Lipid Metabolism Flashcards

1
Q

What is the recommendation for cholesterol?

A

There is none anymore

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2
Q

What kind of fat is good? What is bad?

A

Good: unsaturated
Bad: saturated fat, trans fats

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3
Q

What is a good way to reduce fat?

A

High flavour for low fat content (ex: parmesan)

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4
Q

What are good sources of fat?

A

Olives, olive oil, nuts, cold-water fish, avocados

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5
Q

Name the three types of lipids.

A
  • Triacylglycerols
  • Phospholipids
  • Sterols
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6
Q

What do all lipids have in common?

A

ALL hydrophobic

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7
Q

What are the 6 lipid functions in food?

A
  • Essential fatty acids
  • Concentrated source of E
  • Carry fat soluble vitamins
  • Flavour, texture, aroma
  • Satiety
  • Emulsification
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8
Q

What are the 4 metabolic lipid functions?

A
  • Adipose tissue is a concentrated E store
  • Cell membranes
  • Nerve impulse transmission
  • Eicosanoid synthesis
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9
Q

What can store large quantities of fat?

A

adipose tissue

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10
Q

What are eicosanoids?

A

Lipid derivates of 20-carbon fatty acids; biologically active compounds that help to regulate blood pressure, blood clotting and other body functions.

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11
Q

Describe the structure of triacylglycerols.

A

3 glycerols linked to carboxylic acid liked to carbon chain

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12
Q

What are fatty acids made up of?

A

Carboxylic acid + carbon chain

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13
Q

What is carboxylic acid in fatty acids?

A

Polar “reactive” end

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14
Q

How would we write a saturated fatty acid?

A

C(number of carbons): 0 (no double bonds)

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15
Q

What does monounsaturated mean?

A

One double bond

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16
Q

Where would we start counting for the double bond of unsaturated fatty acids? How would we write it?

A

From the non-reactive end (WITHOUT carboxylic acid)

C(nb of carbons): 1, n-9 (carbon where the double bond starts)

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17
Q

Where is a double bond always located?

A

At 9

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18
Q

Where are the double bonds on omega-6 and omega-3?

A

Omega 6: 6, 9

Omega 3: 3, 6, 9

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19
Q

How would we write omega-6 and omega-3?

A

Omega 6: C18: 2w6

Omega 3: C18: 3w3

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20
Q

What is another name for omega-6 and omega-3?

A

Omega-6: Linoleic acid

Omega-3: Alpha-linolenic acid

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21
Q

What do the number of double bonds influence in a fatty acid?

A

Physical characteristics, more double bonds, more liquid it is at room temperature

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22
Q

Define hydrogenation.

A

Take polyunsaturated fatty acids and turn them into saturated fatty acids by adding H atoms (hydrogenation)

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23
Q

How are fatty acids naturally conformed? What does that create?

A

Cis, a bend

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24
Q

What happens during partial hydrogenation?

