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Drew 922 > Block 3 Lecture 3 -- beta-Oxidation > Flashcards

Block 3 Lecture 3 -- beta-Oxidation Flashcards

1
Q

length of short chain FAs

A

2-4 C

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2
Q

length of medium chain FAs

A

4-12 C

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3
Q

length of long chain FAs

A

12-20 C

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4
Q

length of very long chain FAs

A

> 20 C

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5
Q

What is the most common trans fat?

A

elaidic acid

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6
Q

structure of elaidic acid

A

18:1-trans-∆9

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7
Q

structure of alpha-linolenic acid

A

18:3-cis,cis,cis-∆9,12,15

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8
Q

What are examples of omega-3 FAs?

A

alpha linolenic, EPA, DHA

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9
Q

Where are SCFAs activated?

A

cytosol or mitochondria

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10
Q

Where are MCFAs activated?

A

mitochondrial matrix

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11
Q

Where are LCFAs activated?

A

ER, outer mitochondrial membrane, or peroxisomes

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12
Q

Where do all activated FAs have to go for oxidation?

A

mitochondria

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13
Q

Where is carnitine derived from?

A

side chain of lysine

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14
Q

What is the function of the carnitine carrier system?

A

transporting LCFAs to mito matrix

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15
Q

What are the proteins associated with the carnitine carrier system?

A

1) CPT-1
2) CPT-2
3) translocase

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16
Q

What does CPT stand for?

A

carnitine:palmitoyltransferase

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17
Q

Where are CPT 1/2?

A

1 @ cytosolic side

2 @ matrix side

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18
Q

How is CCS regulated?

A

CPT-1 inhibited by malonyl-CoA

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19
Q

How many ATPs from beta-oxidation of C18 saturated FA?

A

146

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20
Q

4 steps of beta-oxidation?

A

1) FAD-dependent DH
2) hydration
3) NAD+ dependent DH
4) thiolysis

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21
Q

4 enzymes of beta-oxidation?

A

1) Aceyl-CoA DH
2) Enoyl-CoA hydratase
3) L-beta-hydroxyacyl DH
4) beta-ketoacyl thiolase

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22
Q

Describe the 2 problems during beta-oxidation.

A

1) beta-gamma double bond

2) ∆4 conjugated system

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23
Q

How is a beta-gamma double bond fixed?

A

isomerase (- 2 ATP since it skips the FAD-dependent DH step)

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24
Q

How is a ∆4 conjugated system fixed?

A

reductase (-3 ATP since it requires NADPH)

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25
How many ATP from an 18:0?
146
26
How is beta-oxidation regulated?
indirectly by demand for ATP - - reoxidation of FADH2/NADH during the ETC - - produced acetyl-CoA enters TCA cycle
27
What is Zellweger's syndrome?
inherited deficiency of peroxisomes causing accumulation of VLCFAs, especially in the brain
28
What is the indication for clofibric acid and clofibrate?
hyperproteinemia and hyperlipidemia
29
What is the MoA for clofibric acid and clofibrate?
stimulate peroxisomes to oxidize VLCFAs
30
What are omega-3's supposedly good for?
solubilizing cholesterol & TG's without sticking to arteries by forming a micelle of sprirals
31
Why are trans fats bad?
isomerase cannot move trans-beta-gamma to trans-alpha-beta for oxidation; so fatty chain accumulates in arteries
32
What are the 2 major anaplerotic pathways for the TCA?
1) propionyl-coA carboxylase | 2) pyruvate carboxylase
33
What cofactors are required by carboxylases?
biotin
34
What step in converting propionyl-CoA to succinyl-CoA requires B12?
methylmalonyl-CoA mutase
35
What's the end product of odd-numbered FA beta-oxidation?
propionyl-CoA
36
When is peroxisomal beta-oxidation used?
for VLCFAs
37
How many fewer ATPs less per cut in peroxisomal compared to regular beta-oxidation?
2 less
38
Why 2 fewer ATPs in peroxisomal?
FADH2 can't be transported to mitochondria
39
What is the product of peroxisomal beta-oxidation?
C8-acyl-CoAs (transported via carnitine carriers)
40
Where does omega-oxidation occur?
in the ER
41
When does omega-oxidation occur?
normally a minor role unless beta-oxidation is compromised (ex carnitine deficiency)
42
What is the product of omega-oxidation?
C6-8 omega-COOH's excreted in the urine
43
How does omega-oxidation work
1) CYP450 oxidizes omega end to OH 2) 2 NADP-dependent DH's oxidize to omega COOH 3) omega oxidation stopping at C6-8
44
On what molecules does alpha-oxidation occur?
VLCFAs (primarily branched FAs from plants)
45
Where does alpha-oxidation mainly occur?
brain/nervous tissue
46
How does alpha-oxidation occur?
1) alpha H oxidized to alpha-OH 2) NADP-dependent DH to make alpha-ketone 3) NADP dependent decarboxylation 4) beta oxidation yields variety of products
47
Which ketone body is the most stable/energy rich?
d-beta-HB
48
How are ketone bodies synthesized?
from 2 A-CoA in 3 steps 1) thiolase - - claisen condensation 2) HMG-CoA synthase - - claisen condensation + hydrolysis 3) HMG-CoA lyase - - aldol/claisen cleavage
49
Where are ketone bodies synthesized?
mitochondria of liver
50
What are the fates of acetoacetate?
1) decarboxylation to acetone | 2) D-beta-HB-DH to D-beta-HB (determined by NADH/NAD+ ratio)
51
Which ketone body is directly used for energy in tissue?
acetoacetate | -- D-beta-HB must be oxidized to give NADH
52
How is acetoacetate converted to Acetyl CoA?
1) ketoacyl transferase (transesterification) to acetoacetyl-CoA 2) thiolase --> 2 acetyl-CoA
53
What is the cost of activating acetoacetate?
1 ATP equivalent that would have been derived from succinyl CoA
54
Where is acetoacetate activated?
mitochondria (not in liver!)
55
How many ATP from d-beta-HB?
23 (2*2Acetyl-CoA - 1 lost to activation)
56
Why are fatty acids synthesized in fasting?
low malonylCoA levels, activating CPTI
57
Why are ketone bodies synthesized in fasting?
low OAA levels, accumulation of acetyl CoA
58
Which KB is produced most during fasting?
beta-d-HB
59
What causes alcohol-related ketoacidosis?
1) low [glycogen] 2) NADH from acetaldehyde blocks lactate DH 3) FAs released, KBs synthesized
60
How are fatty acids preferred in muscle?
high [acetyl coa] inhibits pyruvate DH through phosphorylation

Drew 922 (12 decks)

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