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Block 3, week 4 Dani > Blomquist Lipid Lectures > Flashcards

Blomquist Lipid Lectures Flashcards

1
Q

What is this:

an essential fatty acid (n-6 family) 18:2 (9,12)

A

linoleic acid

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2
Q

What is this:

an essential fatty acid (n-3 family) 18:3 (9,12,15)

A

linolenic acid

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3
Q

What are 2 important N-3 polyunsaturated fatty acids (PUFAs)?

A 
Eicosapenenoic acid (20:5)
Docosahexenoic acid (22:6)
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4
Q

Where do we find a lot of n-3/ omega 3s?

A

in fish oils

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5
Q

(blank) are associated with less inflammation from prostaglandins and lower incidences of heart disease,

A

N-3/omega 3s

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6
Q

What is the main energy reserve of the body and comprises 24lbs of body weight? How is this stored?

A

TAGs

anhydrously

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7
Q

(blank) is stored anhydrously. However, it takes 2 grams of water to store each gram of (blank). Thus lipid has 6 times more energy per gram then CHO.

A

lipid

glycogen

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8
Q

How much energy do you get from a lipid (TAG)?

A

9kcal/gr

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9
Q

How many calories do you need to lose to lose 1 pound?

A

3600

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10
Q

CHO and (blank) have the same amount of calories which is 4-5 kcal/g

A

protein

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11
Q

adipose cell release (blank) and (blank) into blood stream and the free fatty acids are then carried by albumin.

A

free fatty acids

glycerol

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12
Q

What does ATGL do?

A

a lipase in adipocytes that break down TAGs into fatty acids and DAGs

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13
Q

(blank) is the rate-limiting step in cleaving fatty acids from the triglyceride molecule (turns DAG into MAG when phosphorylated)

A

HSL

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14
Q

HSL is activated by (blank) and inhibited by (blank).

A

catecholamines

insulin

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15
Q

Lipid released from adipose tissue is transported and taken up into cells as (blank) and it is associated with albumin
during transport

A

free fatty acid

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16
Q

Lipid taken up by digestion is transported as (Blank) and hydrolyzed to free fatty acids in capillaries and taken up as free fatty acid.

A

TAG

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17
Q

Once fatty acids enter the cell, the fatty acid oxidation begins with activation which is done how? How much energy does this cost?

A

a thioester bond formed b/w carboxyl group of FA and thiol of CoA-Sh via acyl co synthase
2 ATPs

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18
Q

What is the activated (reactive thioster) fatty acid?

How can we make this?

A

acyl CoA

hydrolyzing fatty acid by pyrophosphate which makes reaction favorable

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19
Q

The inner mitochondrial membrane is (blank), while the outer membrane is very permeable

A

impermeable

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20
Q

How do we get fatty acyl CoA get across the outer and inner mito membrane?

A

just cruises past outter membrane but uses a carnitine shuttle (carnitine acyltransferase) to go across inner membrane

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21
Q

Fatty acyl CoA gets transferred to carnitine which goesacross inner mito membrane and is then transferred to (blank).

A

mitochondrial CoA-SH

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22
Q

(blank) has specificity for acyl groups between 14 and 18 carbons long

A 
Carnitine Palmitoyltransferase (CPT-1)
NOTE: this is a carnitine acyltransferase
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23
Q

Beta-Oxidation of saturated fatty acids. One round of beta-oxidation consists of (blank) enzyme-catalyzed reactions.
Each round generates one molecule each of (blank X 3) and a (blank) molecule two carbon atoms shorter than the molecule that entered the round.

A

four
QH2, NADH, acetyl CoA
fatty acyl CoA

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24
Q

During beta oxidation, fatty acids are cleaved off (blank) carbons at a time and increases (blank and blank) during this cycle. This forms (blank) which then goes into TCA.

A

2
FADH2 and NADH
acetyl CoA

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25
Q

What is the result of one acetyl CoA molecule through the TCA cycle?

A

1 FADH2
3 NADH and H+
1 GTP

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26
Q

How much energy do you get from beta-oxidation?

A

you get 146 ATPs and 8.1 ATPs/Carbon

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27
Q

Do odd numbered fatty acids undergo beta oxidation?

A

yes

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28
Q

Can fatty acids be glycogenic?

A

yes, odd chain fatty acids!

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29
Q

Explain beta oxidation of an odd-numbered FA

A

Odd chain-> Propionyl S CoA-> (via carboxlase) methyl malonyl-S-Coa-> (via mutase) succinyl S CoA-> TCA cycle

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30
Q

In beta oxidation, proprionyl CoA is turned into methyl malonyl s Coa, how?

