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biochem > biochem lecture 8 pt 2 > Flashcards

biochem lecture 8 pt 2 Flashcards

(118 cards)

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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
how do we get fatty acyl CoA to mitochondria
set of interconversion reactions where we swap coenzyme A for carnitine
26
what enzymes are involved
2 acetyl transferases: carnitine acetyl transferase I, carnitine acetyltransferase II
27
what is CAT 1
resides in outer membrane
28
what is CAT II
in inner mitochondrial membrane
29
what is Cat 2 important for
for when we convert fatty acyl carnitine back into fatty acyl coenzyme A
30
describe transportation step
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
31
what is end product after step 2
we end up w/ a fatty acyl CoA which goes through beta oxidation pathway
32
how many stages in beta oxidation
3;
33
stage 1 of beta oxidation
B-oxidation of fatty acids
34
stage 2 of beta oxidation
acetyl CoA oxidized to Co2
35
what is stage 3 of b-oxidation
electrons transferred from NADH/FADH2 to ETC for electron synthesis
36
what do we do in beta oxidation
we are removing 2 Cs at a time off fatty acid, with each round
37
but in all situations what do we have culmination of
culmination of beta oxidation of fats
38
what happens if we have double bonds (one or more)
its about getting rid of those double bonds to generate a fully saturated fatty acid
39
what happens once we have saturated fatty acid
can be sent thru beta oxidation pathway
40
what's the point of beta oxidation pathway
generates acetyl CoA units, which can be fed into TCA cycle
41
what do fats generate a lot of
generate a lot of reducing power (NADH, FADH) in TCA cycle
42
where does that reducing power go
fed into ETC, important for ox phos
43
what are the 4 scenarios of beta oxidation
even & saturated, even & monounsaturated, even & polyunsaturated, odd
44
what's the simplest case
even & saturated
45
what 4 steps
oxidation, hydration, oxidation, thiolysis
46
where is 1st step
fatty acyl CoA (starting point), we are in mitochondrial matrix
47
describe 1st step
fatty acyl CoA oxidized to trans delta 2 enoyl CoA
48
what kinda rxn is 1st step
oxidation rxn
49
what else is produced in 1st oxidation
FADH2
50
why is trans delta 2 enoyl CoA important
because in other pathways, it all boils down to getting to this intermediate
51
2nd step
trans delta 2 enoyl CoA --> 3-hydroxyacyl CoA intermediate
52
what kinda rxn in step 2
hydration step; input of water
53
step 3
second oxidation step, results in another reducing power molecule created
54
describe step 3
3-hydroxyacyl CoA --> 3-ketoacyl CoA intermediate
55
what else is produced in step 3
reduction of NAD+ to NADH, simultaneous oxidataoin
56
step 4
2 products: acyl CoA and acetyl CoA; we keep converting acyl CoA to acetyl CoA until we're done
57
what extra enzyme in even monounsaturated enzyme
enoyl-CoA isomerase
58
how much ATP per double bond does enoyl CoA isomerase use
2 ATP
59
what enzymes does even polyunsaturated fatty acids use
enoyl CoA isomerase AND 2,4-dienoyl CoA reductase
60
how much ATP per double bond in 2,4-dienoyl CoA reductase
3 ATP
61
B-oxidation in odd fatty acids
keep doing beta oxidation until you reach 3Cs
62
what happens to those remaining 3 Cs
succinyl CoA
63
where does succinyl CoA go
into TCA
64
describe b-oxidation for odd stuff
propionyl CoA --> methylmalonyl CoA --> methylmalonyl CoA --> succinyl CoA
65
what 3 enzymes
propionyl CoA carboxylase, methylmalonyl CoA epimerase, methylmalonyl CoA mutase
66
what undergoes lipgenesis
excess dietary glycerol and fatty acids undergo lipogenesis to make triglycerides
67
why is glucose easily converted to fat
acetyl CoA is intermediate in glucose metabolism and starting molecule for fatty acid synthesis
68
what does release of insulin favor
lipogenesis to form triglycerides
69
what else are fats derived from besides excess dietary lipids
glucose
70
liypolysis
breakdown of stored fat
71
what is lipolysis reverse of
reverse of lipogenesis
72
what is necessary for complete oxidation of fat (thru TCA cycle)
oxaloacetete
73
what would happen to acetyl CoA without oxaloacetate
