Midterm 1 - Lecture 6, 7 Flashcards

1
Q

What does the omega end of a FA look like?

A

CH3

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2
Q

What does the alpha end of a FA look like?

A

CH2-COOH

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3
Q

Structural difference between SFA and Monounsaturated FA?

A

1 C=C somewhere in the monounsaturated FA

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4
Q

Structural difference between Polyunsaturated and Monounsaturated FA?

A

Poly has more than 1 C=C and must be separated by 1 -C-

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5
Q

Nomenclature of FAs

A

C16:0 refers to 16 carbons, 0 C=C
C18:1 ω-9 refers to 18 carbons, 1 C=C 9 carbons away from omega end

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6
Q

Degradation of FAs via Beta-oxidation

A

Fatty acyl CoA transporter (requires carnitine) brings FAs into Mitochondria for breakdown into Ac-CoA->TCA cycle; Also requires FAD+ and NAD+

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7
Q

FA synthesis

A
  • occurs in cytosol; adds 2 carbons using Malonyl-CoA
  • Involves acyl-carrier protein (ACP), NADPH, enzymes ACC & FAS;
  • Initial product: palmitate (C16:0)
  • Further products made by elongases & desaturases
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8
Q

What is the limitation of human desaturases?

A

Work only up to α-9; cannot create ω-3 or ω-6 FAs from Palmitic acid (Therefore they are essential FAs)

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9
Q

Synthesis of Long Chain PUFA for Omega-6 FA metabolism

A

Linoleic (ω-6) (18:2) -> Gamma linolenic acid (18:3) -> Arachidonic acid (20:4)

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10
Q

Synthesis of Long Chain PUFA for Omega-3 FA metabolism

A

Alpha-linolenic acid (ω-3) (18:3) -> EPA eicosapentaenoic acid (20:5) -> DHA

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11
Q

Eicosanoids from ω-6 vs. ω-3 FAs

A

Arachidonic -> Pro-inflammatory eicosanoids; Increase blood clotting
EPA -> anti-inflammatory eicosanoids; Decrease blood clotting; reduce heart attack risk

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12
Q

Fxns of Eicosanoids

A

Signaling molecules involved in inflammation & pain

prostaglandins) and blood clotting (thromboxane

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13
Q

How does aspirin affect blood clotting?

A

Aspirin inhibits COX-1, which ultimately inhibits vasoconstriction and inhibits increase in platelet aggregation

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14
Q

Fxns and characteristics of DHA

A
  • Important for brain, eye and heart function.
  • Protect cells in heart and lower lethal arrhythmia.
  • Decreases risk of dementia
  • slows loss of mental function
  • affects volume of the brain (the lower DHA levels in blood, the smaller & more impaired the brain)
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15
Q

Lipid digestion

A
  • They are water insoluble, and thus difficult to hydrolyze
  • Great energy source
  • Small intestine: major site for lipid digestion and FA absorption
  • Lipids in SI -> cholecystokinin (CCK) -> release of bile acids and lecithin from gallbladder and lipases from pancreas -> fat absorbed transferred to lymph
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16
Q

Fxn of Lecithin and bile acids

A

emulsify fats

17
Q

Characteristics of Lecithin

A

A phospholipid; 1 glycerol branched with 2 FAs, 1 phosphate choline

18
Q

Fxns of cholesterol

A

• Essential component of cell membranes
• Produced by the liver (20%) & rest of body (80%)
• Found only in animal products
• Precursor to estrogen, testosterone and vitamin D
• Precursor to bile acids
*NOT ESSENTIAL

19
Q

How does too much dietary cholesterol (e.g. >1 egg) affect a healthy person’s risk of CHD?

A

little change in CHD risk

20
Q

How does too much dietary cholesterol (e.g. >1 egg) affect a diabetic’s or obese’s risk of CHD?

A

great harm to arteries and thus noticeable change in CHD risk; but in general, Sat or Trans fat play larger roles in risk

21
Q

Fxn of Chylomicrons

A

Chylomicrons transport dietary lipids & cholesterol from

SI -> liver and tissues

22
Q

What is a remnant and where is it processed?

A

FA-depleted chylomicron, processed in liver.

23
Q

VLDL - Very low-density lipoprotein

A

-made by liver, rich in lipids, main supplier of liver FA to
tissues where lipoprotein lipase removes lipids.
-As lipids are removed, density increases -> LDL and VLDL remnant.

24
Q

LDL - Low-density lipoprotein

A

Biggest component is cholesterol

25
Q

In healthy people, LDL is removed by:

A

the liver via LDL receptors

26
Q

In diseased people, LDL is removed by:

A

White blood scavenger cells, which can form plaques in arteries
-May be from too much animal or trans fats, or disease

27
Q

HDL - High-density lipoprotein

A

Scavenge cholesterol -> return to liver

28
Q

Atherosclerosis (plaque in artery) risks

A

Risk increased by smoking, diabetes, hypertension, inflammation, obesity, diets high in animal fat.

29
Q

How does higher Total Cholesterol related to CHD risk?

A

Increased risk of CHD

30
Q

2 types of medications for reducing CVD risk

A

Statins

Baby aspirin

31
Q

Effects of statins

A

-inhibitor of cholesterol synthesis
-lowers LDL levels & reduces inflammation.
-Side effects: can damage mitochondrial function & ->
muscle pain & damage, memory loss, diabetes

32
Q

Effects of baby aspirin

A

-reduces inflammation.
-Side effects: damages GI track (~10% of chronic users
get ulcers)

33
Q

Define Lipolysis

A

Mobilization of stored fats in adipose tissue; rate depends on presence of hormones and cytokines

34
Q

Anabolism of stored FA via Feeding

A

Feeding -> Insulin -> inhibits HSL (a lipase) ->Fewer free FAs released from adipose tissue -> Fewer free FAs used for energy

35
Q

Catabolism of stored FA between meals

A

Between meals -> Glucagon -> activates HSL -> more free FAs released from adipose tissue -> More free FAs used for energy

36
Q

Android fat in men

A

in upper body, promoted by testosterone and alcohol
and more mobile (easily shed), but includes visceral (deeper, around organs in abdomen) fat which has more disease associations (Diabetes T2, CVD, hypertension)

37
Q

Fat in women

A

more lower body fat, promoted by estrogen/progesterone and less mobile

38
Q

Types of body fat

A
  • subcutaneous, for insulation

- visceral

39
Q

Why is Partial hydrogenation harmful?

A

FAs become trans FAs, which greatly increase risk of CVD