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BIOL 3421 - molecular biochem > lipid degradation: beta oxidation > Flashcards

lipid degradation: beta oxidation Flashcards

1
Q

beta oxidation converts ____ into ____

A

palmitoyl-CoA into acetyl-CoA

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2
Q

what is the name of first step of beta oxidation

A

dehydrogenation

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3
Q

describe the first step of b-ox

A

acyl-CoA dehydrogenases catalyze the formation of a trans double bond between a and b carbons. FAD gets reduced to FADH2

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4
Q

which enzyme catalyzes the first step of b-ox

A

acyl-CoA dehydrogenase

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5
Q

what are the by-products of step 1 of b-ox

A

FADH2

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6
Q

name step 2 of b-ox

A

hydration

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7
Q

describe step 2 of b-ox

A

water is added to the trans double bond of the a and b carbons = a single bond and an OH on the b carbon

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8
Q

name step 3 of b-ox

A

dehydrogenation #2

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9
Q

describe step 3 of b-ox

A

another dehydrogenation occurs = a ketone on the b carbon. NAD+ is reduced to NADH

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10
Q

what is the by-product of step 3 of b-ox

A

NADH

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11
Q

name step 4 of b-ox

A

thiolysis

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12
Q

describe step 4 of b-ox

A

thiolysis of the two carboxy-terminal carbons via a free molecule of CoA (cleavage between carbons a-b)

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13
Q

what is the end result of the first 4 steps (1 round) of b-ox

A

14C-CoA, acetyl-CoA

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14
Q

how many rounds of b-ox are needed to complete the cleavage of palmitate/palmitoyl-CoA

A

7

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15
Q

how many acetyl-CoA molecules are we left with after 7 rounds of b-ox

A

8 acetyl CoA

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16
Q

after 7 rounds of b-ox, why are we left with 8 acetyl-CoA and not 7

A

each round produces 1 acetyl-CoA, but the last round will produce 2 (when the 4C molecule is cleaved)

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17
Q

after 7 rounds of b-ox, how many FADH2 do we have

A

7

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18
Q

after 7 rounds of b-ox, how many NADH do we have

A

7

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19
Q

after 7 rounds of b-ox, how many H+ do we have

A

7

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20
Q

after b-ox, where do FADH2 and NADH go

A

to the ETC to drop off electrons to O2

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21
Q

each FADH2 produces ___ molecules of ATP in the ETC

A

1.5

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22
Q

each NADH produces ___ molecules of ATP in the ETC

A

2.5

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23
Q

each pair of electrons donated to O2 in the ETC produce ___ H2O molecule(s)

A

1

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24
Q

how many ATP are produced during ONE round of b-ox. Explain (assuming NADH and FADH2 went to the ETC)

A

4 ATP: each round produces 1 FADH2 and 1 NADH. FADH2 produces 1.5 ATP in the ETC and NADH produces 2.5 ATP in the ETC. 1.5 + 2.5 = 4 ATP produced

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25
Q

how many H2O are produced during ONE round of b-ox. Explain (assuming NADH and FADH2 went to the ETC)

A

2 H2O: one electron pair = 1 water. Each round of b-ox produces 2 electron pairs

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26
Q

how many H2O were USED during one round of b-ox

A

1 H2O used per round

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27
Q

what is the net amount of water produced by all 7 rounds of b-ox? explain

A

7 H2O produced (net). 14 were produced via electrons being donated to O2, but 7 were used in the dehydration step

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28
Q

how much ATP was formed after all 7 steps of b-ox, ONLY FROM reduced electron carriers

A

1 round = 4 ATP (1.5 +2.5=4), but there were 7 rounds
4x7 = 28 ATP produced from b-ox

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29
Q

After b-ox, where do the 8 acetyl-CoA molecules go?

A

they go to the CAC

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30
Q

what is the result of the acetyl-CoA from b-ox going to the CAC

A

more ATP will be produced!

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31
Q

each turn of the CAC produces __ NADH

A

3

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32
Q

each turn of the CAC produces __ FADH2

A

1

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33
Q

each turn of the CAC produces __ CO2

A

2

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34
Q

each turn of the CAC produces __ ATP equivalent (GTP)

A

1

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35
Q

how many rounds of CAC (and subsequent ETC) need to occur

A

8 (because there are 8 acetyl-CoA’s)

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36
Q

after 8 rounds of the CAC (and subsequent ETC), how many ATP are produced? explain

A

80
- (3 NADH x 2.5)+ (1 FADH2 x 1.5) = 9 ATP
- 1 ATP equivalent produced in the CAC
- 9 + 1 = 10 ATP

