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Biochem 385 Unit 2 > Lecture 20: Fatty Acid Synthesis > Flashcards

Lecture 20: Fatty Acid Synthesis Flashcards

1
Q

acetyl CoA carboxylase

A

key regulated enzyme in fatty acid synth

generates malonyl CoA using acetyl CoA

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2
Q

malonyl CoA

A

where the growing fatty acids attach

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3
Q

whats the reductant in fatty acid synth

A

NADPH

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4
Q

what moces the acetyl coA equivalents from the mitochondria to the cytosol

A

citrate shuttle

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5
Q

review table in slide

A

3

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6
Q

what is the common metabolite in both the synthesis and degradation pathways

A

acetyl CoA

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7
Q

why does it make sense that fatty acid degredation takes place in the mitochondrial matrix

A

NADH and FADH2 are produced

they’re ready to enter the ETS if they’re present

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8
Q

what purpose does fatty acid synth serve

A

convert excess acetyl CoA to fatty acids to be stored or exported (when glucose levels are high)

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9
Q

key enzymes in FA synth?

A

acetyl coA carboxylase

fatty acid synthase

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10
Q

is the energy charge high or low in the cell when excess acetyl-CoA is available for fatty acid synthesis?

A

high!

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11
Q

swinging arm mechanism

A

2 domain protein and biotin carrier

covalent linkages so intermediate doesn’t diffuse away

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12
Q

How many NADPH must be oxidized in the synthesis of C16 fatty acid palmitate shown on slide 11?

A

14

we need two every time we add 2 carbons
7 x 2= 14 NAPDHs

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13
Q

How many CO2 are released in this process and where are they coming from?

A

7 are released because we go through the process 7 times

they come from the malonyl CoA

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14
Q

review slides 10 and 11

A

review slides 10 and 11

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15
Q

there are 7 dehydration steps required for palmitiate synthesis
why only 6 NET H2O???

A

at the end of the cycle, we still have an acyl chain bound, but it takes water to release it

we produce 7 water molecules but we use one to release the chain

needed for final cleavage rxn to release palmitate from the ACP carrier protein

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16
Q

where do we add the carbon?

A

not at the end, but closer to the begining

17
Q

write the reaction for synth of C18 stearate

__acetyl CoA + __ATP + __NADPH +__H+ —> sterate+__CoA+__ADP+__Pi+__NADP+ + __H2O

A

9 acetyl CoA +8 ATP + 16 NADPH +16 H+ —> sterate+9 CoA+8 ADP+ 8 Pi+ 16 NADP+ + 7 H2O

18
Q

How do we move acetyl CoA

What do we do with it

A

we don’t directly transport it
use shuttle system

make it citrate that we move to cytosol

19
Q

what do we do with the citrate we put it the cytosol

A

make OAA or carbon and acetyl CoA

make it to malate

20
Q

2 things that can happen to malate

A
  1. transport back to matrix, covert to OAA

2. convert to pyruvate and also produce NADPH (one for every acetyl CoA equivalent)

21
Q

where does most NADPH come from for fatty acid synth??

A

pentose phoshphate pathway (oxidative phase)

so lots of glucose 6 phosphate, make lots of NADPH

22
Q

the bulk of NADPH needed for fatty acid synth actually comes from pentose phosphate pathway. Why does this make sense in terms of glucose 6 P lelvels

A

G6P levels are high during FA synth

we can do this and produce lots of NADPH

23
Q

Metabolic reg of acetyl CoA carboxylase:
what stimulates
what inactivates

A

citrate activity stimulates
palmitoyl coA inhibits

BOTH ALLOSTERIC

24
Q

why does it make sense that excess citrate activates acetyl CoA carboxylase activity?

A

high energy charge, so we need to start storing extra nrg just as fast

25
Q

Why should palmotyl CoA inhibit enzyme activity?

A

palmitoyl CoA is in fatty acid degredation. Inhibits enzymes in order to inhibit simultaneous synth and degredation

26
Q

Hormonal regulation of Acetyl-CoA carboxylase

A

glucagon
isnulin
citrate

27
Q

explain the logic of insulin and AMP reg of acetyl CoA carboxylase

A

blood sugar levels high, stim by AMP b.c. low nrg charge

28
Q

Why would high citrate levels partially activate the phosphorylated enzyme?

A

citrate=high nrg charge
allosteric reg=fast response (hormones are slow)
(review slide 18)

29
Q

Glucagon signaling

A

cascade of rxns inside cell
AMPK (kinase) activated at the end–phosphorylates acetyl CoA carboxylase monomeric state

INACTIVATE

30
Q

Citrate

A

polymerization
PARTIAL ACTIVITY
phosphorylated, so inactive, but citrate makes it partially active

31
Q

Insulin signaling

A

protein phosphtase 2 stim: takes off phosphate
active state

ACTIVATE

32
Q

AMPK

A

regulated by AMPKK (this one phosphorylates AMPK)
AMPKK inactivated by insulin
ensures acetyl-CoA carboxylase will stay in active conformation

review slide 19

33
Q

review slide 20

A

review slide 20

Biochem 385 Unit 2 (13 decks)

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