ketogenesis; acetyl CoA converted into ketones
74
when does ketogenesis occur
long term starvation conditions; decline in oxaloacetate levels
75
where does ketogenesis happen
in liver
76
ketone bodies
utilized as a way to generate fatty acids (fatty acid --> beta oxidation --> ATP)
77
what else can ketone bodies be converted into
acetyl CoA
78
what happens w/ ketone bodies in long term starvation conditions
ketone bodies --> acetyl CoA --> into TCA cycle to keep it going
79
what do we see in intermediate to longer term starvation conditions
ketogenesis
80
what's the main idea w ketone bodies
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
basically what is ketogenesis
kind of diverting certain carbon skeletons that can be utilized in longer term starvation conditions
82
what are anabolic and catabolic pathways of lipids reciprocally regulated by
insulin and glucagon
83
when is oxidation of fats unecessary
when diet provides carbohydrate fuel
84
what 2 enzymes for coordinated regulation
acetyl-CoA carboxylase (ACC), carnitine acyl transferase I (CAT I)
85
what is ACC
first enzyme in fatty acid synthesis pathway
86
what does ACC do
takes acetyl CoA, feeds it to biosynthesis pathway for fatty acids
87
what is CAT I important for
uptake/transport of fatty acids in mitochondrial matrix where b-oxidation occurs
88
what does insulin promote
uptake, synthesis, storage of triglycerides
89
what does glucagon promote
degradation/breakdown of triglycerides
90
when is insulin released
high blood glucose conditions
91
when is glucagon released
low blood glucose conditions
92
what kinase mediates these effects
PKA
93
what does glucagon do
stimulates PKA
94
what does insulin
activates PP1
95
what is first intermediate of fatty acid biosynthesis
malonyl CoA
96
what does ACC do
acetyl CoA --> malonyl CoA
97
what is used in synthesis of fatty acid from here
malonyl CoA
98
what happens in low blood glucose conditoins
glucagon --> activates PKA --> phosphorylates & inhibits ACC
99
what does low blood glucose do to ACC
inhibits ACC
100
what does inhibiting ACC do
lowers malonyl CoA (first intermediate in the pathway)
101
what does malonyl CoA do (besides being intermediate in fatty acid synthesis)
allosteric regulator of CAT I
102
what does high malonyl CoA levels mean
inhibit CAT I
103
what happens if we inhibit CAT I
we inhibit the conversion of fatty acyl CoA to fatty acyl Carnitine, and uptake of fatty acyl units into mitochondria
104
basically what does inhibition of CAT I do
prevents beta oxidation (not enough fatty acyl groups feeding into b-oxidation pathway)
105
so describe effects of low blood glucose
glucagon --> inhibits ACC --> inhibits first step of biosynthesis pathway (malonyl CoA) --> increases CAT I activity --> favors uptake and oxidation of fatty acids
106
why does blood glucose condition favor uptake and oxidation of fatty acids
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
describe low blood glucose/glucagon pathway
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
describe high blood glucose conditions
insulin --> stimulates PP1 --> stimulates ACC (dephosphorylates it)
109
what does dephosphorylating ACC do
favors its activation
110
what does activating ACC do
increases malonyl CoA
111
what does increasing malonyl CoA do
inhibits CAT I
112
what does inhibiting CAT I do
inhibits beta oxidation
113
describe high blood glucose / insulin pathway
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
basically what does glucagon/low blood glucose do
inhibits ACC; favors beta oxidation vs. fatty acid synthesis; keeps malonyl CoA levels low
115
basically what does insulin/high blood glucose do
favors fatty acid synthesis by stimulating PP1, activating ACC, higher levels of malonyl CoA, inhibits CAT I and thus beta oxidation
116
what does a high carb meal do
stimulates insulin release
117
what happens in high carb meal
PP1 dephosphorylates and activates ACC, ACC increases malonyl CoA, inhibiting CAT I
118
what happens when blood glucose drops between meals
glucagon activates PKA, phosphorylates & inhibits ACC, lowers malonyl CoA, increases CAT I, stimulates FA oxidation

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