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biochem > biochem lecture 8 pt 2 > Flashcards

biochem lecture 8 pt 2 Flashcards

1
Q

what have we already done in step 1

A

we get fatty acids mobilized and transported, absorbed into muscle cell

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2
Q

what is step 2 in beta oxidation

A

activation of fatty acids, and transportation to mitochondria for degradation

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3
Q

what happens when fatty acids are absorbed into muscle cell

A

need to undergo an activation step in the cell

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4
Q

what happens once those fatty acids have been activated

A

need to be transported into mitochondrial matrix

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5
Q

what happens to individual fatty acids in step 2

A

transported into muscle cell and converted into a fatty acyl CoA

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6
Q

what is coenzyme A

A

important metabolic tag

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7
Q

what does being tagged w/ coenzyme A mean

A

compound is biochemically activated in some way; gonna go into a specific metabolic pathway

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8
Q

what is carnitine

A

molecule needed for the import of fatty acyl CoAs into mitochondria

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9
Q

what do we need to do to fatty acyl CoA

A

convert fatty acyl CoA –> fatty acyl carnitine

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10
Q

why do we need to go through this interconversion from fatty acyl CoA to fatty acyl carnitine

A

because there is a specific transporter that will recognize fatty acyl carnitine and bring it into mitochondrial matrix

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11
Q

what happens once fatty acyl carnitines brought into mitochondrial matrix

A

they are interconverted back into fatty acyl CoAs, where they go thru beta-oxidation

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12
Q

what happens when fatty acyl CoAs are in mitochondria

A

go through beta oxidation pathway

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13
Q

what happens to carnitine released from this step

A

transported out of mitochondria, brings more fatty acids into mitochondria

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14
Q

what is the overall rxn in activation step

A

take fatty acid that’s been brought into cell, and produce fatty acyl CoA

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15
Q

describe thermodynamics of activation step

A

large negative delta G; exergonic

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16
Q

why is it exergonoic

A

cuz we couple it to hydrolysis of ATP

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17
Q

what enzyme for activation step

A

fatty-acyl CoA synthetase

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18
Q

what happens in activation step

A

fatty acid –> fatty acyl adenylate intermediate (by fatty-acyl coa synthetase)

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19
Q

what happens after fatty acyl adenylate intermediate

A

fatty acyl CoA adenylate –> fatty acyl CoA (by fatty-acyl coa synthetase)

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20
Q

basically what happens in activation step

A

fatty acid –> fatty acyl CoA adenylate –> fatty acyl CoA (from 2 rounds of fatty acyl CoA synthetase)

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21
Q

how do we form this thioester bond

A

pyrophosphate leaving group is released, and this generates formation of thioester bond in fatty acyl CoA

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22
Q

why exergonic

A

ATP hydrolyzed; intermediate has a phosphate group from ATP attached

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23
Q

where does generation of fatty acyl CoAs occur

A

in cytoplasm of muscle cell

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24
Q

what happens once we have fatty acyl CoAs

A

we have to get fatty acyl units to mitochondrial matrix

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25
Q

how do we get fatty acyl CoA to mitochondria

A

set of interconversion reactions where we swap coenzyme A for carnitine

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26
Q

what enzymes are involved

A

2 acetyl transferases: carnitine acetyl transferase I, carnitine acetyltransferase II

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27
Q

what is CAT 1

A

resides in outer membrane

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28
Q

what is CAT II

A

in inner mitochondrial membrane

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29
Q

what is Cat 2 important for

A

for when we convert fatty acyl carnitine back into fatty acyl coenzyme A

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30
Q

describe transportation step

A

formation of catty acyl carnitine from fatty acyl CoA. CAT I transfers fatty acyl carnitine to intermembrane space. CAT II is waiting for fatty acyl carnitine in mitochondrial matrix, and will do the second interconversion reaction

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31
Q

what is end product after step 2

A

we end up w/ a fatty acyl CoA which goes through beta oxidation pathway

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32
Q

how many stages in beta oxidation

A

3;

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33
Q

stage 1 of beta oxidation

A

B-oxidation of fatty acids

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34
Q

stage 2 of beta oxidation

A

acetyl CoA oxidized to Co2

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35
Q

what is stage 3 of b-oxidation

A

electrons transferred from NADH/FADH2 to ETC for electron synthesis

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36
Q

what do we do in beta oxidation

A

we are removing 2 Cs at a time off fatty acid, with each round

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37
Q

but in all situations what do we have culmination of

A

culmination of beta oxidation of fats

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38
Q

what happens if we have double bonds (one or more)

