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Block 3; Week 4 Michelle > Blomquist Lipid I > Flashcards

Blomquist Lipid I Flashcards

1
Q

Rank these from healthiest to least healthy:
Trans Unsaturated Fatty Acids
Cis Unsaturated Fatty Acids
Saturated Fatty Acids

A

Most Healthy: Cis unsaturated fatty acids
saturated fatty acids
Least Healthy: Trans unsaturated fatty acids
**trans are the worst & are associated w/ higher rates of heart disease

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2
Q

What are the 2 essential amino acids? Which family do they belong to? Why can’t we make them?

A

Linoleic Acid: 18:2: n-6 family

Linolenic Acid: 18:3: n-3 family

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3
Q

We’re talking n-3 polyunsaturated fatty acids (PUFA)…which type of foods are these found in? Are they healthy for humans?

A

they are high in fish oils

they are healthy & are associated w/ lower rates of inflammation & heart disease…

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4
Q

What type of polyunsaturated fatty acid do they recommend we DON’T eat?

A

n-6

*b/c arachidonic acid is n-6 & produces prostaglandins & is associated w/ inflammation

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5
Q

How many double bonds does eicosapenenoic acid have? How many double bonds does Docosahexenoic acid have?

A

Eicosapenenoic acid: 20 carbons & 5 double bonds

Docosahexenoicacid: 22 carbons & 6 double bonds

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6
Q

What do hibernating bears use for their energy source?

A

TAGs stored anhydrously
It is an efficient mechanism to store energy
the amount of time that you would survive a starvation scenario is dependent on the amount of TAGs you have…

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7
Q

Which is more efficient at storage: lipid or glycogen?

A

Lipid is much more efficient than glycogen…

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8
Q

What is the role of caveolin in lipid mobilization?

A

It inhibits PKA.

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9
Q

What is the pathway for lipid mobilization?

A

Epinephrine activates the G protein & the alpha subunit activates adenylyl cyclase. cAMP increases… & activates the PKA. PKA activates HSL & perilipin-1. Phosphorylated HSL makes DAGs into MAGs. The phosphorylated perlipin-1 releases ABHD5. ABHD5 binds ATGL & activates it. This turns TAGs into DAGs.

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10
Q

What does adipose tissue release into the bloodstream?

A

fatty acids & glycerol

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11
Q

How is lipid taken up into cells?

A

free fatty acids

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12
Q

How do you begin beta oxidation in cells?

A

It begins with fatty acid oxidation.
Fatty Acid + HS-CoA
Enzyme: Acyl CoA Synthetase w/ 2 ATP equivalents
Becomes Acyl CoA

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13
Q

Where does beta oxidation take place?

A

In the mitochondrial matrix.

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14
Q

How do the acyl coAs move from the cytosol to the mitochondrial matrix?

A

Fatty Acyl CoA + L-Carnitine
Enzyme: carnitine acyl transferase
Result: Acyl Carnitine
**While the Acyl CoA was able to get thru the outer mitochondrial membrane…the acyl carnitine is able to pass the inner mitochondrial membrane thru the translocase.
In the mitochondrial matrix: the acyl carnitine bumps into carnitine acyl transferase & becomes acyl CoA again.

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15
Q

What is another name for carnitine acyl transferase? It has a specificity for what types of acyl CoAs?

A 
carnitine palmitoyltransferase (CTP-1)
Acyl groups b/w 14-18 carbons long...
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16
Q

How many steps are in beta oxidation?

What do you begin with? What do you end up with?

A 
4 steps:
oxidation
hydration
oxidation
thiolysis
**begin with fatty acyl CoA
**end w/ Fatty Acyl CoA (2 carbons shorter) & NADH & FADH2 & Acetyl CoA
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17
Q

What is the first step of beta oxidation?

A

Fatty Acyl CoA–>trans delta enoyl CoA
Process: oxidation
Byproduct: FADH2
Enzyme: Acyl CoA dehydrogenase

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18
Q

Why is FAD used in the first step of beta oxidation?

