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Block 3; Week 1 > Valencik Carb Metabolism > Flashcards

Valencik Carb Metabolism Flashcards

1
Q

What are the 4 things that pyruvate can turn into & how?

A
  1. Lactate; reduction
  2. acetyl CoA; oxidative decarboxylation
  3. oxaloacetate; carboxylation
  4. alanine; transamination
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2
Q

Pyruvate dehydrogenase only works under ___ conditions. Describe this step in detail.

A

aerobic conditions.
Pyruvate–>Acetyl CoA
requires NAD+; gives off NADH
Also produces CO2

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3
Q

Where does pyruvate dehydrogenase do its thing?

A

in the mitochondrial matrix. The pyruvate is transported across the membrane.

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4
Q

Pyruvate dehydrogenase is a ____ enzyme that causes a ____ reaction.

A

alpha ketoacid dehydrogenase

irreversible reaction

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5
Q

Aside from pyruvate dehydrogenase, what is another example of alpha ketoacid dehydrogenase?

A

alpha ketoglutarate dehdyrogenase

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6
Q

Oxidative decarboxylation is an ______ reaction.

A

irreversible

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7
Q

What are the 3 catalytic enzymes that make up the pyruvate dehydrogenase complex?

A

E1: on the outside…pyruvate dehydrogenase
E2: in the core…DLTA: dihydrolipoyl transacetylase
E3: in the core…DLDH: dihydrolipoyl dehdyrogenase

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8
Q

What are the 5 coenzymes that make up the pyruvate dehydrogenase complex?

A 
TPP: thiamine pyrophosphate
CoA: coenzyme A
NAD+
FAD+
Lipoamide
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9
Q

What are the vitamins that are required for the coenzymes of pyruvate dehydrogenase to work?

A 
TPP-- requires thiamine (B1)
CoA--requires panthothenic acid (B5)
NAD--requires niacin (B3)
FAD--requires riboflavin (B2)
Lipoamide--doesn't require anything
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10
Q

Beri Beri is caused by a deficiency of what? What 3 things build up in the body as a result? This can impair CNS function etc.

A

thiamine deficiency
pyruvate, lactate, alanine (after you eat lots of carbs)
**body can’t make acetyl CoA very easily

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11
Q

TPP contains what ring? It carries what 2 things? It is bound noncovalently to what?

A

thiazolium
pyruvate
hydroxyethyl group
apoprotein

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12
Q

Lipoamide is required for which enzyme that is a part of the pyruvate dehydrogenase complex?

A

required for E2: the outer edge: a part of DLTA

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13
Q

How is the lipoate attached to the E2 enzyme?

A

bound covalently w/ an amide linkage to the lysine

synthesized directly onto the E2 enzyme to form the lipoyl domain…never free

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14
Q

T/F There is free lipoic acid that is a part of the E2 enzyme.

A

False. B/c the lipoic component of the E2 enzyme is synthesized directly on there–>it is not ever freely hanging around.

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15
Q

What does lipoic acid do in the pyruvate dehdyrogenase complex?

A

participates in redox & carries an acetyl group

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16
Q

What does coenzyme A help activate? What complex is this a part of?

A

DLTA/E2

pyruvate dehydrogenase complex

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17
Q

What vitamin does coenzyme A require?

A

Vitamin B5; pantothenic acid

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18
Q

What are 2 things that are required for activation of DLDH? dihydrolipoyl dehydrogenase

A

NAD+ & FAD

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19
Q 
Talking NAD+ here....
What vitamin does it require to be active?
What enzyme component does it activate? 
Of what complex?
What is its function?
A

VItamin B3; Niacin
DLDH
Pyruvate Dehydrogenase Complex
Hydride Transfers

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20
Q

With NAD & FAD…unlike CoA…??? Talk about a carbon.

A

The number 3 carbon in adenosine is not phosphorylated in NAD & FAD.

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21
Q 
talking FAD here...
What vitamin is required to make it active?
What enzyme component does it activate? 
Of what complex?
What is its function?
A 
Vitamin B2; Riboflavin
FAD is the active form of riboflavin
DLDH
Pyruvate Dehydrogenase Complex
Electron transfers
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22
Q

Aside from the enzymes we have been talking about (the 3 special ones) what are 2 other enzymes that are attached to the pyruvate dehydrogenase complex for the purpose of their regulation?