A

its about getting rid of those double bonds to generate a fully saturated fatty acid

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39
Q

what happens once we have saturated fatty acid

A

can be sent thru beta oxidation pathway

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40
Q

what’s the point of beta oxidation pathway

A

generates acetyl CoA units, which can be fed into TCA cycle

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41
Q

what do fats generate a lot of

A

generate a lot of reducing power (NADH, FADH) in TCA cycle

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42
Q

where does that reducing power go

A

fed into ETC, important for ox phos

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43
Q

what are the 4 scenarios of beta oxidation

A

even & saturated, even & monounsaturated, even & polyunsaturated, odd

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44
Q

what’s the simplest case

A

even & saturated

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45
Q

what 4 steps

A

oxidation, hydration, oxidation, thiolysis

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46
Q

where is 1st step

A

fatty acyl CoA (starting point), we are in mitochondrial matrix

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47
Q

describe 1st step

A

fatty acyl CoA oxidized to trans delta 2 enoyl CoA

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48
Q

what kinda rxn is 1st step

A

oxidation rxn

49
Q

what else is produced in 1st oxidation

A

FADH2

50
Q

why is trans delta 2 enoyl CoA important

A

because in other pathways, it all boils down to getting to this intermediate

51
Q

2nd step

A

trans delta 2 enoyl CoA –> 3-hydroxyacyl CoA intermediate

52
Q

what kinda rxn in step 2

A

hydration step; input of water

53
Q

step 3

A

second oxidation step, results in another reducing power molecule created

54
Q

describe step 3

A

3-hydroxyacyl CoA –> 3-ketoacyl CoA intermediate

55
Q

what else is produced in step 3

A

reduction of NAD+ to NADH, simultaneous oxidataoin

56
Q

step 4

A

2 products: acyl CoA and acetyl CoA; we keep converting acyl CoA to acetyl CoA until we’re done

57
Q

what extra enzyme in even monounsaturated enzyme

A

enoyl-CoA isomerase

58
Q

how much ATP per double bond does enoyl CoA isomerase use

A

2 ATP

59
Q

what enzymes does even polyunsaturated fatty acids use

A

enoyl CoA isomerase AND 2,4-dienoyl CoA reductase

60
Q

how much ATP per double bond in 2,4-dienoyl CoA reductase

A

3 ATP

61
Q

B-oxidation in odd fatty acids

A

keep doing beta oxidation until you reach 3Cs

62
Q

what happens to those remaining 3 Cs

A

succinyl CoA

63
Q

where does succinyl CoA go

A

into TCA

64
Q

describe b-oxidation for odd stuff

A

propionyl CoA –> methylmalonyl CoA –> methylmalonyl CoA –> succinyl CoA

65
Q

what 3 enzymes

A

propionyl CoA carboxylase, methylmalonyl CoA epimerase, methylmalonyl CoA mutase

66
Q

what undergoes lipgenesis

A

excess dietary glycerol and fatty acids undergo lipogenesis to make triglycerides

67
Q

why is glucose easily converted to fat

A

acetyl CoA is intermediate in glucose metabolism and starting molecule for fatty acid synthesis

68
Q

what does release of insulin favor

A

lipogenesis to form triglycerides

69
Q

what else are fats derived from besides excess dietary lipids

A

glucose

70
Q

liypolysis

A

breakdown of stored fat

71
Q

what is lipolysis reverse of

A

reverse of lipogenesis

72
Q

what is necessary for complete oxidation of fat (thru TCA cycle)

A

oxaloacetete

73
Q

what would happen to acetyl CoA without oxaloacetate

A

ketogenesis; acetyl CoA converted into ketones

74
Q

when does ketogenesis occur

A

long term starvation conditions; decline in oxaloacetate levels

75
Q

where does ketogenesis happen

A

in liver

76
Q

ketone bodies

A

utilized as a way to generate fatty acids (fatty acid –> beta oxidation –> ATP)

77
Q

what else can ketone bodies be converted into

A

acetyl CoA

78
Q

what happens w/ ketone bodies in long term starvation conditions

A

ketone bodies –> acetyl CoA –> into TCA cycle to keep it going

79
Q

what do we see in intermediate to longer term starvation conditions

A

ketogenesis

80
Q

what’s the main idea w ketone bodies

A

ketone bodies generated from ketogenesis in liver are used to make acetyl CoA –> goes into TCA cycle, generates reducing power to make ATP in starvation conditions

81
Q

basically what is ketogenesis

A

kind of diverting certain carbon skeletons that can be utilized in longer term starvation conditions