A

Double bonds flip to a lower energy shape (straight) : TRANS

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25
What are the 4 factors to fatty acid structure?
- Chain length - Double bond number - Double bond position - Double bond stereochemistry
26
What are typical saturated fats?
animal fats and tropical oils
27
What are typical monounsaturated and polyunsaturated fats?
Vegetable oils
28
What are we suppose to consume more of: omega-3 or omega-6?
Omega 3 (relatively more)
29
Name some examples of omega-3s and omega-6s.
Omega 3: flaxseed oil, canola | Omega 6: safflower, sunflower
30
Name the 2 essential fatty acids.
Omega-3 | Omega-6
31
Name the two non-essential fatty acids.
Steoric | Oleic
32
How can omega-3s and omega-6s form new families?
Desaturating | Elongating
33
Name the 2 families of omaga-3s and omega-6s that produce eicosanoids.
Arachidonic (n-6) | EPA (n-3)
34
Compare the function of eicosanoids in the omega-6 and omega-3 families.
``` Omega 3: decrease blood clotting decrease platelet aggregation decrease blood pressure decrease CVD risk ```
35
Why is consuming fish better than omega-3 supplements?
Supplements can be toxic, can make an unbalanced eicosanoid production, can result in excess vitamin A and D
36
How many servings of fish should you have a week?
2 servings fatty fish/week
37
What are phospholipids composed of?
Phosphate + Glycerol + Fatty acids | Polar head + non polar tail
38
What helps emulsify?
Eggs and mustard
39
What happens in the mouth during lipid digestion?
Salivary glands produce lipases which digest TG
40
Where does most digestion occur? What organs help
Small intestine | Pancreas and gallbladder
41
What does the pancreas do?
Secretes pancreatic lipase | TG -> (lipase) 2FA + 1 monoacylglycerol
42
What does the gallbladder do?
Stores bile acids and bile salts, emulsifies
43
What does hydrolysis do?
breaking esther bonds -> fatty acids and monoglycerides
44
Where does absorption occur?
Brush border of the small intestine
45
Where are big fat particles taken to?
The lymph --> high pressure blood flow
46
Where are shorter chained fats taken to?
Directly into the bloodstream
47
Define the structure of lipoproteins.
Interior of TG and cholesterol surrounded by phospholipids
48
Define the function of lipoproteins.
Transports hydrophobic fats in the blood plasma
49
What is hydrophobic in a lipoprotein?
Cholesterol-esther
50
Name the 4 types of lipoproteins.
- Chylomicrons - VLDL - HDL - LDL
51
Which lipoprotein is the biggest? What is it mostly made of?
Chylomicron (TG)
52
What explains lipoprotein density?
Content, more protein
53
Which lipoprotein is athrogenic? Which is healthful?
Good: HDL Bad: LDL
54
What are blood samples composed of?
- Red blood cells (heavy) - Platelets - white blood cells (medium) - Plasma (light)
55
What makes plasma clear? What makes it milky?
Clear: no chylomicrons (fasting) Milky: chylomicrons (eating)
56
How do chylomicrons travel? What does the liver eventually transform it in?
Chylomicrons -> lymph -> distributes fat (TG) to peripheral tissues, not much half life -> liver Liver transforms it into VLDL along with fat it has synthesized
57
What does VLDL become? How?
VLDL -> gives up TG, becomes denser -> LDL
58
Where does LDL go? How?
circulates and is taken up by the liver by the LDL receptor
59
If there is a problem with the LDL receptor, what happens?
increase LDL, increase CVD
60
What can induce problems with the LDL receptor? What can help?
Induce: genetic, diet (high sat fat) Help: eating PUFA and MUFA
61
How does HDL circulate?
HDL produced by liver, picks up cholesterol around body, brings it back to liver through a receptor
62
Why are HDLs protective
picks up cholesterol
63
How are TG removed?
Lipoprotein lipase
64
How is cholesterol "removed"? How can we make it more efficient?
Can't catalyze, excrete it through biliary excretion | Can make it more efficient by soluble fibre
65
What kind of organ is adipose tissue?
Endocrine organ
66
What does adipose tissue make? What does it lead to?
Makes adipokines, pro inflammatory | Obesity
67
What is the predominant hormone during fasted state?
Glucagon
68
Are lipoproteins involved during fasted state?
no
69
How does the body produce E during fasting state?
Taking TG out of adipose tissue
70
Fasted State: what happens in the cells?
Glucagon stimulates cell to transform TG -> FAs and MG
71
Fasted State: what does glycerol do?
glycerol goes out of cell and goes to peripheral cells, can be used to produce glucose or oxidize for E