A 
PDH kinase (4 isoforms)
PDH phosphatase (2 isoforms)
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23
Q

What is the purpose of PDH Kinase & PDH Phosphatase?

A

They regulate the activity of the pyruvate dehydrogenase complex. When the kinase does its thing & phosphorylates the complex–>it is inactive. When the phosphatase does its things & dephosphorylates it, it is active.
Called reversible covalent phosphorylation.

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24
Q

Overall: You start with pyruvate & end up with ____. You use the ____ _____ complex. You add in what 5 things? You get out what 3 things?

A 
acetyl CoA
pyruvate dehydrogenase complex
NAD
FAD
TPP
Lipoamide
CoA
You get: acetyl CoA (obviously) & NADH & CO2!!!
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25
Q

Talking from glucose to the TCA cycle…what requires O2 & what doesn’t? And where does everything happen?

A

Glycolysis doesn’t require O2.

Conversion into Acetyl CoA & TCA cycle both happen in the cytosol of the mitochondrion. They both require O2.

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26
Q

What nutrients turn into acetyl CoA eventuallY?

A 
All the major ones!!!
Carbs
Fats
Proteins
Alcohol
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27
Q

What does acetyl CoA turn into?

A 
TCA or...
Acetylated Products
Cholesterol
Ketone Bodies
Fatty Acids
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28
Q

So…what is Danielle’s amazing phrase for TCA & what does each stand for?

A 
Can: Citrate
I: Isocitrate
Keep: alpha ketoglutarate
Selling: Succinyl CoA
Sex: Succinate
For: Fumarate
Money: Malate
Officer: Oxaloacetate
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29
Q

Show the math. 1 glucose molecule…how much energy from TCA??

A 
1 glucose
2 pyruvate
2 acetyl CoA
4 CO2
6 NADH=18 ATP
2 FADH2=4 ATP
2 GTP=2ATP
Overall: 1 glucose (from TCA) = 24 ATP
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30
Q

What is the efficiency of glucose oxidation?

A

40%

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31
Q

How does glucose travel in the blood?

A

attached to albumin

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32
Q

What are the 3 sources of blood glucose?

A

food
glycogen degradation
gluconeogenesis

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33
Q

How long is food good for as a source of blood glucose?

A

a few hours after a meal

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34
Q

The _____ stores ____ of glycogen & supplies it for up to a ____ period of time.

A

liver stores 100 g of glycogen & supplies it for up to 24 hours

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35
Q

How much energy is consumed in degrading glycogen to put it into the blood? Is this process slow or fast?

A

no energy consumed–>free process

Fast!!!!

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36
Q

In the process of gluconeogenesis, what 2 organs start the process? What 3 things do they use to do it?

A 
Liver & Kidneys
amino acids
lactate
glycerol
the 3 things listed above are all non-carbohydrate substrates
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37
Q

Is the liver or the kidneys a greater source of glucose for the blood?

A

The liver–by far!! 90% of the source!!

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38
Q

What is the only source of glucose for the blood after prolonged fasting?

A

the liver!! thru gluconeogenesis

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39
Q

What are 2 cycles that depend on the liver’s gluconeogenesis & then the delivery of that glucose to other tissues?

A 
Cori Cycle (glucose-lactate cycle)
Alanine Cycle (glucose-alanine cycle)
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40
Q

In gluconeogenesis, most of the enzymes are the same as glycolysis (just in reverse) except for which steps? Why?

A

the 3 irreversible energy waterfall steps.
These require different enzymes
Steps 1, 3, 10

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41
Q

Which enzymes replace steps 1, 3, & 10 in gluconeogenesis?

A

Step 1: glucose 6 phosphatase
Step 3: fructose 16 bisphosphatase
Step 10: Part 1: Pyruvate–>OAA (pyruvate carboxylase)
Part 2: OAA–>PEP (PEP carboxykinase)

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42
Q

What is the function of glucose 6 phosphatase? What process is it involved in?
Where is this enzyme found?

A

G6P–>Glucose
Gluconeogenesis
Endoplasmic Reticulum

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43
Q

What is the function of fructose 16 bisphosphatase? What process is this involved in? Where is this enzyme found?

A

Fructose 16 BP–>Fructose 6P
Gluconeogenesis
Cytoplasm

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44
Q

What is the function of PEP carboxykinase?

What process is this involved in? Where is this enzyme found?

