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Block 3 Week 1 > Valenick Carb Metabolism II > Flashcards

Valenick Carb Metabolism II Flashcards

1
Q

What are the four things that pyruvate can turn into?

A

lactate
acetyl coa
oxaloacetate
alanine

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2
Q

How can pyruvate turn into lactate?

A

through reduction

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3
Q

How can pyruvate turn into acetyl CoA?

A

oxidative decarboxylation

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4
Q

How can pyruvate turn into oxaloacetate?

A

through carboxylation

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5
Q

How can pyruvate turn into alanine?

A

through transamination

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6
Q

How does glucose turn into pyruvate?

A

through glycolysis

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7
Q

Under what conditions does pyruvate dehydrogenase work?

A

aerobic conditions

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8
Q

What reaction does pyruvate dehydrogenase participate in?

A

Pyruvate + NAD+ + CoA-SH → Acetyl-CoA + NADH + CO2

C3-> C2 +CO2

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9
Q

The reoxidation of (blank) produces the bulk of ATP by OX-Phos.

A

coenzymes

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10
Q

What is the first step of turning pyruvate into acetyl coA?

A

moving it into the mitochondria

travels through pore of outter membrane and through pyruvate transporter of inner membrane to get to mito matrix.

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11
Q

Once pyruvate enters the mito matrix, what happens to it?

A

it is oxidatively decarboxylated to acetyl co-A

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12
Q

What links glycolysis to the TCA cycle?

A

pyruvate dehydrogenase complex

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13
Q

Where is pyruvate dehydrogenase and what is it essential for?

A

the mito matrix; for cellular respiration

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14
Q

What type of dehydrogenase is pyruvate dehydrogenase? Is it reversible?

A

an alpha ketoacid dehydrogenase

NOOOOOO

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15
Q

What makes up the PDH Complex?

A

3 catalytic enzymes and 5 coenzymes

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16
Q

What are the three catalytic enzymes that make up the PDH complex?

A 
E1 = Pyruvate dehydrogenase (PDH)
E2 = Dihydrolipoyl transacetylase (DLTA)
E3 = Dihydrolipoyl dehydrogenase (DLDH)
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17
Q

What are the five coenzymes that make up the PDH complex?

A 
TPP = Thiamine pyrophosphate
CoA = Coenzyme A
NAD+ = Nicotinamide adenine dinucleotide
FAD + = Flavin adenine dinucleotide
Lipoamide
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18
Q 
4 of the 5 coenzymes of the DHP complex need vitamins for synthesis; what are they?
TPP?
CoA?
NAD?
FAD?
Lipoamide?
A 
Thiamine B1
Panthothenic acid B5
Niacin B3
Riboflavin B2
none
NOTE: a deficiency of any of these vitamins can impair the pyruvate dehydrogenase reaction
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19
Q

In thiamin deficiency (Beriberi), what accumulate after eating lots of carbs and why is this bad?

A

pyruvate, lactate and alanine.
Most pyruvate turns into lactate which leads to lactic acidosis and impaired CNS Function (due to brains dependence on glucose)

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20
Q

What are the components of the coenzyme TPP?

A

pyrimidine ring
thiazole ring,
pyrophosphate (diphosphate) functional group.

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21
Q

Thiamine pyrophosphate is bound (blank) to the apoprotein.

A

noncovalently

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22
Q

TPP acts as a carrier of (blank) and of the hydroxyethyl group that is formed by pyruvate decarboxylation.

A

pyruvate

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23
Q

(blank) is required for E2

A

lipoamide

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24
Q

(blank) is bound covalently with an amide linkage to a lys residue. It participates as a redox system and carrier of the acetyl group.

A

lipoic acid

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25
Q

we synthesize (blank) directly onto the E2 Enzyme and no free lipoic acid is produced.

A

lipoate

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26
Q

What are the components of lipoamide?

A

lipoic acid, lys residue of E2 and polypeptide chain of E2

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27
Q

What is the prosthetic group of DLTA?

A

lipoamide

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28
Q

What is coenzyme A required for?

A

DLTA

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29
Q

What are the components of coenzyme A?

A

acetyl coA, panthothenic acid (vit B5) and 3 phosphoadenosine diphosphate

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30
Q

What 2 coenzymes are required for DLDH?