  • 8 rounds: 8 x 10 = 80 ATP total
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37
Q

combining the numbers from complete b-ox and CAC and ETC, how many ATP do we get

A

108 (28 + 80)

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38
Q

where does b-ox occur in the cell

A

mitochondria matrix

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39
Q

what was the cost of ATP to add CoA to the FA to activate it in preparation for entry to the mito matrix (carnitine shuttle, prior to b-ox)

A

2 ATP needed

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40
Q

when considering the cost of 2 ATP needed PRIOR to b-ox, what is the NET ATP number (b-ox, CAC, ETC)

A

106 ATP

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41
Q

what is the issue with trying to oxidize an unsaturated FA

A

the enzyme for step 1 can only act on trans double bonds at C2, and natural FA bonds are cis, so the enzyme may not work on an unsat FA

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42
Q

what two enzymes do we need to oxidize an unsat FA

A

isomerase and reductase

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43
Q

explain how we oxidize MUFAs (ie oleate)

A

first 3 rounds happen without issue, but at round 4 there will be a cis (we don’t want) at C3 (wrong spot). isomerase converts the natural cis bond to a trans at C2 which fixes the issue

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44
Q

explain how we oxidize PUFAs (ie linoleic acid)

A

the first 3 rounds happen without issue. At round 4, a cis double bond is at C3 and C6 (cis and in the wrong place). Isomerase converts C3 cis to trans at C2. Now it’s in the right spot, but the bond at C6 is in the way. Round 4 completes, round 5 step 1 occurs and a trans-C2 is produced as usual. Now the cis-C4 is in the way of step 2 occurring. Reductase eliminates the cis-C4 bond

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45
Q

in what organism are odd numbered FAs common in (2)

A

many plants, or produced by fermentation of carbs in the stomach chambers of ruminants

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46
Q

what commercial application do odd numbered FAs have

A

they’re used as mold inhibitors in bread

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47
Q

which round of oxidation is impacted by having an odd numbered FA

A

the last round

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48
Q

when oxidizing an odd numbered FA, what molecule do we have right before the last round occurs (instead of acetyl-CoA)

A

propionyl-CoA (3C)

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49
Q

starting from propionyl-CoA (3C), explain how we oxidize odd numbered FAs

A

propionyl-CoA is carboxylated = 4C methylmalonyl-CoA. This requires bicarbonate, ATP, and biotin attached to the propionyl-CoA carboxylase enzyme. Methylmalonyl-CoA is isomerized and then rearranged by a mutase = succinyl-CoA, which then enters the CAC

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50
Q

what is the end result/product of oxidation of odd numbered FAs

A

succinyl-CoA (4C) entering the CAC

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51
Q

in the oxidation of odd numbered FAs, what vitamin does the mutase require

A

B12 derivative

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52
Q

in the oxidation of odd numbered FAs, what does the mutase do?

A

it exchanges an alkyl group off one carbon with a hydrogen off another

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53
Q

where does oxidation of long chain FAs take place

A

the peroxisome

54
Q

list 4 things that peroxisomes do

A

carry out oxidation reactions and produce H2O2, catalase converts H2O2 to water or uses it to oxidize something else, FA/uric acid/AA breakdown, some synthesis of cholesterol/bile salts

55
Q

T or F: the sequence of b-ox reactions are the same in the mitochondria and peroxisomes

A

true

56
Q

which step of b-ox in peroxisomes differs to b-ox in mitochondria

A

step 1

57
Q

describe how step 1 of b-ox in peroxisomes is different to step 1 in mitochondria

A

mito: electrons given to FAD end up in the ETC to make ATP

peroxisome: electrons given to FAD pass directly to O2 to make H2O2, which is cleaved to H2O and O2 by catalase. No ATP is made and the energy is dissipated as heat

58
Q

T or F: in step 1 of b-ox in peroxisomes, ATP is generated by FAD brining electrons to the ETC

A

false: the electrons given to FAD pass directly to O2 to make H2O2, which is cleaved into water and oxygen. No ATP is made

59
Q

which long chain FA do we get from eating dairy and certain animal fats?

A

phytanic acid

60
Q

microbes in ruminant guts produce phytanic acid derivatives as they digest ________

A

chlorophyll a

61
Q

T or F: b-ox is used for branched FAs (phytanic acid)

A

false; it can’t be used because a methyl group blocks the b carbon

62
Q

if we can use b-ox for branched FAs, what do we use?

