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biochem block 3 > polyunsaturated FA > Flashcards

polyunsaturated FA Flashcards

1
Q

two essential C18 PUFA

A 
linolenic acid (18:2w6)- double bonds at 9, 12
a-linolenic acid (18:3w3)- double bonds at 9,12,15
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2
Q

why are these FA “essential”?

A

cannot be synthesized and must be obtained in the diet

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3
Q

essential C18 PUFA can be elongated in the body to form-

A 
arachidonic acid (20:4w6)
docosahexanoic acid "DHA" (22:6w3)
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4
Q

what is true of the location of double bonds in PUFA?

A

never conjugated, always separated by CH2

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5
Q

which PUFA is “omega-3”?

A

a-linolenic acid (18:3w3)

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6
Q

what are dietary sources of a-linolenic w3?

A

soybean and canola oils

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7
Q

what w3 are in fish oil?

A

eicosapentaenotae (20:5w3)

DHA (22:6w3)

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8
Q

what is the importance of PUFA for the fetus in utero?

A

PUFA are obtained from the motor, 80% of DHA in the fetal brain will accumulate between 26-40 weeks

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9
Q

PUFAs in breast milk

A

breast milk usually contains w3 and w6; w3 content will be lower if mother’s diet not rich in w3

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10
Q

how are trans fats forms? (2)

A
  • by partial hydrogenation of polyunsaturated vegetable oils in food processing
  • by microbial metabolism in ruminants, meaning dairy and meats have trans fats
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11
Q

why are trans fats bad?

A

more atherogenic, increase cholesterol and cause leakiness of the plasma membrane that could lead to the development of cancer

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12
Q

what are the “protective fats”?

A

monounsaturated- olive oil

polyunsaturated fats

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13
Q

what is the source of most trans fats in the diet?

A

high carbohydrate/processed foods

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14
Q

elongation product of palmitate

A

stearate (18:0)

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15
Q

desaturation product of stearate

A

oleate (18:1 cis D9)

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16
Q

shortening product of palmitate

A

myrisate (14:0)

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17
Q

which FA are typically not elongated in the body?

A

medium chain FA favor oxidation, usually not elongated

18
Q

3 similarities between FA synthesis and elongation

A

1-malonyl-CoA is the 2C donor
2- uses acetyl-CoA carboxylase
3- uses NADPH for reducing equivalents

19
Q

2 differences between FA synthesis and elongation

A

1- microsomal (not cytosolic)

2- substrate is acyl-CoA (not acyl-ACP)

20
Q

what is the preferred substrate for FA desaturation?

A

stearoyl-CoA –> oleoyl-CoA

21
Q

2 H2O are formed during desaturation, what is the source of electrons?

A

2 from stearate

2 from NADH

22
Q

linolenic acid can be converted to -

A

linolenic (18:2w6) to arachidonic acid (20:4w6)

23
Q

what 2 changes are made to linolenic acid to yield arachidonic acid?

A
  • 2 desaturation steps (D5 and D6 desaturases)

- elongation via addition of one malonyl-CoA to carbonyl end

24
Q

a-linolenic acid can be converted to-

A 
eicosapentaonoic acid (20:5w3) and
DHA (22:6w3)
25
Q

how is the D4 double bond in DHA formed?

A

through an indirect pathway since there is no D4 desaturase; D6 and D5 desaturases work first, then there is an elongation step, followed by the action of D6 desaturase again

26
Q

what will inhibit desaturation of a-linolenic acid?

A

excess linolenic acid

27
Q

what is the benefit of eicosapentanoic acid > arachidonic acid?

A

w3>w6 = more protection against atherosclerosis

28
Q

how are PUFA oxidized?

A

b-oxidation in the mitochondria

29
Q

what is special about PUFA b-oxidation?

A

requires additional enzymes and NADPH
odd number C=C use isomerase
even number C=C use reductase and isomerase

30
Q

what is the significance of the “added steps” in PUFA b-oxidation?

A

additional steps lead to chain shortening without synthesis of FADH2 or NADH, meaning that the amount of ATP obtained will be slightly decreased

31
Q

which PUFA will generate the lowest # ATP from b-oxidation

A

increased double bonds = lesser ATP

32
Q

how do PUFA decrease inflammation? specifically EPA (3)

A

PMNs- dec NFkB and dec PMN infiltration
Monocytes- increased MAPK
dendritic cells- dec migration and IL-12 prod

33
Q

what happens if too much PUFA are consumed?

A

too much = added calories = stored in adipocytes and used later for b-oxidation; vulnerable to oxidation and ROS production = increased CA

34
Q

2 servings of fish rich in DHA and EPA will decrease:

A
  • risk of sudden cardiac death

- risk of death from coronary artery disease

35
Q

when could serum PUFA deficiency occur?

A

on TPN that contains no lipids

36
Q

what is diagnostic for PUFA def?

A

increase in ratio of eicosatrienoic acid (20:3w9) to arachidonic acid (20:4w6)

37
Q

why does (20:3w9) increase in PUFA def?

A

oleate is converted to eicosatrienoic acid (20:3w9)

38
Q

what could be caused by switching TPN lipid from soybean to safflower oil?

A

w3 deficiency

39
Q

what are some sx of w3 deficiency?

A

paresthesias, blurred vision

40
Q

what are the benefits of w6 oils?(4)

A

w6 = linolenic

  • cell membrane fluidity and function
  • prevent excess water loss from skin
  • used to make arachidonic acid that then is used to make LT and prostaglandins
  • longer chain w6 are used in brain and testes
41
Q

what are the benefits of w3 oils? (2)

A

w3= a-linolenic acid

  • DHA = normal brain development, retinal fxn
  • EPA/DHA= dec risk of sudden cardiac death, dec high triglyceride levels

biochem block 3 (7 decks)

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