Week 4: Lipids Flashcards
(120 cards)
1
Q
Simple lipids
A
Two types of products from hydrolysis
2
Q
Compound/complex lipids
A
Three or more products from hydrolysis
3
Q
Derived lipids
A
Combined simple and compound lipids through hydrolysis
4
Q
Types of simple lipids
A
a) Waxes
b) Triglycerides
5
Q
What are triglycerides further broken into?
A
Glycerol and fatty acids
6
Q
What are fatty acids further broken into?
A
Saturated fatty acids
Unsaturated fatty acids
7
Q
What are unsaturated fatty acids further broken down into?
A
Monounsaturated
Polyunsaturated
8
Q
Monounsaturated fatty acids
A
Oleic acid (ex. olive oil)
9
Q
Polyunsaturated fatty acids
A
Linoliec acid (omega-6)
Linolenic acid (omega-3)
10
Q
Compound lipids
A
Phospholipid
Glycolipid (Cerbrosides and gangliosides)
11
Q
Derived lipids
A
a) Steroids
b) Sterols
c) Carotenoids
12
Q
Steroids
A
Bile acids, sex hormones
13
Q
Sterols
A
Cholesterol, ergosterol
14
Q
Carotenoids
A
Carotene, xanthophils
15
Q
What are triglycerides composed of?
A
3 fatty acids with a glycerol
16
Q
Types of triglycerides
A
- Saturated
- Monounsaturated
- Polyunsaturated
17
Q
Saturated fatty acids and bonds
A
No double bonds, all carbons have max amount of hydrogen bonds
18
Q
What foods contain saturated fatty acids ?
A
Animal fats and plant oils
ex. butter, meats
19
Q
Monounsaturated fatty acids and bonds
A
One double bond
20
Q
Polyunsaturated fatty acids and bonds
A
More than one double bond
21
Q
Structure of sterols
A
Four-ring steroid nucleus and at least one hydroxyl group
22
Q
Cholesterol
A
Most common sterol, 25% of plasma membrane in some nerve cells
23
Q
How does cholesterol exist?
A
Can exist in free form or hydroxyl group at C-3 can be esterified w a fatty acid
24
Q
How is cholesterol regulated in membranes
A
Cells esterify excess cholesterol with a fatty acid and store the cholesterol esters in vesicles with the cytosol
When free cholesterol is needed, cholesterol esters are hydrolyzed and it is transported to membrane
25
What is cholesterol a precursor for?
Corticosteroid hormones, sex hormones, bile salts, vitamin D3
26
Lipid digestion in the mouth
Lingual lipase breaks triglycerides into triacylglycerols, fatty acids and diacylglycerols
27
Lipid digestion in the stomach
Gastric lipase breaks them down even more
28
Where does most of lipid digestion occur?
Lumen of small intestine
29
Lipid digestion in the small intestine- bile
Bile breaks down triacylglycerols, fatty acids and diacylglycerols into emulsified triacylglycerols, fatty acids and diacylglycerol micelles via emulsification
30
Lipid digestion in small intestine- pancreatic lipase
Breaks down triacylglycerols, fatty acids and diacylglycerol micelles into monoacylglycerols and fatty acids by enzymatic digestion
31
What do micelles contain?
Contain the final digestion products from lipid hydrolysis such as free long FA, monoacylglycerols, lysophospholipids, free cholesterol, phytoesterols, fat-soluble vitamins
32
What are micelles?
Lipid molecules w a hydrophobic core and a hydrophilic shell that allows lipids to travel through a polar solvent
Produced in liver
33
How do micelles transport lipids into enterocytes?
They are water soluble and penetrate the water layer bathing the enterocytes of the small intestine, they interact w microvilli at the brush border and lipids diffuse into enterocytes
34
What are esterases?
Digestive enzymes that break down dietary lipids in GI tract
35
What do esterases do?
Cleave ester bonds with triglycerides, phospholipids and cholesterol esters
36
How are cholesterol esters absorbed?
Cannot be absorbed, must be hydrolyzed into free cholesterol and fatty acids to be incorporated into micelle
37
Lipid absorption
1. Inside mucosal cells of small intestine, fatty acids and monoglycerides are reassembled into lipids by esterification forming chylomicrons
2. Chylomicrons enter lymph vessel
3. Travel to left subclavian vein and diffuses into circulation
38
What are monoacylglycerols and diacylglycerols and fatty acids reassembled into?
Triglycerides
39
What is cholesterol reassembled into?
Cholesterol ester
40
What are lysophospholipids and fatty acids reassembled into?
Phospholipids
41
Where do chylomicrons bipass?