A

a-oxidation

63
Q

what is a-oxidation

A

an OH is placed on the a carbon instead of the b carbon

64
Q

which carbon gets an OH in a-ox

A

the a carbon

65
Q

where does branched FA oxidation take place in the cell

A

peroxisome

66
Q

what molecule do we get at the end of a-ox

A

propionyl-CoA which is converted to succinyl-CoA (same as we saw with odd numbered FAs in b-ox)

67
Q

FA oxidation is tightly regulated to only occur when the organism ____ ____

A

requires energy

68
Q

T or F: FA oxidation occurs when there is lots of potential fuel around (ie glucose)

A

false; it only occurs when the organism requires energy. The process is tightly regulated

69
Q

what is the commitment step for b-ox

A

carnitine shuttle bring fatty acyl-CoA into the mitochondria

70
Q

which molecule inhibits acyltransferase I? why?

A

malonyl-CoA. It’s unique to FA synthesis, and we don’t want synthesis and oxidation happening at the same time

71
Q

when will malonyl-CoA inhibit carnitine acyltransferase I?

A

when there is ample glucose

72
Q

describe inhibition of FA oxidation when you ingest carbs

A

insulin dependent protein phosphatase dephosphorylates acetyl-CoA carboxylase to activate it. ACC then converts lots of acetyl-CoA to malonyl-CoA, and malonyl is then used to make FAs and prevent FA ox from happening

73
Q

describe activation of FA oxidation when you don’t ingest carbs (3)

A

glucagon activates PKA which phosphorylates ACC to inactivate it. No malonyl-CoA is made = no inhibition of carnitine acyl-transferase I and this fatty-acyl groups into the mito for b-ox

as well, low ATP activates AMP kinase, which phosphorylates and inactivates ACC

glucagon also triggers free FA mobilization from adipocytes, accessing a huge pool of potential fuel for b-ox

74
Q

what happens to FA ox regulation when there is low ATP during fasting

A

activates AMP kinase, which phosphorylates and inactivates ACC = increased ox

75
Q

what does w-oxidation do

A

attacks the two carbons on the methyl end of the FA instead of the carboxyl end

76
Q

where in the body + where in the cell does w-ox occur

A

ER of liver and kidney cells

77
Q

when will w-oxidation occur

A

it substitutes for b-ox if that pathway is defective

78
Q

are ketone bodies water soluble?

A

yes

79
Q

are ketone bodies blood soluble?

A

yes

80
Q

are all ketone bodies ketones?

A

no

81
Q

where in the body are ketone bodies made

A

liver

82
Q

what are ketones made from

A

acetyl-CoA

83
Q

when will ketone bodies be made from acetyl-CoA

A

when there’s no incoming glucose

84
Q

which 3 ketone bodies can be made from acetyl-CoA

A

acetone, acetoacetate, D-B-hydroxybutyrate

85
Q

what happens to the ketone body “acetone” when its in the body

A

it’s exhaled (sweet fruity breath)

86
Q

what happens to the ketone bodies “acetoacetate and D-B-hydroxybutyrate” when they’re in the body

A

they’ll be transported in the blood from the liver to other tissues where they’re reconverted to acetyl-CoA and enter the CAC

87
Q

which does the brain prefer as fuel: glucose or ketone bodies

A

glucose

88
Q

when will the brain use ketone bodies as fuel

A

under starvation conditions when there’s no glucose

89
Q

T or F: fatty acids can be used by the brain for fuel

A

FALSE! only ketone bodies can, which come from fat. FAs themselves cannot be used as fuel because they cannot cross the blood brain barrier

90
Q

why can ketone bodies (fat derivatives) be used for fuel by the brain but FAs can’t be?

A

FAs cannot cross the blood brain barrier. Ketone bodies are water and blood soluble, so they can

91
Q

what is the first step of ketone body synthesis

A

2 acetyl-CoA –> acetoacetyl-CoA by thiolase

92
Q

which enzyme converts 2 acetyl-CoA into acetoacetyl-CoA to make ketone bodies?

A

thiolase

93
Q

ketone body synthesis: what happens once we have 4C acetoacetyl-CoA

A

condensation with another acetyl-CoA occurs = HMG-CoA

94
Q

where does HMG-CoA production occur in FA synthesis? Ketone synthesis?

A

cholesterol synthesis = cytosol
ketone synthesis = mitochondria

95
Q

ketone body synthesis: once HMG-CoA is made, what happens

A

it’s cleaved into acetoacetate by HMG-CoA lyase

96
Q

ketone body synthesis: which enzyme cleaves HMG-CoA into acetoacetate

A

HMG-CoA lyase

97
Q

ketone body synthesis: once we have acetoacetate, how do we get the other two ketone bodies?

