Midterm 1 - Lecture 6, 7 Flashcards
(39 cards)
What does the omega end of a FA look like?
CH3
What does the alpha end of a FA look like?
CH2-COOH
Structural difference between SFA and Monounsaturated FA?
1 C=C somewhere in the monounsaturated FA
Structural difference between Polyunsaturated and Monounsaturated FA?
Poly has more than 1 C=C and must be separated by 1 -C-
Nomenclature of FAs
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
Degradation of FAs via Beta-oxidation
Fatty acyl CoA transporter (requires carnitine) brings FAs into Mitochondria for breakdown into Ac-CoA->TCA cycle; Also requires FAD+ and NAD+
FA synthesis
- 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
What is the limitation of human desaturases?
Work only up to α-9; cannot create ω-3 or ω-6 FAs from Palmitic acid (Therefore they are essential FAs)
Synthesis of Long Chain PUFA for Omega-6 FA metabolism
Linoleic (ω-6) (18:2) -> Gamma linolenic acid (18:3) -> Arachidonic acid (20:4)
Synthesis of Long Chain PUFA for Omega-3 FA metabolism
Alpha-linolenic acid (ω-3) (18:3) -> EPA eicosapentaenoic acid (20:5) -> DHA
Eicosanoids from ω-6 vs. ω-3 FAs
Arachidonic -> Pro-inflammatory eicosanoids; Increase blood clotting
EPA -> anti-inflammatory eicosanoids; Decrease blood clotting; reduce heart attack risk
Fxns of Eicosanoids
Signaling molecules involved in inflammation & pain
prostaglandins) and blood clotting (thromboxane
How does aspirin affect blood clotting?
Aspirin inhibits COX-1, which ultimately inhibits vasoconstriction and inhibits increase in platelet aggregation
Fxns and characteristics of DHA
- 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)
Lipid digestion
- 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
Fxn of Lecithin and bile acids
emulsify fats
Characteristics of Lecithin
A phospholipid; 1 glycerol branched with 2 FAs, 1 phosphate choline
Fxns of cholesterol
• 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
How does too much dietary cholesterol (e.g. >1 egg) affect a healthy person’s risk of CHD?
little change in CHD risk
How does too much dietary cholesterol (e.g. >1 egg) affect a diabetic’s or obese’s risk of CHD?
great harm to arteries and thus noticeable change in CHD risk; but in general, Sat or Trans fat play larger roles in risk
Fxn of Chylomicrons
Chylomicrons transport dietary lipids & cholesterol from
SI -> liver and tissues
What is a remnant and where is it processed?
FA-depleted chylomicron, processed in liver.
VLDL - Very low-density lipoprotein
-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.
LDL - Low-density lipoprotein
Biggest component is cholesterol
