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

Blomquist: Lipid lecture Flashcards

(72 cards)

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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
Oxidation of UNSATURATED fatty acids does not generate as much ATP as saturated fatty acids with the same number of carbons. How so?
For every double bond, 1 less FADH2 generated
26
Oxidation of even number poly-unsaturated fatty acids requires a (blank) step after the isomerase step.
REDUCTASE
27
occurs when the amount of acetyl-CoA produced is excessive compared to the amount of oxaloacetate available to react with it
Formation of ketone bodies
28
Conditions when ketone bodies are formed
Intake high in lipids and low in carbs Diabetes not well controlled Starvation
29
Three ketone bodies
acetone beta-hydroxybutyrate acetoacetate
30
Ketone bodies are formed primarily in (blank) and can be used as fuel in most tissues and organs
liver mitochondria
31
Ketone body formation occurs during (blank), during high (blank) diets, and uncontrolled (blank). It occurs in the (blank)
starvation; fat; diabetes; mitochondrial matrix
32
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)
acetoacetate; beta-hydroxybutyrate and acetate
33
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
acetyl-CoA
34
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)
glucose
35
About how many ATP are generated for each B-hydroxybutyrate broken down?
26ATP
36
During prolonged starvation (at about 4 days), the body prefers (blank) as fuel over glucose
ketone bodies
37
When the brain or body runs out of glucose, it starts to use (blank) for energy
lipids (ketone bodies)
38
Where does biosynthesis of fatty acids occur?
In the cytosol primarily of the liver
39
How is acetyl-CoA transferred to the cytosol for fatty acid biosynthesis? What two things provide the NADPH needed for fatty acid biosynthesis?
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
What is the controlled step in FA biosynthesis? What enzyme catalyzes this reaction?
conversion of Acetyl-CoA to malonyl-CoA; acetyl-CoA carboxylase (transfers a carboxyl group onto acetyl-CoA)
41
Acetyl-CoA carboxylase (contolled step in FA biosynth) is activated by (blank) and inactivated by (blank)
citrate; acyl-CoA
42
Overall reaction of fatty acid synthesis
Acetyl-CoA + 7 malonyl-CoA + 14NADPH-->Palmitic acid (C16:0) + 14NADP+ + 7CO2 + 7CoASH
43
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
thioesterase 2
44
Fatty acid synthetase is has how many catalytic sites? It acts as a (blank) and is very multifunctional.
7; DIMER
45
Where does fatty acid biosynthesis occur in the cell? Where does beta-oxidation occur?
cytosol; mitochondria
46
What is the acyl-carrier in fatty acid biosynthesis? How about in B-oxidation?
acyl carrier protein; coenzyme A
47
What is the redox coenzyme necessary for fatty acid biosynthesis? What about for B-oxidation?
NADPH; FAD when saturated chain (c-C) | NAD+ when hydroxy acid (C-O)
48
Two essential fatty acids. Which one is recommended in the diet? Which one is not?
``` Linoleic acid (n-6) --> not recommended Linolenic acid (n-3) --> recommended ```
49
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
delta-9 double bond
50
Plants CAN desaturate from the (blank) towards the methyl end of the fatty acid
delta-9 double bond
51
Linoleic acid can be converted to (blank) via elongation and desaturation reactions.
arachidonyl-CoA
52
How many carbons are added to linoleic acid when it's elongated? What does it mean that is it "desaturated"?
2 C (from C18 to C20); addition of 2 double bonds
53
``` Inflammation Intensity and duration of pain/fever Reproduction function (induction of labor) Inhibit gastric secretion Regulate BP Inhibit/activate platelet aggregation ```
Biological effects of eicosanoids
54
Clinically relevant prostaglandins (eicosanoids)
prostaglandins thromboxanes leukotrienes lipoxins
55
What step does aspirin block in the synthesis of eicosanoids?
Blocks the cyclooxygenase activity associated with prostaglandin H synthase. This is the step that takes arachidonic acid to prostaglandins
56
What is one problem with taking aspirin?
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
COX2 specific NSAID
Vioxx (taken off market)
58
Dr. Blom's favorite anti-inflammatory drug
Naproxen
59
Acetomenophen (tylenol) is NOT an anti-inflammatory and thus does NOT block (blank) formation.
prostaglandin
60
Cyclooxygenase 1 produces (blank) in the stomach that decrease acid secretion. Cyclooxygenase 2 causes most of the (blank) responses
eicosanoids; inflammation
61
COX-2 inhibitor. Designed not to inhibit COX-1 | and therefore have less stomach ulcer side effects
Celebrex
62
A powerful anti-inflammatory agent that does | not inhibit COX. It represses (at the DNA to RNA level) the synthesis of phospholipase A2
Cortisone
63
TAGs can be synthesized from (blank)
phosphatidic acid
64
Intermediates in TAG synthesis
``` G3P Lysophosphatidic acid Phosphatidic acid DAG TAG ```
65
How many ATP do you get per NADH? | How many ATP do you get per FADH2?
3; 2
66
How many ATP do you generate per 18 C fatty acid going to 9 Acetyl-CoA?
128 ATP
67
Outside of the mitochondria, what pathway would HMG-CoA go down? What if it is IN the mitochondria?
isoprenoid pathway (HMG-CoA to mevalonate via HMG-CoA reductase); ketone bodies via HMG-CoA lyase!
68
3 domains of fatty acid synthetase
1. acyl and malonyl binding and condensation 2. reduction of domain 1 intermediate 3. liberation of palmitate product
69
Essential fatty acids
18: 2 n-6 18: 3 n-3
70
When naming fatty acids, such as 18:2 n-6, what does the 2 indicate? What does the "n-6" indicate?
There are two double bonds; beginning 6 C from the METHYL end
71
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?
Add C=C double bonds and add Carbons from malonyl-CoA | desaturase and elongase
72
What kinds of things can prostaglandins go on to make?!
thromboxanes leukotrienes lipoxins

Block 3 Week 4 Meg (6 decks)

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