A

via enzymatic modification

98
Q

is the formation of acetone from acetoacetate reversible or irreversible

A

irreversible

99
Q

is the formation of D-B-hydroxybutyrate from acetoacetate reversible or irreversible

A

reversible

100
Q

once ketone bodies have been made in the liver, where do they go

A

they’re shipped off to other tissues

101
Q

once acetoacetate and D-B-hydroxybutyrate are in the mitochondria of extrahepatic tissues, what can happen?

A

they can each be reconverted to 2 acetyl-CoA molecules which can then enter the CAC and ETC and make ATP

102
Q

ketosis: without glucose, what happens to CAC intermediates?

A

they’re diverted to use for GNG. This slows the CAC and acetyl-CoA stops being oxidized

103
Q

ketosis: what happens to the build-up of acetyl-CoA when the CAC is slowed down?

A

acetyl-CoA is shifted to make ketone bodies

104
Q

ketosis: what happens to excess ketones in the body

A

released into blood/urine

105
Q

list 3 ways on how to enter ketosis

A
  • fast / intermittent fast
  • very low carb diet
  • untreated diabetes
106
Q

how do you get ketoacidosis

A

excess ketones in the body (2 out of the 3 are acidic and will lower the blood pH)

107
Q

extreme ketoacidosis can lead to __ or __

A

coma or death

108
Q

T or F: diabetic people have a higher risk for ketoacidosis

A

true; they already have too many ketone bodies

109
Q

what does MCAD stand for

A

medium-chain acyl-CoA dehydrogenase

110
Q

what is MCAD responsible for

A

FA oxidation of C6-C12 chains

111
Q

list 5 things that happen when you have MCAD deficiency

A
  • fat accumulation in liver
  • high levels of FAs in blood
  • low blood glucose
  • lethargy, seizures, brain damage, coma
  • 25%-60% mortality in early childhood
112
Q

how much FA oxidation is able to occur when you have MCAD deficiency (ie how short can you get the FAs)

A

medium chain

113
Q

can you produce ketones with MCAD deficiency?

A

no!

114
Q

with MCAD deficiency, can you do GNG when glucose is low?

A

no!

115
Q

T or F: with MCAD deficiency, you cannot produce ketones or glucose (from GNG)

A

true! which sucks so bad because you can’t get fuel to your brain

116
Q

how might you treat MCAD deficiency

A

make sure that blood glucose levels never drop, because then you’ll never have to oxidize fats to get your fuel

117
Q

how does one get Zellweger syndrome

A

arises from an inability to make peroxisomes and thus oxidize very long chain FAs (so they have nowhere to go)

118
Q

list some symptoms of zellweger syndrome

A

enlarged liver, hypomyelination of neurons, vision/hearing loss, carniofacial abnormalities, skeletal abnormalities

119
Q

T or F: humans can excrete ethanol directly

A

false; they must metabolite it in two step process

120
Q

where in the body is ethanol metabolized

A

liver

121
Q

list the products/reactants of ethanol metabolism

A

ethanol –> acetaldehyde –> acetate

122
Q

does ethanol consumption increase or decrease NADH stores

A

increase

123
Q

how does ethanol consumption influence PKA activity

A

reduces it

124
Q

ethanol intake: how might increased NADH affect b-ox

A

down regulates b-ox, which needs NAD+

125
Q

ethanol intake: how might increased NADH affect FA synthesis

A

converted to NADPH, which then promotes FA synthesis

126
Q

ethanol intake: how might increased acetate affect FA synthesis

A

converted to acetyl-CoA, which then promotes FA synthesis

127
Q

ethanol intake: how might downregulated PKA activity affect b-ox

A

TAGs in adipocytes no longer properly metabolized upon hormone signals

128
Q

T or F: overall, increased ethanol intake increases FA synthesis, and in turn increased risk of type II diabetes

A

true

129
Q

high fat diet: how would a lack of carbs affect the processing of fats by b-ox?

A

you’d make lots of acetyl-CoA, which needs to enter the CAC. To enter, it joins with OAA to make citrate. Most OAA is formed by carboxylation of pyruvate, but most pyruvate comes from glycolysis, but you can’t do CAC because of the lack of carbs. Therefore, the acetyl-CoA will be converted to ketone bodies!

130
Q

high fat diet: how do you combat the formation of excess ketone bodies/ketosis?

A

incorporate a supplement of a long chain/odd numbered FA. the final carbons cleaved from b-ox will provide proprionyl-CoA, which is converted to succinyl-CoA, which then enters the CAC = lifts the CAC jam and acetyl-CoA won’t need to make ketones anymore

BIOL 3421 - molecular biochem (20 decks)

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