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Drew 922 > Block 3 Lecture 2 -- Dietary Lipids > Flashcards

Block 3 Lecture 2 -- Dietary Lipids Flashcards

1
Q

How long are FAs/TGs?

A

3-20 C, usually 17 or 15

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2
Q

What is the most common saturated fatty acid?

A

stearic acid

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3
Q

What is the structure of stearic acid?

A

18:0

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4
Q

What are examples of unsaturated FAs?

A

1) oleic

2) linoleic

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5
Q

Oleic acid structure

A

18:1 ∆9

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6
Q

Linoleic acid structure

A

18:2 ∆9,12

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7
Q

What is the natural configuration for glycerophospholipids and sphingolipids?

A

(R)-L

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8
Q

Where is lecithin found?

A

naturally in egg yolk & soybean

also as food additive or dietary supplement

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9
Q

How is lecithin metabolized in the body?

A

lecithin –> GPC –> acetylcholine

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10
Q

What does GPC stand for and where can it be found?

A

glycerophosphorylcholine, milk

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11
Q

Why are sphingolipids more stable than glycerophospholipids?

A

presence of amide bonds

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12
Q

From what are eicosanoids produced?

A

multi-unsaturated C20 arachidonic acid

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13
Q

What is the structure of arachidonic acid?

A

20:4 ∆5,8,11,14

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14
Q

What enzyme converts arachidonic acid to PGs and TXs?

A

PGH2/COX

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15
Q

What structures does arachidonic acid produce?

A

PGs and thromboxanes

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16
Q

What are the functions of eicosanoids?

A

1) BP
2) smooth muscle contractoin
3) pain, fever
4) coag
5) reproduction
6) coagulation
7) bronchoconstriction
8) metabolism regulation

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17
Q

How is naproxen supplied?

A

(s) only

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18
Q

How is ibuprofen supplied?

A

racemic (converted to S in vivo)

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19
Q

What is the backbone for cholesterol?

A

tetracyclic C17 alkane

    • 3 6-membered rings
    • 1 5-membered ring
    • B/C and C/D are always transfused
    • methyls at A/B and C/D fusion points
    • R’s at C12 and end of side chain
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20
Q

For which structures do steroids serve as precursors?

A

1) Vit D3
2) steroid hormones
3) bile acids

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21
Q

Where is cholesterol important?

A

membranes, liver, skin

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22
Q

For bile acids, what are the possibilities for the 2 side chains?

A

1) H or OH

2) OH, HNCH2COOH, or HN(CH2)2SO3H

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23
Q

Describe the structure of a liposome?

A

stable bilayered vesicle, relatively large (several 100 A)

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24
Q

What do corticoids do?

A

downregulate proinflammatory cytokines

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25
Q

What enzyme do the sex hormones need?

A

aromatase for aromatization of the A ring

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26
Q

What is cortisone’s side chain?

A

acetone

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27
Q

What are the side chains for the androgens?

A

trans hydroxyl

28
Q

What are the side chains of the fat-soluble vitamins?

A

all iso-prenoid derivatives

29
Q

Where are TGs mainly digested?

A

in intestine by pancreatic lipase

30
Q

What are the products of TG digestion?

A

2 FA + MAG

31
Q

Describe the action of pancreatic lipase

A

operates at ph 6; hydrolyzes 1,3 FAs

32
Q

Describe the function of colipase.

A

makes PL more active (binds fat and another lipase)

33
Q

Describe the action of phospholipase

A

digests phospholipids

34
Q

Where are shorter FAs digested?

A

hydrolyzed by mouth/stomach lipases

35
Q

Where are bile acids re-absorbed?

36
Q

Describe the structure of a micelle

A

small (10 - 100 A) lipid monolayer complexes

37
Q

When are bile acids not required?

A

for small FAs (4-12 C MCTs)

38
Q

How are TGs absorbed?

A

as 2 FA + 2-MAGs packaged into micelles with other lipids

39
Q

What happens in TG absorption after micelle absorption?

A

epithelial cells resynthesize TGs in SER

40
Q

what is the major apo-protein of chylomicrons?

41
Q

What is the major apoprotein of VLDL?

42
Q

Where are apoproteins synthesized?

A

RER of hepatocytes

43
Q

How are lipids packaged for blood transport?

A

into lipoproteins

44
Q

Describe structure of lipoproteins.

A

aphipathic phospholipids on surface

cholesterol, ADEK in lumen

45
Q

Where are lipoproteins assembled?

46
Q

Why are ADEK not found in VLDL?

A

VLDL not from diet

47
Q

How are lipoproteins secreted?

A

into lymph via exocytosis

48
Q

What proteins are present in HDL that are transferred for development of mature chylomicrons?

A

ApoE and ApoCII

49
Q

What is the function of ApoE?

A

allows rEcognition by tissue membrane receptors

50
Q

What is the function of ApoCII

A

aCtivates LPL attached to glycoproteins of capillary epithelium

51
Q

What does LPL do?

A

digests TGs to FAs and glycerol

52
Q

What do the TGs resulting form LPL do?

A

1) taken up by adipose for storage

2) minorly taken up by muscle for beta-oxidation

53
Q

What happens to glycerol resulting from LPL?

A

to liver for recycling or gluconeogenesis

54
Q

What happens to the chylomicron remnans from LPL?

A

recycle by liver

1) liver receptors recognize apoE
2) endocytosis then phagolysosome

55
Q

What happens to VLDL

A

converted –> IDL –> LDL

56
Q

What happens to LDL

A

cellular LDL receptors recognize apoB100 and trigger clarithin coated endocytosis

57
Q

What is the function of adipose lipase?

A

releases FAs from adipose during fasting

58
Q

How are FAs transported in the blood when released from adipose?

A

complex with albumin

59
Q

What is Km?

A

the michaelis constant; the substrate concentration at which the reaction rate is 1/2 Vmax (inverse measure of affinity)

60
Q

How do Adipose LPL and Muscle LPL compare?

A

adipose LPL has higher Km

61
Q

When is ALPL hydrolysis preferable to MLPL?

A

only in fed state with high [CM]

62
Q

What factors activate AL?

A

glucagon, epinephrine, norepi, corticoadrenals

63
Q

What factors inhibit AL?

64
Q

What is the cause of abetalipoproteinemia?

A

genetic disorder in which b-apoproteins are not produced sufficiently

65
Q

What are the consequences of abetalipoproteinemia?

A
    • can’t form VLDL or CM
    • TGs accumulate in intestine and liver
    • can’t burn dietary fat
    • SCFAs can be burned
    • fat-soluble things are not available
66
Q

What is the cause of CF?

A

mucous secretions block the pancreatic duct and prevent excretion of exocrine enzymes

67
Q

What are symptoms of CF?

A

steatorrhea, ADEK deficiency, eicosanoid deficiency

Drew 922 (12 decks)

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