A

b/c it is dealing w/ C-C

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19
Q

What is the second step of beta oxidation?

A

trans delta enoyl CoA–>L-3-hydroxyacyl CoA
Process: Hydration
Enzyme: Enoyl CoA hydratase

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20
Q

What is the 3rd step of beta oxidation?

A

L-3-hydroxyacyl CoA–>3-ketocyl CoA
Process: oxidation
Byproduct: NADH
Enzyme: L-3-hydroxyacyl CoA dehydrogenase

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21
Q

Why is NAD used in the third step of beta oxidation?

A

b/c we are dealing w/ a C-O connection…

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22
Q

What is the fourth step of beta oxidation?

A

3-ketocyl CoA–>Fatty Acyl CoA (2 fewer carbons)
Process: thiolysis
Byproduct: Acetyl CoA
Enzyme: 3-ketoacyl thiolase

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23
Q

Where does the Acetyl CoA produced by beta oxidation go?

A

stays in the mitochondrial matrix & enters the TCA cycle.

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24
Q

Let’s talk TCA.
What’s your mnemonic?
What do you get from 1 cycle, 1 Acetyl CoA?

A 
OC (orange county)
I
KSS FM (radio station)
1 cycle = 3 NADH; 1 FADH2; 1 GTP
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25
Q

How many steps are in the TCA cycle?

A

8

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26
Q

What happens step 1 of TCA?

A

OAA + Acetyl CoA–>Citrate

Enzyme: citrate synthase

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27
Q

What happens step 2 of TCA?

A

Citrate –> Isocitrate

Enzyme: aconitase

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28
Q

What happens step 3 of TCA?

A

Isocitrate–>alpha ketoglutarate
Byproducts: 1 NADH; 1 CO2
Enzyme: isocitrate dehydrogenase

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29
Q

What happens step 4 of TCA?

A

alpha ketoglutarate–>succinyl CoA
Byproduct: 1 NADH
Enzyme: alpha ketoglutarate dehydrogenase complex

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30
Q

What happens step 5 of TCA?

A

succinyl CoA–>succinate
Byproduct: 1 GTP
Enzyme: succinyl CoA synthetase

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31
Q

What happens step 6 of TCA?

A

succinate–>fumarate
Byproduct: 1 FADH2
Enzyme: succinate dehydrogenase

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32
Q

What happens step 7 of TCA?

A

fumarate–>malate

Enzyme: fumarase

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33
Q

What happens step 8 of TCA?

A

malate–>OAA
Byproduct: 1 NADH
Enzyme: malate dehydrogenase

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34
Q

Can odd chain fatty acids undergo beta oxidation? Where are odd chain fatty acids found?

A

Yes, they can…they just have different products.

Found in 2% of the fatty acids in beef meat.

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35
Q

What does your body do with odd-chain number fatty acids?

A

They undergo beta oxidation, but instead of producing Acetyl CoA, they produce propionyl CoA (3C).

36
Q

How does having a bunch of propionyl CoA do you any good?

A

Propionyl CoA is converted into methyl malonyl SCoA, which is converted to succinyl S CoA. This has four carbons & is fed into TCA.

37
Q

The step of changing propionyl CoA into methyl malonyl SCoA involves what?

A

CO2 & ATP are fed in…
this is a step of carboxylation
**this enzyme contains biotin

38
Q

The step of changing methyl malonyl SCoA into succinyl SCoA involves what?

A

Rearrangement

  • *it involves a cobalt containing mutase
  • *this enzyme is affected by cobalamin or vitamin B12 deficiencies…
39
Q

Can fatty acids be glycogenic?

A

Yes, odd chain fatty acids.

40
Q

What is involved in getting a mono-unsaturated fatty acid (w/ a cis double bond) ready for beta oxidation?

A

cis–>trans isomerization

  • *basically you make it into a trans unsaturation
  • enzyme: cis-delta-enoyl CoA isomerase
41
Q

Do fatty acids with double bonds give the same amount of energy thru beta oxidation as do fatty acids w/o them?