The liver so that they aren't catabolized
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Lipoproteins
Lipids are transported in blood as components of lipoproteins
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Types of lipoproteins
Chylomicrons
Very low density lipoproteins (VLDL)
Low density lipoproteins (LDL)
Intermediate-density lipoprotein (IDL)
High-density lipoprotein (HDL)
44
Lipoprotein metabolism differs depending on
1. Which lipids are transported (triglycerides, cholesterol, phospholipids)
2. Where lipids are delivered (liver, skeletal muscle, adipose tissue)
3. Lipoprotein metabolic fate
45
Exogenous lipid transport
Transport of dietary lipids (triacylglycerols) from the intestine to peripheral tissues for storage and energy utilization
46
Pathway of exogenous transport
After chylomicrons enter the blood stream, triglycerides are transferred to skeletal muscle and adipose tissue, leading to the formation of a chylomicron remnant which results in delivery of cholesterol to liver
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When does exogenous lipid transport occur?
Operates only after a fat containing meal
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What happens to chylomicrons at the end of exogenous lipid transport?
Chylomicrons disappear after all dietary triacylglycerols are delivered to target tissues
49
What lipoprotein is involved in exogenous lipid transport?
Chylomicrons
50
Endogenous lipid transport
Transport of triglycerides (already in body) from liver to peripheral tissue for storage or energy utilization
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What lipoproteins are involved in endogenous lipid transport?
VLDL, IDL, LDL
52
Reverse cholesterol transport
Ability of HDL to pick up excess cholesterol from peripheral tissues and deliver it to liver for excretion from body by bile
53
Lipoprotein involved in reverse cholesterol transport
HDL
54
Step 1 of reverse cholesterol transport
Lipid free ApoA-1 is secreted by liver and intestines and released from chylomicrons and VLDL during hydrolysis
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Step 2 of reverse cholesterol transport
ApoA-1 acquires PL and C from interaction w liver resulting in nascent HDL particles
56
Step 3 of reverse cholesterol transport
Nascent HDL acquires more PL and C from non-hepatic tissues
57
Step 4 of reverse cholesterol transport
LCAT enzyme (carried on HDL) forms cholesterol esters by catalyzing the transfer of fatty acids to free cholesterols and CE migrates to core of HDL particle
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Step 5 of reverse cholesterol transport
Continuous binding to cell receptors and continued action of LCAT causes HDL to grow in size
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Step 6 of reverse cholesterol transport
Accumulated CE can be transferred to other lipoproteins through CEPT which distributes VLDL to LDL so that HDL is reduced in size to optimize interaction with receptors
60
Step 7 of reverse cholesterol transport
HDL binds with receptors on hepatocytes and either CE is deposited in liver cells and depleted HDL returns to circulation OR entire HDL is internalized and degraded
61
Why is a larger HDL beneficial?
Greater ability to gather cholesterol and deliver it to the liver and therefore reduced CVD risk
62
Atherosclerosis
Progressive narrowing of the arteries caused by a buildup of plaque in the lining of the artery; major cause of CVD
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Plaque
Composed of fats, cholesterol etc.
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Steps of developing atherosclerosis
1. Dysfunctional endothelial cells and retention of ApoB containing lipoproteins
2. Triggers an inflammatory response
3. Fatty streak formation
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Formation of foam cells- atherosclerosis pathogenesis
1. Initiation of inflammatory response triggers monocytes and T-lymphocytes to adhere to the endothelium of arteries, changing their shape and loosening their tight junctions
2. Allows LDL (carrying triglycerides and cholesterol) to enter arterial wall and become trapped in intima
3. LDL is oxidized
4. Monocytes become macrophages which accept oxidized LDL by phagocytosis, forming foam cells
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Foam cells function
Recruitment and proliferation of smooth muscle cells, further LDL oxidation, recruitment of other inflammatory cells and additional impairment of endothelial function
LEAD TO FATTY STREAK
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Plaque formation- atherosclerosis
Over time, accumulation of foam cells results in a fibrous plaque in the walls of the arteries
68
LDL-C and risk of CVD
Causal and cumulative effect
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The lipid hypothesis
States that elevated plasma cholesterol (LDL cholesterol) has a causal role in the development of heart disease and CVD
70
Does dietary cholesterol impact blood cholesterol?
Not necessarily bc 80% of cholesterol is produced in the body and only 20% comes from the food you eat
71
Ratio of ApoA to ApoB and CVD risk
Decreasing ratio = decreased risk
72
Dangerous cholesterol levels
Total= 240+
LDL= 60+
HDL male= under 40, female = under 50
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Healthy cholesterol levels
Total= under 200
LDL= under 100
HDL 60+
74
What impact do saturated fats have on LDL receptors?
Saturated fat decreases sensitivity of LDL receptor on liver, increasing LDL cholesterol
75
Does dose matter in studies that try to replace saturated fats in diet?
Yes
Only a certain range of %energy from saturated fat will increase risk of CVD event
76
Does nutrient replacement matter when replacing saturated fats in diet?
Yes
No effect when replaced w carbs or MUFA
Positive effect when replaced with PUFA
77
Does source matter when replacing saturated fat in diet?
Yes
Vegetable sources of fat and PUFA reduce risk of CVD more than dairy fat, and especially more than animal fat
78
Does type of carb matter when replacing saturated fat in diet?
