from?

A
  1. a free ammonia
  2. amino group of aspartate
  3. CO2
226
Q

What is the first step in the urea cycle and what is it catalyzed by?

A

NH3 + CH3O —-> carbamoyl phosphate

CPS-1

227
Q

How many ATP does the first step of the urea cycle cost?

A

2

228
Q

What is the rate limiting step of the Urea cycle?

A

1st
CPS-1

229
Q

The activity of CPS-1 in the urea cycle is dependent on ___________

A

NAG

230
Q

The concentration of __________ determines the rate and activity of the urea cycle

A

NAG

231
Q

What is NAG formed from in the urea cycle?

A

acetyl coA

232
Q

NAG synthase in the Urea cycle is activated by _________

A

arginine

233
Q

Activation of the urea cycle via stimulation of carbamoyl phosphate synthase -1 (CPS-1) occurs only when there is …
#1
#2
#3

A

1 NH3 to maintain glutamate levels

#2 acetyl CoA + glutamate to make NAG
#3 arginine to activate NAH synthase

234
Q

How is the urea cycle and the TCA cycle interlinked?

A

aspartate goes from TCA to urea and fumarate comes out of urea cycle and into TCA

235
Q

Any defect in urea synthesis results in _____________

A

hyperammonemia

236
Q

What are the 2 main causes of urea cycle defects?

A

liver disease
genetic defects

237
Q

How is lactulose used as a treatment for urea cycle disorders?

A

reduces ammonia in blood
gut bacteria ferment the lactulose and will acidify the gut which allows NH3 from blood to enter gut and protonate into NH4+ and is peed out

OLD "MBS 602" (7 decks)

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