A

via a biotin containing carboxylase

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31
Q

In beta oxidation, methyl malonyl s CoA is rearranged into succinyl s Coa, how?

A

via a cobalt containing mutase (i.e cobalamin Vit B12)

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32
Q

Proprionyl S- CoA is made up of how many carbons?

Succinyl-S CoA is made up of how many carbons?

A

3 x C

4 x C

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33
Q

A (blank) is needed to convert unsaturated FA to acetyl-CoA called isomerase.

A

cis-trans isomerization

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34
Q

If you have an unsaturated FA you have to (Blank) for oxidation.

A

rearrange

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35
Q

Oxidation of (blank) FA does not generate as much ATP relative to (blank) FA.

A

unsaturated

saturated

36
Q

Oxidation of unsaturated FA does not generate as much ATP relative to saturated FA with the same # of carbons you will get (blank) less FADH2 for unsaturated.

A

1

37
Q

Oxidation for an even # poly-unsaturated FA requires a (Blank) step.

A

reductase

38
Q

If you have a poly-unsat or unsaturated FA, you need (Blank) for beta oxidation.

A

additional steps

39
Q

Formation of (blank) occurs when the amount of acetyl-CoA produced is excessive compared to the amount of oxaloacetate available to react with it.

A

ketone bodies

40
Q

What are these:

acetone, beta-hydroxybutyrate, and acetoacetate

A

ketone bodies

41
Q

When will we have ketone bodies?

A

when we have high lipids and are low in carbs
when diabetes isnt controlled
starvation

42
Q

Where are ketone bodies made and what are they used for?

A

made mostly in liver mitochondria and can be used as a fuel in most tissues and organs

43
Q

What diet is this:
high in fats, protein,
ketosis is the goal

A

atkins

44
Q 
What diet is this:
based on what
cavemen supposedly ate. Low in
carbohydrates, ketosis would be
normal.
A

paleolithic diet

45
Q

Give me the creation of ketone bodies

A

In mito matrix:
2 acetyl CoA->acetoacetyl coA-> makes HMG CoA ( notice this is the same key intermediate in cholesterol intermediate but instead we make ketone bodies here) -> acetoacetate-> Acetoacetate and D-3Hydroxy butyrate are the main ketones.

46
Q

Once we make ketone bodies,where do they go?

A

then enter the blood stream and hit up the mitochondrias of muscle, brain and other tissues

47
Q

When ketone bodies enter the mitochondria of other tissues after exiting the liver and blood, what happens to them?

A

they are broken down into acetoacetate-> acetoacetyl CoA–> 2 acetyl CoA-> TCA cycle

48
Q

What is the oxidizing agent for the conversion of ketones to the acetyl CoA?

A

NAD+-> NADH

49
Q

How much energy do you get from ketone bodies?

A

26 ATPs (significantly less than Lipid breakdown)

50
Q

How many ATPs per carbon do you get for ketone bodies and glucose?
How many ATPs per carbon do you get from fat?

A

6.5 ATPs

8 ATPs

51
Q

As you begin to starve what happen?

A

Glucose decreases and Ketone bodies increase signif. and FAs increase a little

52
Q

Brain is normally an obligate glucose user but after a day or 2 of starvation it can switch to (blank). (i.e switch fron carbs to ketone/lipids)

A

ketone bodies

53
Q

Where do fatty acid biosynthesis take place?

A

in the cytosol of the liver from excess glucose or acetyl coA from citrate from the mitochondria

54
Q

Is fatty acid biosynthesis that exact reversal of oxidation?

A

no

55
Q

Explain fatty acid biosynthesis from products in the mitochondria.

A

pyruvate->oxaloacetate + acetyl CoA-> citrate-> acetyl Coa-> Fatty acid
OR
pyruvate->oxaloacetate + acetyl CoA-> citrate-> oxaloacetate->malate->Fatty acid (Needs NADPH)

56
Q

If you are making fatty acids from glucose what do you need?

A

NADPH

57
Q

Since you need NADPH to make fatty acids (most of the time), where will you get this?

A

from the PPP

58
Q

What is the source of acetyl CoA for fatty acid synthesis?

A

from citrate from the TCA cycle

59
Q

What is the controlled step in fatty acid biosynthesis?

A

Conversion of acetyl CoA to Malonyl Coa via acetyl coa carboxylase (needs biotin)

60
Q

What does acetyl-CoA carboxylase need to work?

A

Biotin

61
Q

How is acetyl-CoA carboxylase regulated (the controlled step in FA biosynthesis)?

