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MONOGASTRIC GI > 6.2a – Lipid Digestion and Absorption > Flashcards

6.2a – Lipid Digestion and Absorption Flashcards

1
Q

Lipids are heterogenous:

A

-relatively insoluble in water
-soluble in nonaqueous (nonpolar) solvents (ex. chloroform, alcohols)

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2
Q

What are the functions of lipids?

A

-high energy value
-low heat increment
-thermal insulation
-essential FA
-storage and transport of fat-soluble vitamins
-transmembrane signalling and cell regulation

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3
Q

What is the importance of lipids having a low heat increment?

A

-don’t generate lots of metabolic heat
Ex. can change their diet to more lipids during heat stress

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4
Q

What are the primary lipids available?

A

-triacylglycerols (TAG)
>acyl=long carbon chain
*90%

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5
Q

What are other lipids available?

A

-FFA
-cholesterol
-phospholipids
-galactolipids
-fat soluble vitamins

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6
Q

What are lipids derived from?

A

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

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7
Q

What affects the digestibility of TAGs?

A

-saturation of FAs
-position on the glycerol
Ex. 80% of C16:0 and C18:0 of beef fat are at sn-1 and sn-3 positions
>would be better absorbed if at the sn-2 position

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8
Q

What are FAs?

A

-carboxylic acids with a long hydrocarbon side chain
-most dietary ones have 12-20 carbons
>bovine milk fat is an exception
-even number of carbons

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9
Q

How can FAs differ?

A

How can FAs differ?
-length of hydrocarbon side chain
-degree of unsaturation
-position and orientation of double bonds

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10
Q

IUPAC nomenclature:

A

-C-1 is the carboxyl
-omega is the carbon furthest from C-1

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11
Q

Omega 3 and omega 6 are essential FAs:

A

-the double bonds will always be 3 or 6 from the omega C
>modifications occur on the other end to get different FAs

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12
Q

Unsaturated fatty acids:

A

-double bonds in diets are usually in cis (H on same side)
-trans: act more like saturated, not metabolized as well (melt at a higher T)

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13
Q

Double bonds are always:

A

-methylene interrupted=always separated by 2 carbons

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14
Q

What are fatty acids called if double bonds are not methylene interrupted?

A

-conjugated fatty acids
Ex. conjugated linoleic acid
>inhibit growth of tumor mammary cells
>may contribute to weight loss

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15
Q

Conjugated linoleic acid for companion animals?

A

-may have weight loss effects (increased fat breakdown)
-certain ones cause insulin resistance
>pre-diabetic
*more studies needed

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16
Q

What positions do most mammalian tissues introduce double bonds?

A

-4-6
-9
>usually not beyond 9
*due to desaturase enzymes
*linoleic and linolenic are considered essential

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17
Q

Linoleic and linolenic FAs and double bond positions:

A

-linoleic: C18:2 (cis 9,12)
-linolenic: C18:3 (cis 9, 12,15)
*important precursors for C20 FAs (eicosanoids)
*elongation and desaturation are important for their synthesis

18
Q

What are the 2 groups of essential fatty acids?

A

-omega-3 (alpha-linolenic acid)
-omega-6 (linoleic acid)

19
Q

What is omega-6 the precursor for?

A

-arachidonic acid
Ex. not in cats

20
Q

What is omega-3 the precursor for?

A

-eicosapentaenoic acid (EPA)
-docosahexaenoic acid (DHA)

21
Q

Cats:

A

-lack delta 6=can’t put a double bond in position 6
*need to have arachidonic acid (ex. meat products)

22
Q

What is important in the synthesis of long chain PUFAs from essential FAs linoleate and linolenic?

A

-elongation and desaturation

23
Q

Why are some long-chain unsaturated FAs (ex. palmitoleic w/delta 9) not essential?

A

-mammalian tissues have a delta 9 desaturase

24
Q

What are the 2 fatty acids that are essential for most mammals?

A

-linoleic
-alpha-linolenic
*in most mammals arachidonic acid can be formed form linoleic acid (not in cats)
>essential in cats

25
Q

Why are essential FAs important?

A

-precursor for eicosanoids
>bioactive derivatives of 20C FAs

26
Q

Eicosanoids:

A

-signalling molecules
-role in initiation and resolution of immune responses to infection and injury
>comparable to cytokines

27
Q

What are all the areas that eicosanoids are involved?

A

-vasodilation and vasoconstriction
-up or down regulation of inflammatory cytokines
-pain
-fever
*actions may vary depending on tissues

28
Q

What is the difference between eicosanoids derived from omega-6 FA vs. omega-3 FA?

A

-omega-6: inflammatory
-omega-3: less active
*if have too much omega-6 relative to omega-3=can cause inflammation
>enzymes are busy converting omega-6s and can’t ‘keep up’ on the omega-3 conversion

29
Q

Omega-6 (linoleic acid)

A

-thromboxanes
-prostacyclins

30
Q

Thromboxanes:

A

-synthesised in platelets
-cause vasoconstriction and platelet aggregation

31
Q

Prostacyclins:

A

-potential inhibitors of platelet aggregation

32
Q

Omega-3 (alpha-linolenic acid)

A

-prostanoids
-leukotrienes

33
Q

Where can arachidonic be derived from?

A

-diet
-membrane phospholipids via phospholipase A2

34
Q

Prostanoids (group 3)

A

-PGE3 and TXA3
>inhibit release of AA from phospholipids
>inhibit formation of PGD2 and TXA2 (group 2)

35
Q

PGI2 + PGI3 and TXA3 + TXA2

A

-PGI: antiaggregators of platelets
*TXA: 3 is weaker than 2: favours longer clotting times

36
Q

How does aspirin work?

A

-inhibits cyclooxygenase which catalyzes the first step in the synthesis of eicosanoids from AA
>low does: inhibits COX-1
>high dose: inhibits COX-2

37
Q

COX-1

A

-constitutive enzyme (always on)
-generates signal ligand for homeostatic intercellular signalling

38
Q

COX-2:

A

-inducible enzymes
-increased activity accompanying acute and chronic inflammatory conditions

39
Q

COX-3:

A

-uniquely involved in hyperestesia (increased pain perception) and fever

40
Q

Development of specific NSAIDS:

A

-to reduce side effects (GI bleeding and kidney necrosis)
*COX-2 was specifically targeted as an inducible enzyme
>trying to target the inflammation

MONOGASTRIC GI (24 decks)

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