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Block 3 Week 4 Meg > Blomquist: Lipid lecture > Flashcards

Blomquist: Lipid lecture Flashcards

1
Q

Common saturated fatty acid

A

stearate

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2
Q

Which fatty acids have a lower boiling point: saturated or unsaturated?

A

unsaturated

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3
Q

Which fatty acids are the worst?

A

trans fatty acids

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4
Q

Two essential fatty acids

A 
linoleic acid (n-6)
linolenic acid (n-3)
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5
Q

These fatty acids are high in fish oils, associated with less inflammation from prostaglandins, and experts recommend we eat foods high in them

A

n-3 polyunsaturated fatty acids

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6
Q

Lipid is stored (blank), meaning that it does not require water to store it. Each gram of glycogen takes 2 grams of water to store, so lipid has (blank) times more energy per gram than CHO.

A

anhydrously; 6

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7
Q

Are glucagon receptors found on adipose tissue?

A

No

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8
Q

What is the lipase called on lipid droplets that takes TAGs to DAGs and FFAs?

A

ATGL = adipose TAG lipase

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9
Q

PKA, when stimulated by epinephrine, phosphorylates (blank) on the surface of the lipid droplet to cleave DAG into MAG and FFA.

A

HSL

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10
Q

When insulin binds to fat cells, phosphodiesterase ultimately blocks (blank) from activating PKA

A

cAMP

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11
Q

Lipid released from adipose tissue is transported and takenup into cells as (blank)

A

free fatty acid

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12
Q

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

A

TAG; FFA

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13
Q

Fatty acid oxidation (breakdown) begins with (blank). A thioester bond is formed between the carboxyl group of the FA and the thiol of (blank)

A

activation of fatty acid; CoA-SH

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14
Q

What do fatty acids become when they are “activated”? What enzyme is this dependent on? How many ATP equivalents are invested?

A

Acyl-CoA; Acyl-CoA synthase; 2 ATP equivalents

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15
Q

The Acyl-CoA crosses the outer mitochondrial membrane, but to get into the matrix, the acyl group must be transferred first to (blank), carried across the membrane, and then transferred to (blank)

A

carnitine; CoA-SH

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16
Q

Carnitine Palmitoyltransferase (CPT-1) has specificity for acyl groups between (blank) carbons long

A

14-18

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17
Q

4 steps in beta oxidation of fatty acyl CoA

A
  1. Fatty acyl-CoA shortened by 2 C and then oxidized
  2. Hydration (gains an OH)
  3. Oxidation (OH become =O)
  4. Thiolysis (release of acetyl-CoA)
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18
Q

Acetyl-CoA can enter the TCA cycle by combining with OAA to form (blank)

A

citrate

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19
Q

Per Acetyl-CoA that enters, the TCA cycle generates how many FADH2? NADH? GTP?

A

1; 3; 1

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20
Q

The last beta-oxidation cycle of a fatty acid with an odd number of carbons gives (blank)

A

propionyl-CoA

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21
Q

What happens to Propionyl-S-CoA so that it may enter the TCA cycle? How many carbons does propionylCoA have? What are the enzymes that catalyze these steps?

A

Propionyl-S-Coa (3C) —-> Methyl-malonyl-S-CoA via a biotin containing carboxylase
Methyl-malonyl-CoA —–> succinyl-CoA (4C) via a cobalt containing mutase

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22
Q

Can fatty acids be glycogenic?

A

Yes, odd chain fatty acids, because succinyl-CoA can go to TCA cycle

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23
Q

The cobalt containing mutase that takes methyl-malonyl-S-CoA to succinyl-S-CoA is dependent on what vitamin?

A

Vit B12

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24
Q

What is needed to convert a UNSATURATED fatty acids to acetyl-CoA? What is the enzyme known as?

A

a cis-trans isomerization; isomerase

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25
Q

Oxidation of UNSATURATED fatty acids does not generate as much ATP as saturated fatty acids with the same number of carbons. How so?

A

For every double bond, 1 less FADH2 generated

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26
Q

Oxidation of even number poly-unsaturated fatty acids requires a (blank) step after the isomerase step.

A

REDUCTASE

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27
Q

occurs when the amount of acetyl-CoA produced is excessive compared to the amount of oxaloacetate available to react with it

A

Formation of ketone bodies

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28
Q

Conditions when ketone bodies are formed

A

Intake high in lipids and low in carbs
Diabetes not well controlled
Starvation

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29
Q

Three ketone bodies

A

acetone
beta-hydroxybutyrate
acetoacetate

30
Q

Ketone bodies are formed primarily in (blank) and can be used as fuel in most tissues and organs

A

liver mitochondria

31
Q

Ketone body formation occurs during (blank), during high (blank) diets, and uncontrolled (blank). It occurs in the (blank)

A

starvation; fat; diabetes; mitochondrial matrix

32
Q

Production of ketone bodies starts with 2 acetyl-CoA which combine with acetoacetyl-CoA to form HMG-CoA. If in the mito, HMG-CoA will form (blank) which can form the two ketones (blank) and (blank)

A

acetoacetate; beta-hydroxybutyrate and acetate

33
Q

When ketone bodies enter the blood stream and travel to mitochondria of other tissues outside the liver, they can then be reversed and taken back to 2 (blank) which can enter the TCA cycle

A

acetyl-CoA

34
Q

Since ketone bodies can enter the TCA cycle once they are broken down into 2 acetyl-CoA, they generate about as much energy per carbon as (blank)

35
Q

About how many ATP are generated for each B-hydroxybutyrate broken down?