A

NAD and FAD

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31
Q

What does this describe?
A hydroxyl group of pantothenic acid is joined to a modified ADP moiety by a phosphate ester bond, and its carboxyl group is attached to β-mercaptoethylamine in amide linkage.
The hydroxyl group at the 3′ position of the ADP moiety has a phosphoryl group not present in free ADP.
The -SH group of the mercaptoethylamine moiety forms a thioester with acetate in Acetyl-CoA.

A

Coenzyme A

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32
Q

What participates in hydride transfers?

What participates in electron transfers?

A

NAD+

FAD

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33
Q

what are the components of NAD+?

A

adenine, di phosphate, Niacin (vit B3)

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34
Q

What are the components of FAD?

A

adenine, di phosphate, riboflavin (vit B2)

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35
Q

What are 2 enzymes found tethered to the PDH complex? What do these enzymes do? Phosphorylation causes what?

A

PDH kinase (4 isoforms) and PDH phosphatase (2 isoforms)
They regulate PDH activity through reversible covalent phosphorylation
inactivation of PDH

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36
Q

Complete glucose oxidation begins where and ends where?

A

begins in the cytoplasm

ends in the mitochondria

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37
Q

Describe the steps of complete glucose oxidation

A

D glucose->glycolysis->2 pyruvate -> PDH-> 2 acetyl CoA->TCA-> 4 CO2

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38
Q

Is there an 02 requirement for glycolysis?

Is there an O2 requirement for pyruvate dehydrenase plus TCA cycle activity?

A

no

yes

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39
Q

The catabolic pathways convert the carbon of substrates to (blank)

A

carbon dioxide

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40
Q

The hydrogen initially is transferrred to the coenzymes NAD+ and FAD. The reduced coenzymes then are reoxidized by the respiratory chain. Most of the ATP is produced in the process of (Blank), which couples the oxidation of the reduced coenzymes to ATP synthesis.

A

oxidative phosphorylation

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41
Q

(blank) is the gateway to oxidative metabolism of the food we eat.

A

acetyl coA

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42
Q

What four things can make acetyl coa?

A

AA, FA, Ketones, Pyruvate

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43
Q

explain how you can start with glucose and get to reduced coenzymes?

A

glucose->pyruvate->acetyl CoA-> TCA-> reduced coenzymes

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44
Q

For the generation of metabolic energy, all major nutrients are degraded to (blank). These include carbs, fats, protein and alchol.

A

acetyl CoA

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45
Q

What can Acetyl Co A become?

A

acetylated products, cholesterol, ketone bodies, fatty acids, into the TCA cycle

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46
Q

What is the final common pathway for the oxidation of all major nutrients.

A

TCA cycle

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47
Q

What are the irreversible steps of the TCA cycle?

A

isocitrate dehydrogenase
Alpha-ketoglutarate dehydrogenase complex
citrate synthase

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48
Q

What is the limiting step of the TCA cycle?

A

oxaloacetate

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49
Q

What two steps of the TCA cycle can leave the mitochondria?

A

citrate, malate

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50
Q

What step of the TCA cycle is bound to the inner mitochondrial membrane?

A

succinate dehydrogenase

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51
Q

What three steps of the TCA cycle give off NADH?

A

isocitrate dehydrogenase
alpha ketoglutarate dehydrogenase complex
malate dehydrogenase

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52
Q

To balance the two carbons of acetyl-CoA that enter the TCA cycle, each turn of the cycle releases two carbons as (blank). THe hydrogen in the substrate does not form water, but is transferred to the coenzymes (blank) and (blank).

A

carbon dioxide

NAD+ and FAD

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53
Q

How many molecules of NADH and FADH2 are formed in each turn of the cycle?

A

3 of NADH

1 of FADH2

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54
Q

The energy yield of the TCA cycle is about (blank) ATP for NADH oxidation and (blank) ATP for FADH2 oxidation.

A

3

2

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55
Q

Therefore the overall energy yield from the oxidation of one acetyl residue is (blank) high-energy phosphate bonds: one from substrate-level phosphorylation and 11 by the reoxidation of the reduced coenzymes.

A

12

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56
Q

Where in the TCA cycle do you produce ATP (GTP)?