A

OAA–>PEP
gluconeogenesis
Cytoplasm or mitochondria

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45
Q

What is the function of pyruvate carboxylase?

What process is this involved in? Where is this enzyme found?

A

Pyruvate–>OAA
gluconeogenesis
mitochondria

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46
Q

Which enzyme involved in gluconeogenesis is biotin dependent?

A

pyruvate carboxylase

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47
Q

Explain the bypass process in gluconeogenesis.

A

Need to convert pyruvate–>PEP.
Transport pyruvate across the mitochondrial membrane.
Convert to OAA thru pyruvate carboxylase (ATP dependent)
Either:
Stay in the mitochondrion.
Or leave the mitochondrion via malate or aspartate.
Convert OAA to PEP via PEP carboxykinase (GTP dependent)

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48
Q

What is the net cost of the bypass of gluconeogenesis?

A

1 ATP & 1 GTP per pyruvate

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49
Q

What is the driving force for the bypass in gluconeogenesis?

A

The fact that there is so much ATP & GTP & Pyruvate in the cell.

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50
Q

So…if the glucose 6 phosphatase enzyme is found on the luminal membrane of the ER….how does that help with gluconeogenesis???!!!

A

Well…there is a G6P transporter into the ER.
The G6Pase is on the luminal surface of the ER. It converts the G6P into Glucose & Pi.
There is a transporter to get the glucose & Pi out of the ER.

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51
Q

What is von Gierke’s Disease?

A

it is a disease caused by a defect in either the G6P transporter into the ER or the G6Pase. Sad.

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52
Q

What are 2 efficient feed-ins for gluconeogenesis b/c they are readily converted to pyruvate? What converts them?

A

Lactate (lactate dehydrogenase)

Alanine (a transaminase)

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53
Q

What is totally awesome about the conversion of lactate to pyruvate?

A

You don’t get any loss of NADH, b/c it generates NADH thru this conversion.

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54
Q

What do the cori & alanine cycles have in common?

A

They both convert into pyruvate & are then shuttled into the mitochondria to become OAA. Then they are shuttled back out to become glucose.

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55
Q

How many times must the Cori or alanine cycle be run in order to generate a glucose molecules?

A

TWICE!!!

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56
Q

How does the cost of gluconeogenesis differ b/w alanine & lactate as starting molecules?

A

Lactate–>Pyruvate generates NADH (2 total)
Alanine–>Pyruvate is free
Overall: takes less energy to make glucose from lactate.

57
Q

Considering that you have to use 2 lactate or alanine molecules to make 1 glucose molecule…what are the energy costs at each step in the process?

A

Lactate: +2 NADH
Pyruvate carboxylase: -2 ATP
PEP carboxykinase: -2GTP
Phosphoglycerate Kinase: -2ATP

58
Q

What does the body use for energy after a carb-heavy meal? After fasting?

A

Carb-heavy meal: glycolysis–lots of it!!

Fasting: fatty acid oxidation

59
Q

T/F It is okay for gluconeogenesis & glycolysis to be running at the same time.

A

FALSE! It would be futile & just consume a lot of ATP. That is why it is so important to have regulators!!

60
Q

What regulates pyruvate kinase? (allosteric)

A

An inhibitor is ATP. Another inhibitor is alanine.

Like, dude….stop the glycolysis already we have enough ATP. Just store & calm yourself down.

61
Q

What regulates pyruvate carboxylase? (allosteric)

A

Acetyl CoA activates Pyruvate Carboxylase. ADP inhibits it.

Like, we have way too much acetyl CoA lying around…can be please go back home & be glucose. It’s crowded.

62
Q

What regulates fructose 1,6 bisphosphatase? (allosteric)

A

Two activators are Citrate & ATP.

63
Q

What regulates PFK1? (allosteric)

A

Citrate & ATP are both inhibitors.

64
Q

What regulates F26BPase?

A

It is hormonally regulated.

65
Q

How is fructose-2,6-bisphosphate involved in regulation?

A

It activates PFK1, meaning that it activates glycolysis.

It inhibits F-1,6BPase, meaning that it inhibits gluconeogenesis.

66
Q

What is F26BP made from?

A

F6P!!!

67
Q

What are the activators of pyruvate kinase? What type of activators are they?

A

Activator: Fructose-1,6-bisphosphate
allosteric
feed forward mechanism

68
Q

What are the inhibitors of pyruvate kinase? What types of inhibitors are they?