A

NO

for each double bond they give off -1 FADH2 worth of energy…

42
Q

What is involved in getting a poly-unsaturated fatty acid (w/ cis double bonds) ready for beta oxidation?

A

It requires cis-delta-enoyl CoA isomerase

  • *it also requires 2,4 dienoyl CoA reductase
  • *remember for each double bond -1FADH2 worth of energy…
43
Q

When do ketone bodies form?

A

when more acetyl CoA is produced than there is available OAA to react with it…

44
Q

What conditions favor the formation of ketone bodies?

A

Starvation (begins day 2)
Uncontrolled Type I Diabetes (dangerous ketoacidosis)
High Fat Diet (Atkins)
*in ketosis

45
Q

What are the 3 types of ketone bodies?

A

acetone
beta-hydroxybutyrate
acetoacetate

46
Q

Where are ketone bodies formed & what are they used for?

A

formed mainly in liver mitochondria & used for fuel in most tissues

47
Q

What does your breath smell like if you are in ketosis?

A

sweet, from the acetone

48
Q

Explain the process of ketone body formation.

A 
2 Acetyl CoA-->Acetoacetyl CoA
Acetoacetyl CoA + Acetyl CoA-->HMG CoA
Enzyme: HMG-CoA Synthase
HMG CoA-->Acetoacetate
Byproduct: Acetyl CoA
Enzyme: HMG CoA Lyase
Acetoacetate-->Acetone OR -->Beta hydroxybutyrate
49
Q

Where does ketone body formation take place?

A

the mitochondrial matrix

**if it were in the cytosol–>it would result in cholesterol formation

50
Q

When runners “hit the wall” what is really happening?

A

they have run out of their available stores of glycogen & their bodies are switching from carbohydrate energy to lipid energy (including ketone bodies)

51
Q

Where does fatty acid biosynthesis take place?

A

in the cytosol

mainly in the liver w/ excess glucose

52
Q

What are the 2 main feed-ins to fatty acid biosynthesis?

A

NADPH

Acetyl CoA

53
Q

Where does the NADPH come from that is fed into fatty acid biosynthesis?

A

The conversion of malate to pyruvate

hexomonophosphate shunt of the pentose phosphate pathway…

54
Q

Where does the acetyl CoA come from that is involved in fatty acid biosynthesis?

A

glycolysis in the cytosol shuttle pyruvate into mitochondrial matrix…it is converted into acetyl CoA…changed into citrate to be shuttled back into the cytosol…and changed back into acetyl CoA

55
Q

How many steps & how many shuttles are involved in getting the body set up for fatty acid biosynthesis?

A

2 shuttles

5 steps

56
Q

What is the first shuttle?

A

the first shuttle is getting the pyruvate from glycolysis into the mitochondrial matrix

57
Q

What is the first step of fatty acid biosynthesis?

A

Pyruvate is converted into OAA by pyruvate carboxylase.

Pyruvate is converted into Acetyl CoA by pyruvate dehydrogenase complex.

58
Q

fatty acid biosynthesis

What is the second step?

A

The OAA & Acetyl CoA made from pyruvate in the mitochondrial matrix are converted into Citrate via the enzyme: citrate synthase.

59
Q

What is the second shuttle in fatty acid biosynthesis?

A

The citrate is shuttled from the mitochondrial matrix into the cytosol.

60
Q

fatty acid biosynthesis

What is the third step?

A

Citrate is broken up into OAA & Acetyl CoA by ATP-citrate lyase

61
Q

The Acetyl CoA that is separated from the citrate is fed into the fatty acid biosynthesis…but what is the fourth step?

A

OAA–>Malate

via malate dehydrogenase

62
Q

fatty acid biosynthesis

What is the fifth step?

A

Malate–Pyruvate
via Malic Enzyme
Byproducts: CO2 & NADPH

63
Q

Rando: anything with a dehydrogenase requires ____.

A

NAD+

64
Q

What enzyme do mammary glands use to make medium & short chain fatty acids from growing fatty acids for milk?