Yes
Replacing saturated fat with high quality carbs reduces risk of CVD but replacement with refined starch and added sugars doesn't
79
Three main types of omega-3 (polyunsaturated fat)
1. EPA
2. DHA
3. ALA
80
Roles of omega-3
1. Components of phospholipid (increase permeability of plasma membrane)
2. Precursor for inflammatory molecules: resolvins, protectins, maresins
3. Cardiovascular benefits
81
Sources of omega-3
Fish-salmon
Flax seed
82
DRI of omega-3 for adults
Men 19+= 1.6g/day
Women 19+= 1.1 g/day
83
AI for ALA for ages 0-12 months
0.5g/day
84
AI for ALA for ages 1-3
0.7g/day
85
AI for ALA for ages 4-8
0.9g/day
86
AI for ALA for ages 9-13 boys
1.2g/day
87
AI for ALA for ages 9-13 girls
1.0g/day
88
AI for ALA for ages 14-18 boys
1.6g/day
89
AI for ALA for ages 14-18 girls
1.1g/day
90
Recommended intake of ALA per week
2 servings of oily fish per week
91
History of Omega-3 literature- cross sectional studies
Greenland eskimos have reduced risk of CVD bc they have more EPA in diet
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History of omega-3 literature- case control studies
Risk of a CV event decreased the most when subjects ate btwn 2.94 and 5.54g of fish per week
93
Omega-3 index
Level of EPA and DHA in erythrocyte (RBC) phospholipids
Used as a risk factor for CHD and death from CHD
94
Levels on the omega-3 index
<4% high risk
4-8% moderate-high risk
>8% lowest risk
95
Blood levels of DHA and EPA and risk of death from CHD
Low = increased risk
96
Primary prevention
Intervening before health effects occur (usual risk population)
97
Secondary prevention
Known CVD/CHD, previous MI, stroke etc.
98
Primary outcome measures
Cardiovascular outcomes
Coronary outcomes
- Myocardial infarction
- Percutaneous intervention
- Sudden cardiac arrest
- coronary bypass graft
All-cause mortality
Hospitalization for CV reasons
99
Composite measure
Usually studies measure for a variety of primary outcome measures
100
Pre-2018 major trials
Found that omega-3 fatty acid had no effect on death from CHD
101
VITAL (2019)
Found no sig diff btwn placebo and omega-3 group
102
VITAL(2019): Subgroup analysis
People who ate less than 1.5 servings/week of fish saw a greater reduction in risk of MI and CV event when supplementing omega-3 than people who already ate a lot fish
103
REDUCE-IT (2019)
Found a greater reduction in risk of a CV event in the secondary prevention cohort when supplementing w omega-3 compared to primary prevention cohort
104
Post 2018 Major trials
Included the REDUCE-IT study
Found a stronger association that showed that omega-3 reduces risk of CV events
105
Cochrane review
Found that increasing omega-3 reduces risk of CHD events, mostly in secondary prevention group
106
Omega-3 literature limitations
1. Support for omega-3 benefit comes from low quality studies
2. Issues with control vs omega-3 pills (fishy taste)
3. Analyses are not controlled for all variables (ex. protein consumption)
4. Generalizability limitations (only benefit for secondary prevention populations and no standardized dose)
107
Omega-3 supplementation for skeletal muscle
Increases EPA and DHA composition in skeletal muscle
108
Fish oil supplementation and muscle protein synthesis
Omega-3 spikes MPS causing you to lose less muscle mass
It potentiates MPS in response to an amino acid and insulin infusion
109
Omega-3 intake in older adults for skeletal muscle
Increases muscle mass and strength
Increased mitochondrial gene expression (easier to generate energy)
110
Krill oil supplementation in older adults
Increased muscle function and size
111
Omega-3 supplementation in older women
Exercise induced (RT) increases in muscle quality
112
Omega-3 supplementation in older men
Don't see the same benefit on muscle quality as older women
113
Omega-3 fatty acid intake and muscle anabolism
Improves ability to gain and maintain muscle
(But this is done in older pop. who are more susceptible to muscle loss)
114
Omega-3 fatty acid and muscle disuse atrophy
Those who take omega-3 with an immobilization injury will lose less muscle and gain more muscle back than those who don't
115
Does EPA have a benefit for health?
Yes, but when combined with DHA
116
Fates of LDL once it enters intima of artery wall
1. Moves back in to bloodstream
2. Becomes oxidized
3. Taken up by monocyte/macrophages which form foam cells
117
Progression of atherosclerosis
1. Foam cell
2. Fatty streak
3. Intermediate lesions
4. Atheroma
5. Fibrous plaque
6. Complicated lesion/rupture
118
Why are LDL third in line to be taken up by liver and non-hepatic tissue?
Can survive in body for 3-5 days bc LDL doesn't supply cholesterol to organs
119
What happens if LDL receptors are defective?
Increased plasma cholesterol which will accelerate atherosclerosis
120
What can all cells do with cholesterol?
Synthesize cholesterol, but only liver can degrade it