A

Inhibitors:
ATP: allosteric
Alanine: allosteric
Glucagon Signaling

69
Q

What are the activators of pyruvate carboxylase? What types of activators are they?

A

Activator:

Acetyl CoA: allosteric

70
Q

What are the inhibitors of pyruvate carboxylase? What types of inhibitors are they?

A

Inhibitor:
ADP: competitive

71
Q

What are the activators of PFK1? What types of activators are they?

A

Activator:

Fructose-2,6-bisphosphate: allosteric

72
Q

What are the inhibitors of PFK1? What types of inhibitors are they?

A

Inhibitor:
ATP: allosteric
Citrate: allosteric

73
Q

What are the inhibitors of Fructose-1,6-Bisphosphatase? What types of inhibitors are they?

A

Inhibitor:
Fructose-2,6-bisphosphate
competitive

74
Q

What are the activators for fructose-1,6-bisphosphatase? What types of activators are they?

A

Activator:
ATP: allosteric
Citrate: allosteric

75
Q

What is the overall way that gluconeogenesis is stimulated?

A

By the repression of glycolysis…at its waterfall sites or by the repression of the synthesis of the enzymes for the waterfall sites.

76
Q

When does glucagon rise? What does it do?

A

Rises in response to low blood glucose during fasting.
Reduces glucose consumption.
Increase glucose production by the liver.

77
Q

When does insulin rise? What does it do?

A

Rises in response to elevated blood glucose after a meal.

It stimulates glucose consumption in many tissues.

78
Q

What 2 things generally increase the levels of glycolytic enzymes in the body?

A

Insulin

Glucose

79
Q

What are the component parts of TPP?

A

thiamine= pyrimidine ring + thiazolium ring

pyrophosphate

80
Q

What 2 things generally decrease the levels of glycoloytic enzymes in the body?

A 
Glucagon
Fatty Acids (present during starvation)
81
Q

Aside from glucagon & fatty acids what else is used to increase blood glucose?

A

Epinephrine!

82
Q

What is glucagon released from? In response to what? What does it do & how?

A

pancreatic alpha cells
Hypoglycemia
Raises blood glucose thru increase cAMP levels

83
Q

What is the effect of epinephrine or glucagon in the liver? How?

A

It favors gluconeogenesis over glycolysis in the liver thru a rise in cAMP levels.

84
Q

Does glucagon increase or decrease F26BP? What does this mean in terms of enzymes?

A

Decreases F26BP.
Means less activation of PFK1 & less inhibition of F16Bisphosphatase.
Decreases glycolysis in the liver.

85
Q

Does insulin increase or decrease F26BP? What does this mean in terms of enzymes?

A

Increases F26BP.
Means more activation of PFK1 & more inhibition of F16Bisphosphatase.
Increases glycolysis in the liver.

86
Q

F26BP activates/inhibits PFK1 in what way? Activates/inhibits F16Bisphosphatase in what way?

A

F26BP activates PFK1 allosterically

F26BP inhibits F16Bisphosphatase competitively.

87
Q

What is the name of the special enzyme that has both kinase & phosphatase powers & forms Fructose 26BP?

A

Phosphofructokinase 2-Fructose-2,6-Bisphosphatase

88
Q

What part of the special enzyme with 2 powers turns F6P–>F26BP?

A

Phosphofructokinase 2 part

89
Q

What part of the special enzyme w/ 2 powers turns F26BP–>F6P?

A

Fructose-2,6-Bisphosphatase

90
Q

In the human…where is the only place that has glucagon receptors?

A

the liver!!!

91
Q

F6P–>F26BP is promoted by which hormone? Which activity of PFK2-F26BPase is promoted? Does this mean that the enzyme is phosphorylated or dephoshporylated?

A

Insulin
Kinase activity favored
Dephosphorylated enzyme

92
Q

F26BP–>F6P is promoted by which hormone? Which activity of PFK2-F26BPase is promoted? Does this mean that the enzyme is phosphorylated or dephosphorylated?

A

Glucagon
Phosphatase activity favored
Phosphorylated enzyme

93
Q

When there is a ton of F6P lying around…what happens to the PFK2-F26BPase activity?

A

F6P activates the kinase activity & inhibits the phosphatase activity. Thus, if there is a ton of F6P chillin’ around the house–>you’re gonna start to see some F26BP b/c that kinase will be going crazy. It does this allosterically.