72
Fasted State: what do free fatty acids do?
albumin carries them to cells -> generates to acetylCOA -> produces E
73
What can be toxic in its free form?
free fatty acids
74
What is the predominant hormone during fed state?
Insulin
75
How is energy stored during fed state?
TG -> chylomicrons in the gut -> distribution to body -> liver, rearranges with synthesized fat -> VLDL -> gives up triglycerides to STORE in adipose tissues, catalyzed by LP lipase
76
Where is energy stored during fed state?
Adipose tissue
77
What study informed us of the link between cholesterol, mortality and CVD?
1960s study | Reducing cholesterol by 1%, CVD decreases by 2%
78
Define atherosclerosis.
Plaque that forms within arterial walls
79
What are arteries like before atherosclerosis?
Smooth, elastic, wide lumen
80
Name the 3 steps to atherosclerosis.
- Fatty Streak - Fibrous Plaque - Complicated Lesion
81
What happens during fatty streak?
- LDL particles slip in endothelial cells, stuck under lining - Immune macrophages break down LDL particles
82
What are foam cells?
Unhealthy macrophages
83
What happens during fibrous plaque?
Foam cells increase, inflammation increases, fibrous accumulation -> hard
84
What happens during complicated lesion?
Calcification leads to rigid, narrow lumen, rough Can produce ulceration and thrombosis Platelets stick and can block blood flow or break away (peripheral artery disease)
85
What is thrombosis?
Blood clot
86
Name the 4 ways LDLs can be damaged.
- Inflammation (oxidation) - Smoking - Glycation, blood glucose increase (type II diabetes) - The longer they are in transit (we need GOOD receptors)
87
Why is it important to prevent LDL damage?
IF they are damaged they are more likely to invade arterial walls.
88
Name the 5 risk factors of atherosclerosis.
- High energy - High fat - High alcohol - Low complex CHO/fibre - Low/High vitamins/minerals
89
Name 2 factors that increase LDL.
``` Saturated fats (animal fats) Trans fats (hydrogenation) ```
90
Name 2 factors that decrease LDL.
``` Monounsaturated fats (mediterranean diet) Omega 3s ```
91
Why can high CHO diets increase LDL?
excess CHO is synthesized into saturated FAs which increase LDL
92
What should we measure for atherosclerosis disease risk?
NUMBER of LDL particles
93
Name 5 treatment options for someone with high cholesterol.
- Increase MUFA and PUFA, decrease Sat fats - Phytosterols - Statins - Ezetimide - Lovaza
94
Name the two types of cholesterol reducing pharmaceuticals.
- Cholesterol absorption inhibitors | - Cholesterol synthesis inhibitors
95
Why is it better to decrease trans fats and sat fats than to eat less cholesterol?
Decreasing cholesterol intake has little effect on cholesterol status since liver monitors intake and will produce more
96
When energy yielding nutrients are consumed in excess, which one(s) can lead to storage of fat?
Fat, carbohydrate and protein
97
Define lipoprotein.
A cluster of lipids wrapped with proteins circulating in plasma.
98
Name some approaches to decrease CVD.
- PUFAs and MUFAs vs Saturated Fat - Weight loss, exercise, moderate alcohol - Soluble fibre to bind cholesterol - CHOs with low GI - Plant sterols - Cholesterol Binding Drugs - Cholesterol synthesis inhibiting drugs
99
What should fat intake be for toddlers?
40%
100
How much n-3 and n-6 PUFAs?
n6: 5 to 10% (12-17 grams) n3: 0.6 to 1.2% (1.1-1.6 grams)
101
How do we get omega 3 eggs?
Feed chickens flaxseed
102
Why don't we feed cows flaxseed? What do we do instead?
Rumen metabolizes omega-3 | Add fish oil or flax oil (not good taste)
103
What do consumers want their fat substitutes to be?
Mouthfeel, flavour, low in E, non toxic, no side effects
104
What do manufacturers want their fat substitutes to be?
Stable in mfg and storage, non-toxic (consumers, envr.)
105
Name the 5 fat substitutes.
- Oatrim - Maltodextrin - Simplesse - Olestra - Salatrim, Caprenin
106
How does Oatrim work?
oat-fibre based, healthy, didn't catch on
107
How does Maltodextrin work?
Core of starches, corn, melts when sprinkled
108
How does Simplesse work?
Egg protein or whey + air, microparticulated protein
109
How does Olestra work?
Sucrose polyesther instead of glycerol triesther, not absorbed, no calories
110
How does Salatrim, Caprenin work?
Structured lipids with SCFAs, or poorly absorbed FAs
111
How do anti-absorption drugs work?
Will go down by 30% roughly, but needs a good diet | Pancreatic lipase inhibitor