Lipid Digestion and absorption Flashcards

1
Q

Lipids

A

-heterogeneous
-relative insolubility in water
-soluble in nonaqueous (nonpolar) solvents such as chloroform, alcohols

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2
Q

Function of lipids

A

-high energy value, low heat increment (don’t generate much heat during digestion and therefore would be better to feed carbohydrates when heat stress present)
-thermal insulation
-essential fatty acids (EFA)
-storage and transport of fat-soluble vitamins
-transmembrane signaling and cell regulation

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3
Q

Main form of lipids

A

-triacylglycerols

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4
Q

What are lipids derived from?

A

-diet
-lipids secreted into the intestinal lumen as part of bile
-lipids in sloughed off epithelial cells

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5
Q

Lipids available for digestion

A

-more than 90% triacylglycerols (TAG, tryglycerides)
-Also FFA, cholesterol/cholesterol esters, phospholipids (from meat based diets membrane layers), sphingolipids (nervous tissue), glactolipids, fat soluble vitamins (A, D, E, K carotenoids)

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6
Q

Triglycerols

A

-composed of glycerol and 3 fatty acids

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7
Q

How do triacylglycerols affect digestibility?

A

-saturation of the fatty acid and position of glycerol
Ex.~80% of C16:0 and C18:0 of beef fat are located on the sn-1 and sn-3 positions but it would be better absorbed in the sn-2

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8
Q

Fatty acids

A

-carboxylic acids with long hydrocarbon side chain (even number; 12-20 carbons)

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9
Q

How do fatty acids differ?

A

-differ depending on:
>length of hydrocarbon side chain
>degree of unsaturation
>position and orientation of the double bonds

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10
Q

Fatty acid nomenclature

A

-1. Delta nomenclature= C-1 is carboxyl
-2. also use alpha, beta, gamma
- 3. w (omega) nomenclature= carbon furthest from carboxyl C

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11
Q

Omega 6

A

-can’t synthesize passed 6 carbon so anything with a bond at the 6th carbon will always be derived from omega 6
-more pro-inflammatory

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12
Q

Omega 3

A

-anything with a double bond at carbon 3
-more anti-inflammatory

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13
Q

Trans vs. cis

A

-referring to unsaturated (bonds); position of hydrogens around the double bonds
-trans are not well digested in our body; cis is more easily digested
>double bonds in diets= cis

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14
Q

Methylene interrupted

A

-2 carbon interruptions between each double bonds

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15
Q

Conjugated

A

-when double bonds are not separated by single carbons

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16
Q

Palmitic acid

A

C16:0

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17
Q

Linoleic acid

A

C18:2 cis-9,12
-18 carbons
-2 double bonds (at C9 and C12)
-omega 6 FA

18
Q

Conjugated linoleic acid

A

-linked with possible weight loss due to increased lipid digestion
-also could be linked with insulin resistance

19
Q

Mammals introduction of double bonds

A

-different enzymes used to introduce double bonds
-double bonds can be placed at delta 4, 5, 6, 9, positions but not possible to go past delta 9

20
Q

Linoleic FA

A

-omega 6
-C 18:2 (cis 9,12)

21
Q

Linolenic FA

A

-omega 3
-C18:3 (cis 9, 12, 15)

22
Q

Linoleic (omega 6) and Linolenic (omega 3) essential FAs

A

-because their double bonds are positioned past delta 9 so we cannot create them ourselves
-these are precursors for C20 fatty acids (eicosanoids)= eicosapentaenoic acid (EPA), docosahexaenoic acid (DHA), arachidonic acid (AA)

23
Q

Elongation and desaturation

A

-required for the synthesis of long chain polyunsaturated fatty acids from essential fatty acids linoleate (C18:2n-6) and linolenic (C18:3n-3)

24
Q

Non-essential long-chain unsaturated fatty acids

A

-ability to be made because mammalian tissues have a delta 9 desaturase
-ex. Palmitoleic acid (C16) & oleic (C18)

25
Q

Essential fatty acids

A

1.Linoleic acid (omega 6)
2.Linolenic acid (omega 3)

26
Q

Arachidonic acid

A

-C20
-formed from linoleic acid

27
Q

Why can cats not form Arachidonic acid?

A

-because they lack a delta 6 double bond

28
Q

Eicosanoids

A

-bioactive derivatives for the 20-carbon fatty acids (Arachnidonic (20:4n-6), eicosapentaenoic (EPA 20:5n-3) and dihomo-gamma-linolenic (DGLA 20:3n-6)

29
Q

Eicosanoids importance

A

-they are signalling molecules comparable to cytokines
-play a role in initiation and resolution of immune responses to infection and injury
-also involved in inflammation and homeostasis
>vasodilation and vasoconstriction, up and down regulation of inflammatory cytokines (pain, fever)

30
Q

Groups of Eicosanoids

A

1.thromboxanes
2. prostacyclins
3. leukotrienes
4.lipoxins

31
Q

Thromboxanes (TXA)

A

-synthesized in platelets
-cause vasoconstriction and platelet aggregation

32
Q

Inhibition of thromboxanes

A

-thromboxane synthesis is inhibited by aspirin

33
Q

Prostacyclins (PGI)

A

-potent inhibitors of platelet aggregation

34
Q

PGI3, PGI2, TXA3, TXA2

A

-PGI2 and PGI3 are both anti-aggregators
-TXA3 is a weaker aggregator than TXA2 resulting in longer clotting time

35
Q

Where can arachidonic come from?

A

-diet
-membrane phospholipids via phospholipase A2

36
Q

Aspirin

A

-inhibits cyclooxygenase which catalyzes the first step in the synthesis of eicosanoids from amino acids

37
Q

Cox 1

A

-a constitutive enzyme that generates the signal ligand for homeostatic intercellular signaling

38
Q

Cox 2

A

-an inducible enzyme with increased activity accompanying acute and chronic inflammatory conditions

39
Q

Cox 3

A

-uniquely involved in hyperesthesia (increased pain perception) and fever (splice variant of Cox 1)
**still need research

40
Q

NSAIDS

A

-development of specific NSAIDS are undertaken to reduce the side effects (GI bleeding, kidney necrosis)
-Targets cox-2 (inducible enzyme with increased activity/inflammatory conditions) which means targeting inflammation