94
Q

Explain the process by which glucagon @ the liver slows glycolysis & increases gluconeogenesis.

A

Glucagon goes to the liver.
G protein active
adenylyl cyclase active
cAMP increases
PKA active
PPP inhibitor activated
Phosphoprotein phosphatase inhibited
Phosphatase activity of PFK2-F26BPase promoted
More F6P accumulates
F26BP can’t stimulates PFK1–glycolysis slows
F26BP can’t inhibit F16BPase–gluconeogenesis increases

95
Q

When glucagon is high what happens?

A

Gluconeogenesis goes up & glycolysis goes down.

96
Q

When insulin is high what happens?

A

Glycolysis is high & glucoeneogenesis is low.

97
Q

Explain the process by which insulin @ the liver increases glycolysis & slows gluconeogenesis.

A

Insulin @ the liver activates a cAMP degrading phosphodiesterase.
cAMP decreases.
PKA not active.
PPI not active.
Promotes kinase activity of PFK2-F26BPase.
More F26BP accumulates
F26BP activates PFK1=more glycolysis
F26BP inhibits F16BPase=less gluconeogenesis.

98
Q

What do glucocorticoids do?

A

They stimulate gluconeogenesis by inducing the synthesis of gluconeogenic enzymes.

99
Q

When are glucocorticoids usu released?

A

during times of high stress

100
Q

T/F The effects of glucocorticoids are often short-lived.

A

False. They are long-lasting.

101
Q

What are some feed-ins (aside from carbs) for gluconeogenesis?

A

Lactate & Alanine go directly to Pyruvate
Other AA go to TCA intermediates to OAA & feed in
Glycerol (from triglycerides in fat) feeds in as DHAP
Odd chain fatty acids

102
Q

T/F Even chain fatty acids are another good feed-in to gluconeogenesis.

A

FALSE!! Odd chain–yes.

Even chain–>acetyl CoA which can’t go backwards!

103
Q

What are some feed-ins (aside from carbs) for gluconeogenesis?

A

Lactate & Alanine go directly to Pyruvate
Other AA go to TCA intermediates to OAA & feed in
Glycerol (from triglycerides in fat) feeds in as DHAP
Odd chain fatty acids

104
Q

T/F Even chain fatty acids are another good feed-in to gluconeogenesis.

A

FALSE!! Odd chain–yes.

Even chain–>acetyl CoA which can’t go backwards!

105
Q

What is the process for the breakdown of ethanol?

A

Ethanol
Acetaldehyde
Acetate
Acetyl CoA

106
Q

What is the enzyme that catalyzes the reaction of ethanol to acetaldehyde & what does it give off?

A

Alcohol Dehydrogenase

Gives off NADH (can increase ATP eventually)

107
Q

What is the enzyme that catalyzes the reaction of acetaldehyde to acetate? What does it give off?

A

Aldehyde Dehydrogenase

Gives off NADH (can increase ATP eventually)

108
Q

What is the enzyme that catalyzes the reaction of acetate to acetyl CoA? What does it give off?

A

Acetyl CoA Synthase aka Acetate Thiokinase

AMP & PPi

109
Q

Where does the reaction of acetate to acetyl CoA usu happen?

A

In the liver

the acetate travels thru the blood to the liver.

110
Q

What is the rate limiting step of ethanol degradation?

A

the first step

ethanol to acetaldehyde

111
Q

What does it take to saturate the first step of ethanol metabolism & what type of kinetics does it demonstrate?

A

1 drink saturates it

zero order kinetics

112
Q

What is the Vmax of alcohol dehydrogenase & what does this mean in terms of blood alcohol levels?

A

Vmax=10 gram/hour

blood alcohol level increases 0.15g/hour

113
Q

Antabuse (used to treat alcoholism) acts on which enzyme? What is another name for this drug?

A

aka disulfiram

acts on aldehyde dehdyrogenase

114
Q

What causes “oriental flush”?

A

an isoform of aldehyde dehydrogenase…an isoform that has a lower affinity.

115
Q

How many drinks can cause a toxic buildup of acetaldehyde? What does this do? What step is this?

A

1 or 2 drinks
cirrhosis
acetaldehyde–>acetate

116
Q

What are the main products of ethanol metabolism? Given these products–>which pathways are inhibited?

A

Acetyl CoA
NADH
ATP
Glycolysis, TCA, & Beta oxidation are all inhibited.

