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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
Q

How many ATP from an 18:0?

A

146

26
Q

How is beta-oxidation regulated?

A

indirectly by demand for ATP

    • reoxidation of FADH2/NADH during the ETC
    • produced acetyl-CoA enters TCA cycle
27
Q

What is Zellweger’s syndrome?

A

inherited deficiency of peroxisomes causing accumulation of VLCFAs, especially in the brain

28
Q

What is the indication for clofibric acid and clofibrate?

A

hyperproteinemia and hyperlipidemia

29
Q

What is the MoA for clofibric acid and clofibrate?

A

stimulate peroxisomes to oxidize VLCFAs

30
Q

What are omega-3’s supposedly good for?

A

solubilizing cholesterol & TG’s without sticking to arteries by forming a micelle of sprirals

31
Q

Why are trans fats bad?

A

isomerase cannot move trans-beta-gamma to trans-alpha-beta for oxidation; so fatty chain accumulates in arteries

32
Q

What are the 2 major anaplerotic pathways for the TCA?

A

1) propionyl-coA carboxylase

2) pyruvate carboxylase

33
Q

What cofactors are required by carboxylases?

A

biotin

34
Q

What step in converting propionyl-CoA to succinyl-CoA requires B12?

A

methylmalonyl-CoA mutase

35
Q

What’s the end product of odd-numbered FA beta-oxidation?

A

propionyl-CoA

36
Q

When is peroxisomal beta-oxidation used?

A

for VLCFAs

37
Q

How many fewer ATPs less per cut in peroxisomal compared to regular beta-oxidation?

A

2 less

38
Q

Why 2 fewer ATPs in peroxisomal?

A

FADH2 can’t be transported to mitochondria

39
Q

What is the product of peroxisomal beta-oxidation?

A

C8-acyl-CoAs (transported via carnitine carriers)

40
Q

Where does omega-oxidation occur?

A

in the ER

41
Q

When does omega-oxidation occur?

A

normally a minor role unless beta-oxidation is compromised (ex carnitine deficiency)

42
Q

What is the product of omega-oxidation?

A

C6-8 omega-COOH’s excreted in the urine

43
Q

How does omega-oxidation work

A

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
Q

On what molecules does alpha-oxidation occur?

A

VLCFAs (primarily branched FAs from plants)

45
Q

Where does alpha-oxidation mainly occur?

A

brain/nervous tissue

46
Q

How does alpha-oxidation occur?

A

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
Q

Which ketone body is the most stable/energy rich?

A

d-beta-HB

48
Q

How are ketone bodies synthesized?

A

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
Q

Where are ketone bodies synthesized?

A

mitochondria of liver

50
Q

What are the fates of acetoacetate?

A

1) decarboxylation to acetone

2) D-beta-HB-DH to D-beta-HB (determined by NADH/NAD+ ratio)

51
Q

Which ketone body is directly used for energy in tissue?

A

acetoacetate

– D-beta-HB must be oxidized to give NADH

52
Q

How is acetoacetate converted to Acetyl CoA?

A

1) ketoacyl transferase (transesterification) to acetoacetyl-CoA
2) thiolase –> 2 acetyl-CoA

53
Q

What is the cost of activating acetoacetate?

A

1 ATP equivalent that would have been derived from succinyl CoA

54
Q

Where is acetoacetate activated?

A

mitochondria (not in liver!)

55
Q

How many ATP from d-beta-HB?

A

23 (2*2Acetyl-CoA - 1 lost to activation)

56
Q

Why are fatty acids synthesized in fasting?

A

low malonylCoA levels, activating CPTI

57
Q

Why are ketone bodies synthesized in fasting?

A

low OAA levels, accumulation of acetyl CoA

58
Q

Which KB is produced most during fasting?

A

beta-d-HB

59
Q

What causes alcohol-related ketoacidosis?

A

1) low [glycogen]
2) NADH from acetaldehyde blocks lactate DH
3) FAs released, KBs synthesized

60
Q

How are fatty acids preferred in muscle?

A

high [acetyl coa] inhibits pyruvate DH through phosphorylation

Drew 922 (12 decks)

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