A

succinate dehydrogenase

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57
Q

The efficiency of glucose oxidation is close to (blank) percent.

A

40%.

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58
Q

What are the sources of blood glucose?

A

food
glycogen degredation (liver)
gluconeogenesis (liver and kidney)

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59
Q

What is the only source of glucose during prolonged fasting?

A

liver

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60
Q

How does the liver and kidney make glucose?

A

during gluconeogenesis using AAs, lactate and glycerol

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61
Q

(blank) is the net synthesis or formation of glucose from non-carbohydrate substrates.

A

gluconeogenesis

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62
Q

gluconeogenesis produces glucose from (blank x 3)

A

amino acids, lactic acid, glycerol

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63
Q

liver gluconeogenesis is linked to glycolysis in other (blank)

A

tissues

64
Q

Both the (blank) cycle and the (blank) cycle depend on gluconegenesis in the liver followed by delivery of glucose and its use in a peripheral tissues

A

cori cycle

alanine cycle

65
Q

What are the three irreversible steps of glycolysis?

During gluconeogenesis, how do you bypass these irreversible steps?

A

glucokinase
phosphofructokinase 1
pyruvate kinase
by using different enzymes

66
Q

What are the different enzymes used to bypass the irreversible steps of gluconeogenesis? And where are these reactions taking place?

A

1) pyruvate carboxylase (Mitochondria) and PEP carboxykinase (cytoplasm or mitochondria) bypass pyruvate kinase
2) Fructuse 1,6 bisphosphate (cytoplasm) bypasses phosphofructokinase 1
3) Glucose 6 phosphatase (ER) bypasses glucokinase

67
Q

What pushes all the other reversible steps in the gluconeogenesis pathway?

A

mass action

68
Q

What enzyme is biotin dependent?

A

pyruvate carboxylase

69
Q

PEP is transported across the inner mitochondrial membrane, whereas (blank) is shuttled into the cytoplasm after being reduced to malate or transaminated to aspartate.

A

oxaloacetate

70
Q

Since the pyruvate kinase reaction of glycolysis is irreversible two enzymes (pyruvate carboxylase and PEP carboxykinase) must bypass this step at what cost? What is the driving force behind this?

A 
1 ATP and 1 GTP per pyruvate molecule
Driving force: greater concentration of:
ATP than ADP
GTP than GDP 
Pruvate than PEP
71
Q

The other two irreversible steps of glycolysis that must be bypassed for gluconeogenesis are PFK and hexokinase. THese are bypassed via F1,6BP and G6P, How does these ezymes accomplish this?

A

hydrolytic removal of phosphate

72
Q

(blank) is caused by a defect in Glucose 6-Phosphatase or the Glucose 6-phosphate transporter in the ER membrane.

A

Von Gierke’s disease

73
Q

What three transporters are involved in the third bypass (G6pase) of gluconeogenesis?

A

one moves g6p into lumen
one moves phosphate to cytoplasm
one moves glucose to cytoplasm

74
Q

Lactate generates a (blank) when it is converted to pyruvate. Is there a net loss of NADH in gluconeogenesis from lactate?

A

NADH

No

75
Q

Lactate (cory cycle) and alanine (alanine cycle) are convenient substrates of gluconeogenesis because they are readily converted to pyruvate by (blank) and (blank)

A

lactate dehydrogenase and transamination

76
Q

Explain how the cori cycle works with gluconeogenesis?

What is the difference between the cori cycle and the alanine cycle?

A

you start with lactate-> pyruvate-> go into mitochondria to make OAA-> shuttle OAA out of mito or convert OAA to PEP and then shuttle out of mito-> continue process in cytosol->G6P gets its phosphate taken by G6Pase in the ER-> GLUCOSE :)
Alanine will be converted into pyruvate instead of lactate

77
Q

Gluconeogenesis must run (blank) times to produce one glucose

A

2 times

78
Q

What does glucagon do?

A

makes glucose!!!!!

79
Q

What does insulin do?

A

gets rid of glucose!!!

80
Q

Does it cost any ATP to convert alanine to pyruvate?

What does it cost to turn lactate into pyruvate?

