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
how is the D4 double bond in DHA formed?
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
what will inhibit desaturation of a-linolenic acid?
excess linolenic acid
27
what is the benefit of eicosapentanoic acid > arachidonic acid?
w3>w6 = more protection against atherosclerosis
28
how are PUFA oxidized?
b-oxidation in the mitochondria
29
what is special about PUFA b-oxidation?
requires additional enzymes and NADPH odd number C=C use isomerase even number C=C use reductase and isomerase
30
what is the significance of the "added steps" in PUFA b-oxidation?
additional steps lead to chain shortening without synthesis of FADH2 or NADH, meaning that the amount of ATP obtained will be slightly decreased
31
which PUFA will generate the lowest # ATP from b-oxidation
increased double bonds = lesser ATP
32
how do PUFA decrease inflammation? specifically EPA (3)
PMNs- dec NFkB and dec PMN infiltration Monocytes- increased MAPK dendritic cells- dec migration and IL-12 prod
33
what happens if too much PUFA are consumed?
too much = added calories = stored in adipocytes and used later for b-oxidation; vulnerable to oxidation and ROS production = increased CA
34
2 servings of fish rich in DHA and EPA will decrease:
- risk of sudden cardiac death | - risk of death from coronary artery disease
35
when could serum PUFA deficiency occur?
on TPN that contains no lipids
36
what is diagnostic for PUFA def?
increase in ratio of eicosatrienoic acid (20:3w9) to arachidonic acid (20:4w6)
37
why does (20:3w9) increase in PUFA def?
oleate is converted to eicosatrienoic acid (20:3w9)
38
what could be caused by switching TPN lipid from soybean to safflower oil?
w3 deficiency
39
what are some sx of w3 deficiency?
paresthesias, blurred vision
40
what are the benefits of w6 oils?(4)
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
what are the benefits of w3 oils? (2)
w3= a-linolenic acid - DHA = normal brain development, retinal fxn - EPA/DHA= dec risk of sudden cardiac death, dec high triglyceride levels