Block 3 PUFAs

Question 1

What is the formula for oleic acid, linoleate?

Answer 1

Oleic: c9-18:1 (18:1 d9)
Linoleate: c9,c12-18:2 (18:2 d9,12)

Question 2

What are formulas for arachindonic acid and DHA? What are they synthesized from?

Answer 2

AA: 20:4 w6, by elongation and desat of linoleate (18:2 w6)
DHA: 22:6 w3, by elong, desat of a-linolenate (18:3 w3)

Question 3

What is the makeup of lard?

Answer 3

40% sat fat, 45% oleic acid, 9% linoleic acid (w6)

Question 4

What are dietary sources of w3 FAs?

Answer 4

Soybean, canola oils (a-linolenate), cold water marine fish (DHA and eicosapentaenoate 20:5 w3)
NOT corn, safflower oils

Question 5

Why are PUFAs important in infant formulas?

Answer 5

80% fetal brain 22:6 w3 acc b/w weeks 26-40; w3, w6, C20-22 polyenes, C18s in human milk

Question 6

What are trans FAs?

Answer 6

Partial hydrogenation PU veg oils, microbial metabolism in ruminants, and dairy products/meat; makes more solid, atherogenic and ^ plasma chol (MU and PU oils protective)

Question 7

How are w3 and w6 obtained?

Answer 7

Linoleic and a-linolenic essential; longer chain synth by desat, elong these 2

Question 8

How do FA elongation and synth differ?

Answer 8

Microsomal vs. cytosolic, substrate acylCoA vs. acylACP

Question 9

What is d9 desaturase?

Answer 9

AKA stearoyl-CoA DS; stearate -> oleic acid (c9-C18) & palmitate -> palmitoleate (c9-C16). *Stearoyl-CoA preferred substrate; adds cis C9=10; on ER, uses O2 and removes 2 e- from both stearate & NADH

Question 10

How is dietary linoleic acid converted to AA?

Answer 10

2 desats with d5 desat, elong with malCoA, d6 desat (all substrates acylCoAs)

Question 11

What are the formulas for EPA and DHA? How are these created?

Answer 11

From a-linolenic acid (ALA, 18:3 d9,12,15) -> desat, elong, desat -> EPA (20:5 d5,8,11,14,17) —> DHA (22:6 d4,7,10,13,16,19)

Question 12

Why are excess w3 or w6 FAs bad? Which is better?

Answer 12

Excess 18:2 w6 inhibits desat of 18:3 w3; replacing w6 with w3 alters eicosanoid synth and protects from athero

Question 13

What are the products of B-ox? How might any PUFA be oxidized?

Answer 13

AcCoA, reducing eqs; additional enzymes and NADPH to rearrange double bonds

Question 14

How are odd or even-numbered double bonds handled differently? Why is this important?

Answer 14

Odd: isomerase
Even: reductase & isomerase
Chain shortening w/o synthesis of FAD/NADH so each double bond = less ATP from B-ox

Question 15

What fats decrease risk of heart disease?

Answer 15

Sat FA ^ plasma chol, CHD mortality, trans also ^ plasma LDL = atherogenic
MU and PU oils protective

Question 16

How does AA cause inflammation? How does EPA resolve inflammation?

Answer 16

AA -> LTB4 -> BLT1 activates PMN
EPA -> RvE1 –| BLT1 on PMN to inhibit NFkB activation and IMN infiltration; RvE1 act ChemR23 on mono (increase MAPK act) and DC (decrease IL-12 production and migration)

Question 17

What is classic PUFA deficiency?

Answer 17

Lack of dietary linoleic acid bc of fat-free TPN -> dermatitis, flaky skin. Tx: parenteral lipid emulsions

Question 18

What is EFAD?

Answer 18

Normally linoleate w6 is major PUFA desat/elong substrate; oleate -> 20:3 w9; dx by increased 20:3 w9 to 20:4 w6 ratio

Question 19

What is w3 PUFAD?

Answer 19

ALA def worse bc ^ linoleum acid intake; distal numbness, paresthesia, vision blurring

Question 20

What are w6 FAs/linoleic acid essential for?

Answer 20

Maintaining membrane fluidity and fxn; AA precursor to PGs and LKTs; 22:4/5 w6 required for brain/testes
Def: fragile RBCs and dehydration through skin

Question 21

What are w3 FAs for?

Answer 21

DHA (22:6 w3) for brain dev, retinal fxn; lower req than w6; fish oils (20:5 w3, 22:6 w3) v risk CAD, plasma TG in hyperTG patients

Question 22

What happens when there is an excess of PUFA?

Answer 22

Add calories to diet, stored in adipocytes or B-oxed; vulnerable to ox, ROS production -> may increase cancer risk