A

no!

nothing, you actually gain 2 NADH’s so it costs less energy to make lactate than pyruvate

81
Q

Most tissues glycolyze (undergo glycolysis) after a carbohydrate meal but switch to (blank) during fasting.

A

fatty acid oxidation

82
Q

it is mandatory to control the irreversible reactions at all three bypasses to ensure that only the glycolytic reactions or only the gluconeogenic reactions take place, but not both.
Therefore, F2,6 BP is regulated by (blank)

A

hormones

83
Q

F2,6 BP stimulates (blank) and inhibits (blank)

A

glycolysis

gluconeogenesis

84
Q

(blank) fine-tune glycolysis and gluconeogenesis in the liver.

A

effectors

85
Q

The levels of (blank) and (blank) are elevated during fasting because of fatty acid oxidation. Therefore, they stimulate gluconeogenesis.

A

ATP, acetyl-CoA

86
Q

(blank) is the most important regulated enzyme in the PEP-pyruvate cycle.

A

pyruvate kinase

87
Q

What is an activator for pyruvate kinase? What is an inhibitor of pyruvate kinase?

A

F1,6 BP

ATp, Alanine, glucagon

88
Q

What is an activator for pyruvate carboxylase? What is an inhibitor of it?

A

acetyl CoA

ADP

89
Q

What is an activator of PFK1? What is an inhibitor of it?

A

F2,6 BP

ATP, citrate

90
Q

(blank) turns ON glycolysis and OFF gluconeogenesis (hormonally regulated).

A

F2,6bis-P

91
Q

In general, (blank) and (blank) increase the levels of glycolytic enzymes, whereas glucagon and fatty acids have the opposite effect.

A

insulin and glucose

92
Q

(blank) rises in response to low blood glucose during fasting. It reduces glucose consumption and stimulates glucose production by the liver.

A

glucagon

93
Q

(blank) signal to increase blood glucose. They lead to phosphorylation of key regulatory enzymes in a pathway. So when you think of phosphorylation you think of these.

A

glucagon and epinephrine

94
Q

(blank) signal to decrease blood glucose. This changes the expression of regulatory enzymes,reduces phosphorylation of enzymes and modulates the localization of reguated steps.

A

insulin

95
Q

(blank) is released from pancreatic alpha cells

(blank) is released from pancreatic beta cells during hyperglycemia.

A

glucagon

insulin

96
Q

Describe the G-protein coupled receptor signaling

Is there signal amplification?

A 
hormone  binds receptor
GDP is released-> GTP binds.
Gq translocates to adenylate cyclase
Second messenger cAMP is generated
PKA is activated
regulated proteins get phosphorylated

YES!

97
Q

(blank) regulates pyruvate kinase in the liver, if glucagon works on pyruvate kinase it will phosphorylate it rendering it (Blank)

A

glucagon

inactive!

98
Q

If you inactivat pyruvate kinase, PEP cannot reenter (blank)

A

glycolysis

99
Q

The amount of F2,6BP is regulated by (blank)

A

hormones

100
Q

F2,6 BP is a competitive inhibitor of (blank) and an allosteric effector of (blank). SOOO you can think of F2,6 BP as being glycolysis loving and gluconeogenesis hating!

A

F1,6 bisphosphatase

PFK1

101
Q

In humans, only the (blank) has glucagon receptors

A

liver

102
Q

Kinase favors (blank) while phosphatase favors (blank)

A

glycolysis

gluconeogenesis

103
Q

(blank) makes more F6P while (blank) makes F26BP

A

gluconeogenesis

glycolysis

104
Q

How is phosphoprotein phosphatase (the enzyme that promotes glycolysis) inhibited and what does it do?

A

phosphoprotein phosphatase allows F6P to turn into F 2,6 BP to promote glycolysis. It is inhibited by glucagon by the PPP inhibitor being phosphorylated.

105
Q

PFK2-F2 F2,6 Bpase( the enzyme that converts F2,6 BP to F6P) decreases the concenrtation of (blank) when it is phosphorylated.

A

F2,6 BP

106
Q

PFK2 F2,6 BPase is an enzyme with a dual function. When this enzyme is phosphorylated it works as a (blank). When it is dephosphorylated,i it works as a (Blank)

A

phosphatase

kinase

107
Q

When PFK2-F2,6BPase is phosphorylated, the level of fructose 6 phosphate is increased turning on gluconeogenesis and slowing glycolysis. During this time, the liver generates energy from (blank)

A

fatty acid oxidation.