A

via Citrate and acyl Coa

These both activate it

62
Q

What is the overall reaction of fatty acid synthase?

A

acetyl-CoA + 7 malonyl-CoA +14 NADPH–> palmitic acid + 14 NADP +7CO2 +7CoASH

63
Q

(blank) have a separate protein, a thioesterase 2 that interacts with the growing fatty acid to make medium and short chain fatty acids typical of milk fatty acids.

A

mammary glands

64
Q

What do mammary glands have that allow for the breakdown of large fatty acids into smaller ones typical of milk fatty acids?

A

have thioesterase 2

65
Q

Fatty acid synthetase is made up of (blank) different catalytic sites in a single polypeptide (active as a dimer) ‘multifunctional’

A

7

66
Q

What is this:
3 enzyme activities from one monomer interact with 4 enzyme activities from the other monomer. Absolute need for a dimer for activity.

A

Fatty Acid Synthetase

67
Q

What do the first three domains of fatty acid synthetase do?

A

1) acyl and malonyl binding and condensation
2) reduction of domain I
3) liberation of palmitate product

68
Q

What is malonyl coA used for?

A

Fatty acid biosynthesis

69
Q

What kind of fatty acids are required in the diet.

A

essential fatty acids

70
Q

n6 fatty acids are called (blank)

n3 fatty acids are called (blank)

A

linoleic acid

linolenic acid

71
Q

(blank) (18:2, n-6, 18:3, n-3) are essential because humans cannot desaturate between the delta-9 position and the methyl end of the molecule.. However humans can desaturate where?

A

essential fatty acids

between D9 and carboxyl end of fatty acid

72
Q

How do we further process fatty acids from lineoly coA to arachidonoyl CoA?

A

we desaturate and elongate via addition of 2 carbons

73
Q

What is a precursor of eicosanoids?

A

arachidonoyl CoA

74
Q

What are the biological effects of eicosanoids?

A

Inflammation (primarily of joints, skin, eyes)
Intensity and duration of pain and fever
Reproduction function (including induction of labor)
Inhibit gastric acid secretion
Regulate blood pressure
Inhibiting or activating platelet aggregation and
thrombosis

75
Q

What are the 4 clinically relevant prostaglandins?

A

Prostaglandins PG
Thromboxanes TX
Leukotrienes LT
Lipoxines LX

76
Q

The major pathways for the formation of eicosanoids via the prostaglandin H synthase (PGHS) pathway leads to (blank).

A

prostaglandin H2, which can be converted to prostacyclin, thromboxane A2 and a variety of prostaglandins

77
Q

The major pathway for the formation of eicosanoids via the lipoxygenase pathway produces (blank), a precursor of some other leukotrienes. The cyclooxygenase activity of PGHS (prostaglandin H synthase) is inhibited by (Blank).

A

leukotriene A4

aspirin

78
Q

What does prostaglandin H synthase do? What inhibits this?

A

it converts arachidonate to prostaglandin G2 (via the ecosanoid synthesis pathway)
inhibited by COX inhibitor (Aspirin)

79
Q

Why is aspirin not awesome for your stomach?

A

aspirin blocks Cox-1 and Cox-2, Cox-1 is important for mucin production to protect stomach wall from acid

80
Q

What was the drug recalled for myocardial risk?

A

rofecoxib (vioxx)

81
Q

(blank) is not an anti-inflammatory and

does not block prostaglandin formation. It works by a different mechanism than NSAIDS.

A

acetomenophen (tylenol)

82
Q

What kind of drug is naproxen?

A

anti-inflammatory

83
Q

(blank) produces eicosanoids in the stomach that decrease acid secretion.

A

Cyclooxygenase 1

84
Q

(blank) causes most of the inflammation responses.

A

Cyclooxgenase 2

85
Q

What is this:
COX-2 inhibitor. Designed not to inhibit COX-1
and therefore have less stomach ulcer side effects. It does have
other side effects and its sisters, Vioxx and Bextra, both COX 2
inhibitors, are no longer used. New COX 2 inhibitors are in the
pipeline and will undoubtedly be available in the future.

A

Celebrex

86
Q

(blank) is a powerful anti-inflammatory agent. It does not inhibit cycloxygenase and works by repressing the synthesis of phospholipase (at the DNA to RNA level). If you don’t have phospholipase A2, then you wont make eicosanoids.

A

Cortisone

87
Q

(blank) is a metabolic pathway which synthesizes glycerol 3-phosphate or triglyceride from precursors other than glucose

A

glyceroneogenesis

Block 3, week 4 Dani (10 decks)

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