82
Q

what are anabolic and catabolic pathways of lipids reciprocally regulated by

A

insulin and glucagon

83
Q

when is oxidation of fats unecessary

A

when diet provides carbohydrate fuel

84
Q

what 2 enzymes for coordinated regulation

A

acetyl-CoA carboxylase (ACC), carnitine acyl transferase I (CAT I)

85
Q

what is ACC

A

first enzyme in fatty acid synthesis pathway

86
Q

what does ACC do

A

takes acetyl CoA, feeds it to biosynthesis pathway for fatty acids

87
Q

what is CAT I important for

A

uptake/transport of fatty acids in mitochondrial matrix where b-oxidation occurs

88
Q

what does insulin promote

A

uptake, synthesis, storage of triglycerides

89
Q

what does glucagon promote

A

degradation/breakdown of triglycerides

90
Q

when is insulin released

A

high blood glucose conditions

91
Q

when is glucagon released

A

low blood glucose conditions

92
Q

what kinase mediates these effects

A

PKA

93
Q

what does glucagon do

A

stimulates PKA

94
Q

what does insulin

A

activates PP1

95
Q

what is first intermediate of fatty acid biosynthesis

A

malonyl CoA

96
Q

what does ACC do

A

acetyl CoA –> malonyl CoA

97
Q

what is used in synthesis of fatty acid from here

A

malonyl CoA

98
Q

what happens in low blood glucose conditoins

A

glucagon –> activates PKA –> phosphorylates & inhibits ACC

99
Q

what does low blood glucose do to ACC

A

inhibits ACC

100
Q

what does inhibiting ACC do

A

lowers malonyl CoA (first intermediate in the pathway)

101
Q

what does malonyl CoA do (besides being intermediate in fatty acid synthesis)

A

allosteric regulator of CAT I

102
Q

what does high malonyl CoA levels mean

A

inhibit CAT I

103
Q

what happens if we inhibit CAT I

A

we inhibit the conversion of fatty acyl CoA to fatty acyl Carnitine, and uptake of fatty acyl units into mitochondria

104
Q

basically what does inhibition of CAT I do

A

prevents beta oxidation (not enough fatty acyl groups feeding into b-oxidation pathway)

105
Q

so describe effects of low blood glucose

A

glucagon –> inhibits ACC –> inhibits first step of biosynthesis pathway (malonyl CoA) –> increases CAT I activity –> favors uptake and oxidation of fatty acids

106
Q

why does blood glucose condition favor uptake and oxidation of fatty acids

A

low blood glucose means E levels are low, and we need to use fats as an E source (since glycogen stores depleted we can’t use that as E source)

107
Q

describe low blood glucose/glucagon pathway

A

Low blood glucose conditions → glucagon → PKA → phosphorylates and inhibits ACC → lower levels of malonyl CoA (allosteric regulator of CAT I) → higher levels of CAT I, together w/ presence of fatty acyl coAs → conversion into fatty acyl carnitines → import into mitochondrial matrix → fatty acids undergo oxidation (E source)

108
Q

describe high blood glucose conditions

A

insulin –> stimulates PP1 –> stimulates ACC (dephosphorylates it)

109
Q

what does dephosphorylating ACC do

A

favors its activation

110
Q

what does activating ACC do

A

increases malonyl CoA

111
Q

what does increasing malonyl CoA do

A

inhibits CAT I

112
Q

what does inhibiting CAT I do

A

inhibits beta oxidation

113
Q

describe high blood glucose / insulin pathway

A

high blood glucose conditions → insulin → PP1 → dephosphorylates and activates ACC → higher levels of malonyl CoA (allosteric regulator of CAT I) → inhibits CAT I, inhibits beta oxidation

114
Q

basically what does glucagon/low blood glucose do

A

inhibits ACC; favors beta oxidation vs. fatty acid synthesis; keeps malonyl CoA levels low

115
Q

basically what does insulin/high blood glucose do

A

favors fatty acid synthesis by stimulating PP1, activating ACC, higher levels of malonyl CoA, inhibits CAT I and thus beta oxidation

116
Q

what does a high carb meal do

A

stimulates insulin release

117
Q

what happens in high carb meal

A

PP1 dephosphorylates and activates ACC, ACC increases malonyl CoA, inhibiting CAT I

118
Q

what happens when blood glucose drops between meals

A

glucagon activates PKA, phosphorylates & inhibits ACC, lowers malonyl CoA, increases CAT I, stimulates FA oxidation

biochem (15 decks)

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