108
Q

After a good meal, insulin cAMP->AMP and PFK2-F2,6Bpase acts as a (blank), and stimulated (Blank).

A

kinase

glycolysis

109
Q

Insulin regulates gene expression, and it reduces the cyclic AMP (cAMP) level in the liver by activating a cAMP-degrading phosphodiesterase. This decreases the phosphorylation of Phosphofructokinase 2-Fructose2.6 bisphosphatase leading to an increase of (blank). This stimulates glycolysis and inhibits gluconeogenesis.

A

fructose 2,6 bisphosphate

110
Q

F2,6BP stimulates PFK1 (glycolysis)and inhibits (blank)

A

F1,6 BPase

111
Q

What all does insulin increase?

A

PFK1, PFK2, pyruvate kinase expression

112
Q

(blank) are long term effectors and stimulate gluconeogenesis by inducing the synthesis of gluconeogenic enzymes..

A

glucocorticoids

113
Q

(blank) are released during sustained stress. They stimulate gluconeogenesis by inducing the synthesis of gluconeogenic enzymes.
The hormones regulate the synthesis of the distinctive glycolytic and gluconeogenic enzymes at the level of transcription. Because this involves the synthesis of new enzyme protein and most of the enzymes have lifespans of a few days in the cell, regulation of enzyme synthesis works on a time scale of days rather than minutes.

A

glucocorticoids

114
Q

Besides carbs, what else can be glucogenic (make glucose)?

A

Lactate, Alanine, all other AAs except for leucine and lysine, Glycerol, ODD chain fatty acids.

115
Q

Glycerol, derived from triglyceride hydrolysis in adipose tissue, enters gluconeogenesis (and glycolysis) through (blank) at the level of the (blank) phosphates

A

DHAP

triose

116
Q

(blank) is not only a gluconeogenic intermediate but also a member of the TCA cycle. THis is important so that TCA cycle intermediates can enter gluconeogenesis at this point.

A

Oxaloacetate

117
Q

Can acetyl coenzyme A be converted to glucose?

A

no

118
Q

The (blank) reaction is irreversible, and there are no alternative reactions to channel acetyl-coA into gluconeogenesis. (blank) are degraded to acetyl coA. Therefore the ones that are released from adipose tissue during fasting cannot be turned into glucose.

A

pyruvate dehydrogenase reaction

Fatty acids

119
Q

(blank) depends on amino acids and, to a lesser extent, on lactic acid and glycerol.

A

Gluconeogenesis

120
Q

WHy can odd chain fatty acids become glucose but even cant?

A

because odd have an extra carbon so it can become pyruvate

121
Q

Although (blank) enters the TCA cycle, it is not a substrate of gluconeogenesis because the citrate synthase reaction does not involve the net synthesis of a TCA cycle intermediate.

A

acetyl-CoA

122
Q

Describe the process of ethanol degredation

A

ethanol->acetaldehyde->acetate->acetyl CoA

123
Q

What are the enzymes involved in ethanol degredation and where are they located?

A

alcohol dehydrogenase complex (cytoplasm)
aldehyde dehydrogenase (mitochondrial)
acetyl CoA synthase (mito in muscle, cytoplasm)

124
Q

What are the products of ethanol degredation?

A

NADH, ATP

125
Q

Where does most of the acetate from ethanol degredation go?

A

most goes into the blood where it is oxidized by the liver

126
Q

What is this?

H3C-CH2OH → H3C-CHO → H3C-COO- → Acetyl-CoA

A

ethanol degredation

127
Q

What is the rate limiting step of alcohol metabolism? How many drinks of alcohol will saturate this enzyme? What is it dependent upon and why order kinetics does this enzyme follow?

A

ADH (alcohol dehydrogenase)
1!
NAD+ availability
zero

128
Q

Aldehyde dehydrogenase can be inhibited by (blank).

A

disulfiram (antabuse)

129
Q

How does antabuse work? What is it used for?

A

it blocks aldehyde dehydrogenase which leads to a build up of aldehyde which makes you sick. Used to treat alcoholism.