A

thioesterase 2

65
Q

What is the most controlled step in fatty acid biosynthesis?

A

Acetyl CoA + Bicarb –>Malonyl CoA

Enzyme: Acetyl CoA Carboxylase

66
Q

What does Acetyl CoA carboxylase require to function?

A

biotin

67
Q

What 2 things activate Acetyl CoA?

A

citrate

acyl coA

68
Q

What is the overall reaction of fatty acid synthesis?

A

Acetyl CoA + 7 Malonyl-CoA + 14 NADPH
–>
Palmitic Acid + 14 NADP + 7 CO2 + 7 COASH
Enzyme: fatty acid synthase

69
Q

How many carbons are in palmitic acid?

A

16 carbons

70
Q

What’s the deal w/ fatty acid synthase?

A

It is a dimer, requires both monomers to function.

It has 7 enzymatic activities.

71
Q

Once again, what are the 2 essential fatty acids? Why are they essential?

A

18:2 (n-6)
18:3 (n-3) **better to eat them more of these!
We can’t desaturate b/w delta 9 & the methyl end of the molecule…

72
Q

How do you convert linoleoyl CoA to arachidonyl CoA?

A

thru a series of desaturation & elongation steps

Note: the formation of arachidonyl CoA is clinically significant as this is the precursor to eicosanoids.

73
Q

What are some biological effects of eicosanoids?

A 
Inflammation
Pain
Induction of Labor
Inhibition of Gastric Acid secretion
BP regulation
Control of Platelet Aggregation
74
Q

What are 4 clinically relevant eicosanoids?

A

Prostaglandins
Thrombaxanes
Leukotrienes
Lipoxins

75
Q

Explain eicosanoid synthesis.

A

Arachidonate goes to 1/2 places.

  1. Prostaglandins
  2. leukotrienes
76
Q

Explain eicosanoid synthesis w/ the prostaglandin pathway.

A

Arachidonate–>Prostaglandin G2
Enzyme: Prostaglandin G2
synthase/Cyclooxygenase
Prostaglandin G2–>Prostaglandin H2
Enzyme: Prostaglandin H Synthase/hydroperoxidase
Prostaglandin H–>thrombaxane or prostacyclin or other things.

77
Q

Explain the eicosanoid synthesis w/ the leukotriene pathway.

A

Arachidonate–>Leukotrienes

via arachidonate lipoxygenase & dehydrase

78
Q

What do aspirin & other NSAIDs inhibit?

A

Cyclooxygenase. Prevents the formation of prostaglandin G2.

79
Q

What is COX 1 responsible for? COX 2?

A

COX 1: decreases stomach acid secretions

COX 2: inflammation

80
Q

In terms of COX 1 & COX 2…what does aspirin inhibit?

A

COX 1 & COX2

81
Q

In terms of COX 1 & COX 2…what does ibuprofen inhibit?

A

COX 2>COX1

82
Q

In terms of COX 1 & COX 2…what does acetaminophen inhibit?

A

Neither! It has a different pathway than NSAIDs

83
Q

In terms of COX 1 & COX2…what does celebrex inhibit?

A

COX 2 only

**Note: Vioxx & Bextra are COX 2 only too…but they are off the market now.

84
Q

What is the advantage to taking a COX 2 only inhibitor?

A

you would probably not have as many stomach ulcers, b/c your COX 1 & decreased stomach acid secretions could still go strong…

85
Q

What does cortisone do?

A

Okay…so a phospholipid is chillin’ there with 2 fatty acids. @ the 2 position is a fatty acid that can become arachidonic acid. Phosphlipase A2 cleaves it off. The arachidonic acid becomes eicosanoids.
Cortisone @ the DNA/RNA level represses the levels of Phosphlipase A2. This decreases the formation of prostaglandins & leukotrienes & stuff.

86
Q

Explain TAG synthesis.

A

From glycolysis…you get G-3-P

G-3-P–>lysophosphatidic acid–>phosphatidic acid–>DAG–>TAG

Block 3; Week 4 Michelle (9 decks)

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