36
Q

During prolonged starvation (at about 4 days), the body prefers (blank) as fuel over glucose

A

ketone bodies

37
Q

When the brain or body runs out of glucose, it starts to use (blank) for energy

A

lipids (ketone bodies)

38
Q

Where does biosynthesis of fatty acids occur?

A

In the cytosol primarily of the liver

39
Q

How is acetyl-CoA transferred to the cytosol for fatty acid biosynthesis? What two things provide the NADPH needed for fatty acid biosynthesis?

A

citrate cleavage pathway: citrate shuttled from mito to cytosol, is cleaved to form OAA and acetyl-CoA (OAA can go to malate and pyruvate)

  1. from the pentose phosphate pathway
  2. OAA –> malate –> pyruvate (malate DH generates NADPH)
40
Q

What is the controlled step in FA biosynthesis? What enzyme catalyzes this reaction?

A

conversion of Acetyl-CoA to malonyl-CoA; acetyl-CoA carboxylase (transfers a carboxyl group onto acetyl-CoA)

41
Q

Acetyl-CoA carboxylase (contolled step in FA biosynth) is activated by (blank) and inactivated by (blank)

A

citrate; acyl-CoA

42
Q

Overall reaction of fatty acid synthesis

A

Acetyl-CoA + 7 malonyl-CoA + 14NADPH–>Palmitic acid (C16:0) + 14NADP+ + 7CO2 + 7CoASH

43
Q

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

A

thioesterase 2

44
Q

Fatty acid synthetase is has how many catalytic sites? It acts as a (blank) and is very multifunctional.

45
Q

Where does fatty acid biosynthesis occur in the cell? Where does beta-oxidation occur?

A

cytosol; mitochondria

46
Q

What is the acyl-carrier in fatty acid biosynthesis? How about in B-oxidation?

A

acyl carrier protein; coenzyme A

47
Q

What is the redox coenzyme necessary for fatty acid biosynthesis? What about for B-oxidation?

A

NADPH; FAD when saturated chain (c-C)

NAD+ when hydroxy acid (C-O)

48
Q

Two essential fatty acids. Which one is recommended in the diet? Which one is not?

A 
Linoleic acid (n-6) --> not recommended
Linolenic acid (n-3) --> recommended
49
Q

Essential fatty acids (18:2, n-6, 18:3, n-3) are essential because humans cannot desaturate between the (blank) position and the
methyl end of the molecule

A

delta-9 double bond

50
Q

Plants CAN desaturate from the (blank) towards the methyl end of the fatty acid

A

delta-9 double bond

51
Q

Linoleic acid can be converted to (blank) via elongation and desaturation reactions.

A

arachidonyl-CoA

52
Q

How many carbons are added to linoleic acid when it’s elongated? What does it mean that is it “desaturated”?

A

2 C (from C18 to C20); addition of 2 double bonds

53
Q 
Inflammation
Intensity and duration of pain/fever
Reproduction function (induction of labor)
Inhibit gastric secretion
Regulate BP
Inhibit/activate platelet aggregation
A

Biological effects of eicosanoids

54
Q

Clinically relevant prostaglandins (eicosanoids)

A

prostaglandins
thromboxanes
leukotrienes
lipoxins

55
Q

What step does aspirin block in the synthesis of eicosanoids?

A

Blocks the cyclooxygenase activity associated with prostaglandin H synthase. This is the step that takes arachidonic acid to prostaglandins

56
Q

What is one problem with taking aspirin?

A

It blocks COX 1 and COX2, and COX1 is important for production of mucus to protect from stomach acid. Too much aspirin can lead to ulcers.

57
Q

COX2 specific NSAID

A

Vioxx (taken off market)

58
Q

Dr. Blom’s favorite anti-inflammatory drug

59
Q

Acetomenophen (tylenol) is NOT an anti-inflammatory and thus does NOT block (blank) formation.

A

prostaglandin

60
Q

Cyclooxygenase 1 produces (blank) in the stomach that decrease acid secretion.
Cyclooxygenase 2 causes most of the (blank) responses

A

eicosanoids; inflammation

61
Q

COX-2 inhibitor. Designed not to inhibit COX-1

and therefore have less stomach ulcer side effects

62
Q

A powerful anti-inflammatory agent that does

not inhibit COX. It represses (at the DNA to RNA level) the synthesis of phospholipase A2

63
Q

TAGs can be synthesized from (blank)

A

phosphatidic acid

64
Q

Intermediates in TAG synthesis

A 
G3P
Lysophosphatidic acid
Phosphatidic acid
DAG
TAG
65
Q

How many ATP do you get per NADH?

How many ATP do you get per FADH2?

66
Q

How many ATP do you generate per 18 C fatty acid going to 9 Acetyl-CoA?

67
Q

Outside of the mitochondria, what pathway would HMG-CoA go down? What if it is IN the mitochondria?

A

isoprenoid pathway (HMG-CoA to mevalonate via HMG-CoA reductase); ketone bodies via HMG-CoA lyase!

68
Q

3 domains of fatty acid synthetase

A
  1. acyl and malonyl binding and condensation
  2. reduction of domain 1 intermediate
  3. liberation of palmitate product
69
Q

Essential fatty acids

A

18: 2 n-6
18: 3 n-3

70
Q

When naming fatty acids, such as 18:2 n-6, what does the 2 indicate? What does the “n-6” indicate?

A

There are two double bonds; beginning 6 C from the METHYL end

71
Q

T/F: Fatty acids can be DESATURATED and ELONGATED. What does this mean? Where do the extra carbons come from?! What are the enzymes involved?

A

Add C=C double bonds and add Carbons from malonyl-CoA

desaturase and elongase

72
Q

What kinds of things can prostaglandins go on to make?!

A

thromboxanes
leukotrienes
lipoxins

Block 3 Week 4 Meg (6 decks)

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