117
Q

With the buildup of NADH…what happens to lactate?

A

Buildup of NADH prevents the transformation of lactate–>pyruvate; & so the lactate builds up & is released into the blood as lactic acid

118
Q

What 2 things can alcohol become?

A

Fatty Acids or Ketones

119
Q

T/F Alcohol is both ketogenic & glucogenic.

A

FALSE. It is only ketogenic. NOT glucogenic.

120
Q

So…you have a bunch to drink. How could this lead to ketoacidosis?

A

Tons of Alcohol
metabolized to a bunch of acetate.
Goes to the liver.
Becomes acetyl CoA
Becomes ketones–that can’t be metabolized
Therefore, the plasma pH will drop & you get ketoacidosis…

121
Q

How do people who drink a lot get fatty liver? What is another name for this condition?

A

Hepatic Steatosis
they get this b/c the only option for acetyl CoA is ketone & fatty acid synthesis.
**you also get the release of a bunch of VLDL (bad cholesterol)

122
Q

T/F The heart and kidneys have a bunch of acetylCoA synthase in their ER.

A

FALSE
the heart & SKELETAL MUSCLE
have a bunch of acetyl CoA synthase in their mitochondria…

123
Q

T/F the liver metabolizes ketones.

A

FALSE
b/c the liver does not…only the extra-hepatic tissues do.
The extra hepatic tissues have the SCOT enzyme

124
Q

Which enzyme is necessary to metabolize ketones into acetyl CoA? What is this reaction? Where is this enzyme found?

A

SCOT: acetoacetate-succinyl CoA transferase
Rxn:
Acetoacetate + Succinyl CoA–>Acetoacetyl CoA + Succinate
Found in extra-hepatic tissues (NOT the liver)

125
Q

Which 2 vitamins does ethanol disrupt?

A

Vitamin A aka retinol

Vitamin B1 aka thiamine

126
Q

How does ethanol disrupt Vitamin A? What is another name for this vitamin?

A

It is a competitive inhibitor of retinol dehydrogenase

**retinol

127
Q

How does ethanol disrupt thiamine? What is another name for this vitamin? What disease can this cause?

A

Decreases absorption of thiamine
aka Vitamin B1
Wernicke-Korsakoff Syndrome

128
Q

What does Wernicke-Korsakoff Syndrome do generally? What are 2 specific ways?

A

brain damage

  • *Wernicke: encephalopathy–damages the hypothalamus & the thalamus
  • *Korsakoff: psychosis–damages the area of the brain responsible for memory
129
Q

T/F Ethanol is an energy source.

A

True. At the rate of 7.1kcal/g

130
Q

Where does the ethanol metabolism begin in males? Where is it accomplished predominately?

A

begins in the stomach wall

predominately occurs in the liver

131
Q

T/F the ethanol consumed doesn’t distribute to the different compartment of the body very well–>it mainly stays in the abdomen.

A

False. It distributes about equally.

132
Q

How much alcohol consumption per day would be required to provide the energy of half the basal metabolic rate?

A

1-200 grams/day

133
Q

What are the 3 stages of liver damage? And what happens at each stage? Caused by alcoholism.

A

Fatty Liver: b/c of increased triacylglycerol synthesis
Alcoholic Hepatitis: liver inflammation
Cirrhosis: hepatocytes die & there is replacement fibrosis

134
Q 
Ethanol in excess causes NADH in excess and leads to excessive amounts of which of the following & low amounts of which of the following?
Lactate
Pyruvate
Malate
OAA
A

Lots of Lactate & Malate

Not very much Pyruvate or OAA

135
Q

What are some important pathways that are inhibited b/c of excess alcohol?

A

TCA
Fatty Acid Oxidation
Gluconeogenesis

136
Q

How can lots of alcohol lead to hypoglycemia? What would be the results of this?

A

If there is already low liver glycogen, then hypoglycemia could result b/c gluconeogenesis is impossible.
Hypoglycemia will cause an increase in G3P & FFA
This will cause an increase in TAG & VLDL

137
Q

How much energy does it take to go from pyruvate to glucose in gluconeogenesis?

A

4 ATP
2 GTP
2 NADH

138
Q

How much energy does it produce to go from glucose to pyruvate in glycolysis?

A

2 ATP

2 NADH

Block 3; Week 1 (11 decks)

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