Lipid Digestion and absorption Flashcards
Lipids
-heterogeneous
-relative insolubility in water
-soluble in nonaqueous (nonpolar) solvents such as chloroform, alcohols
Function of lipids
-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
Main form of lipids
-triacylglycerols
What are lipids derived from?
-diet
-lipids secreted into the intestinal lumen as part of bile
-lipids in sloughed off epithelial cells
Lipids available for digestion
-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)
Triglycerols
-composed of glycerol and 3 fatty acids
How do triacylglycerols affect digestibility?
-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
Fatty acids
-carboxylic acids with long hydrocarbon side chain (even number; 12-20 carbons)
How do fatty acids differ?
-differ depending on:
>length of hydrocarbon side chain
>degree of unsaturation
>position and orientation of the double bonds
Fatty acid nomenclature
-1. Delta nomenclature= C-1 is carboxyl
-2. also use alpha, beta, gamma
- 3. w (omega) nomenclature= carbon furthest from carboxyl C
Omega 6
-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
Omega 3
-anything with a double bond at carbon 3
-more anti-inflammatory
Trans vs. cis
-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
Methylene interrupted
-2 carbon interruptions between each double bonds
Conjugated
-when double bonds are not separated by single carbons
Palmitic acid
C16:0
Linoleic acid
C18:2 cis-9,12
-18 carbons
-2 double bonds (at C9 and C12)
-omega 6 FA
Conjugated linoleic acid
-linked with possible weight loss due to increased lipid digestion
-also could be linked with insulin resistance
Mammals introduction of double bonds
-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
Linoleic FA
-omega 6
-C 18:2 (cis 9,12)
Linolenic FA
-omega 3
-C18:3 (cis 9, 12, 15)
Linoleic (omega 6) and Linolenic (omega 3) essential FAs
-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)
Elongation and desaturation
-required for the synthesis of long chain polyunsaturated fatty acids from essential fatty acids linoleate (C18:2n-6) and linolenic (C18:3n-3)
Non-essential long-chain unsaturated fatty acids
-ability to be made because mammalian tissues have a delta 9 desaturase
-ex. Palmitoleic acid (C16) & oleic (C18)
Essential fatty acids
1.Linoleic acid (omega 6)
2.Linolenic acid (omega 3)
Arachidonic acid
-C20
-formed from linoleic acid
Why can cats not form Arachidonic acid?
-because they lack a delta 6 double bond
Eicosanoids
-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)
Eicosanoids importance
-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)
Groups of Eicosanoids
1.thromboxanes
2. prostacyclins
3. leukotrienes
4.lipoxins
Thromboxanes (TXA)
-synthesized in platelets
-cause vasoconstriction and platelet aggregation
Inhibition of thromboxanes
-thromboxane synthesis is inhibited by aspirin
Prostacyclins (PGI)
-potent inhibitors of platelet aggregation
PGI3, PGI2, TXA3, TXA2
-PGI2 and PGI3 are both anti-aggregators
-TXA3 is a weaker aggregator than TXA2 resulting in longer clotting time
Where can arachidonic come from?
-diet
-membrane phospholipids via phospholipase A2
Aspirin
-inhibits cyclooxygenase which catalyzes the first step in the synthesis of eicosanoids from amino acids
Cox 1
-a constitutive enzyme that generates the signal ligand for homeostatic intercellular signaling
Cox 2
-an inducible enzyme with increased activity accompanying acute and chronic inflammatory conditions
Cox 3
-uniquely involved in hyperesthesia (increased pain perception) and fever (splice variant of Cox 1)
**still need research
NSAIDS
-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