130
Q

(blank) accumulates to toxic levels after only 1 or 2 drinks (believed to cause cirrhosis).

A

Acetaldehyde

131
Q

(blank) is caused by a isoform of the enzyme aldehyde dehydrogenase which results in a higher Km, making it the rate limiting step. This results in build up of acetylaldehyde.

A

“Oriental Flush”

132
Q

(blank) metabolism is not subject to negative control. THe major products are acetyl CoA, NADH, and ATP.

A

ethanol

133
Q

Ethanol metabolism inhibits what process by inhibiting which enzymes?

A

glycolysis

PFK1 and PDH

134
Q

During ethanol metabolism, beta oxidation and high NADH levels shut down both beta-oxidation of (blank) and the (blank).

A

fatty acids

TCA cycle

135
Q

Durin alcohol metabolism you end up with excess NADH, what does it do to your body?

A

Makes LDH reaction irreversible and lactic acid accumulates and is released into the blood

136
Q

What are the two components that alcohol can be broken into?

A

ketones and fatty acids

137
Q

In the liver, what happens to acetate?

A

In the cytoplasm it is converted to acetyl coa and then to ketones

138
Q

Can ketones be metabolized by the liver, and why do they do to plasma pH?

A

NO

decreases it resulting in acidosis (ketoacidosis)

139
Q

Alcohol is (blank), not glucogenic

A

ketogenic

140
Q

Following the consumption of ethanol, acetate levels can be elevated by as much as (blank)

A

20 fold.

141
Q

In alcohol metabolism, the fatty acid oxidation is (blank), therefore acetyl coA generated is diverted to ketones and fatty acid synthesis.

A

inhibited

142
Q

What is the primary cause of fatty liver syndrome?

A

the build up of fatty acids in the liver due to the shut down of fatty acid oxidation. These fatty acids are esterified and triglycerides synthesized and exported as VLDL (bad cholesterol)

143
Q

Most Acetate from alcohol metabolism leaves the liver and is metabolized by (blank) and (blank) (contain high levels of mitochondrial Acetyl CoA synthase) generating Acetyl CoA.

A

heart and skeletal muscle

144
Q

Why doesnt the liver metabolize ketones?

A

because the liver doesnt have SCOT (acetoacetate succinyl Coa Transferase) ….other tissues do

145
Q

(blank) disrupts vitamin metabolism.

A

ethanol

146
Q

Ethanol is a competitive inhibitor of retinol dehydrogenase thereby disrupting the metabolism of which vitamin?

A

vitamin A (retinol)

147
Q

Ethanol decreases the absorption of what vitamin?

A

Vitamin B1 (thiamine)

148
Q

What disease can B1 deficiency cause?

A

Wernick-Korksakoff syndrome (brain damage)

149
Q

(blank) results from damage to areas of the brain involved with memory.

A

Korsakoff psychosis

150
Q

(blank) is caused by brain damage in the thalamus and hypothalamus.

A

Wernicke’s encephalopathy

151
Q

What does this describe:

In males metabolism begins in the stomach wall, but in general most of the metabolism takes place in the liver.

A

ethanol

152
Q

(blank) is an intoxicant and energy source

A

ethanol

153
Q

Being a water-miscible organic solvent, (blank) rapidly distributes through the aqueous compartments of the body, with tissue concentrations similar to the blood alcohol level.

A

ethanol

154
Q

Ethanol leads to excess NADH which favors (blank), depletes (blank), stops (blank), favors (blank) so it depletes OAA.

A

lactate (acidosis)
Pyruvate
TCA cycle
malate

155
Q

Ethanol makes gluconeogenesis becomes impossible, so if liver glycogen levels are low,what can result?

A

hypoglycemia and increase in G3P and fatty acids, increase in triacylglycerides and increase in VLDL, and slows fatty acid oxidation

156
Q

Unlike most metabolic pathways, alcohol metabolism is not (blank). Therefore, alcohol is metabolized over the oxidation of other nutrients.

A

negatively regulated.

157
Q

What are the three stages of liver damage?

A

fatty liver from increased TAG synthesis
alcoholic hepatitis : liver inflammation caused by drinking
cirrhosis: hepatocytes due and there is replacement fibrosis

Block 3 Week 1 (18 decks)

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