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1) Nutrition & Health > Lipid Metabolism > Flashcards

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
Q

What are the 4 factors to fatty acid structure?

A
  • Chain length
  • Double bond number
  • Double bond position
  • Double bond stereochemistry
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26
Q

What are typical saturated fats?

A

animal fats and tropical oils

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27
Q

What are typical monounsaturated and polyunsaturated fats?

A

Vegetable oils

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28
Q

What are we suppose to consume more of: omega-3 or omega-6?

A

Omega 3 (relatively more)

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29
Q

Name some examples of omega-3s and omega-6s.

A

Omega 3: flaxseed oil, canola

Omega 6: safflower, sunflower

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30
Q

Name the 2 essential fatty acids.

A

Omega-3

Omega-6

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31
Q

Name the two non-essential fatty acids.

A

Steoric

Oleic

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32
Q

How can omega-3s and omega-6s form new families?

A

Desaturating

Elongating

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33
Q

Name the 2 families of omaga-3s and omega-6s that produce eicosanoids.

A

Arachidonic (n-6)

EPA (n-3)

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34
Q

Compare the function of eicosanoids in the omega-6 and omega-3 families.

A 
Omega 3: 
decrease blood clotting
decrease platelet aggregation
decrease blood pressure
decrease CVD risk
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35
Q

Why is consuming fish better than omega-3 supplements?

A

Supplements can be toxic, can make an unbalanced eicosanoid production, can result in excess vitamin A and D

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36
Q

How many servings of fish should you have a week?

A

2 servings fatty fish/week

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37
Q

What are phospholipids composed of?

A

Phosphate + Glycerol + Fatty acids

Polar head + non polar tail

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38
Q

What helps emulsify?

A

Eggs and mustard

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39
Q

What happens in the mouth during lipid digestion?

A

Salivary glands produce lipases which digest TG

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40
Q

Where does most digestion occur? What organs help

A

Small intestine

Pancreas and gallbladder

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41
Q

What does the pancreas do?

A

Secretes pancreatic lipase

TG -> (lipase) 2FA + 1 monoacylglycerol

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42
Q

What does the gallbladder do?

A

Stores bile acids and bile salts, emulsifies

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43
Q

What does hydrolysis do?

A

breaking esther bonds -> fatty acids and monoglycerides

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44
Q

Where does absorption occur?

A

Brush border of the small intestine

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45
Q

Where are big fat particles taken to?

A

The lymph –> high pressure blood flow

46
Q

Where are shorter chained fats taken to?

A

Directly into the bloodstream

47
Q

Define the structure of lipoproteins.

A

Interior of TG and cholesterol surrounded by phospholipids

48
Q

Define the function of lipoproteins.

A

Transports hydrophobic fats in the blood plasma

49
Q

What is hydrophobic in a lipoprotein?

A

Cholesterol-esther

50
Q

Name the 4 types of lipoproteins.

A
  • Chylomicrons
  • VLDL
  • HDL
  • LDL
51
Q

Which lipoprotein is the biggest? What is it mostly made of?

A

Chylomicron (TG)

52
Q

What explains lipoprotein density?

A

Content, more protein

53
Q

Which lipoprotein is athrogenic? Which is healthful?

A

Good: HDL
Bad: LDL

54
Q

What are blood samples composed of?

A
  • Red blood cells (heavy)
  • Platelets - white blood cells (medium)
  • Plasma (light)
55
Q

What makes plasma clear? What makes it milky?

A

Clear: no chylomicrons (fasting)
Milky: chylomicrons (eating)

56
Q

How do chylomicrons travel? What does the liver eventually transform it in?

A

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
Q

What does VLDL become? How?

A

VLDL -> gives up TG, becomes denser -> LDL

58
Q

Where does LDL go? How?

A

circulates and is taken up by the liver by the LDL receptor

59
Q

If there is a problem with the LDL receptor, what happens?

A

increase LDL, increase CVD

60
Q

What can induce problems with the LDL receptor? What can help?

A

Induce: genetic, diet (high sat fat)
Help: eating PUFA and MUFA

61
Q

How does HDL circulate?

A

HDL produced by liver, picks up cholesterol around body, brings it back to liver through a receptor

62
Q

Why are HDLs protective

A

picks up cholesterol

63
Q

How are TG removed?

A

Lipoprotein lipase

64
Q

How is cholesterol “removed”? How can we make it more efficient?

A

Can’t catalyze, excrete it through biliary excretion

Can make it more efficient by soluble fibre

65
Q

What kind of organ is adipose tissue?

A

Endocrine organ

66
Q

What does adipose tissue make? What does it lead to?

A

Makes adipokines, pro inflammatory

Obesity

67
Q

What is the predominant hormone during fasted state?

68
Q

Are lipoproteins involved during fasted state?

69
Q

How does the body produce E during fasting state?

A

Taking TG out of adipose tissue

70
Q

Fasted State: what happens in the cells?

A

Glucagon stimulates cell to transform TG -> FAs and MG

71
Q

Fasted State: what does glycerol do?

A

glycerol goes out of cell and goes to peripheral cells, can be used to produce glucose or oxidize for E

72
Q

Fasted State: what do free fatty acids do?

A

albumin carries them to cells -> generates to acetylCOA -> produces E

73
Q

What can be toxic in its free form?

A

free fatty acids

74
Q

What is the predominant hormone during fed state?

75
Q

How is energy stored during fed state?

A

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
Q

Where is energy stored during fed state?

A

Adipose tissue

77
Q

What study informed us of the link between cholesterol, mortality and CVD?

A

1960s study

Reducing cholesterol by 1%, CVD decreases by 2%

78
Q

Define atherosclerosis.

A

Plaque that forms within arterial walls

79
Q

What are arteries like before atherosclerosis?

A

Smooth, elastic, wide lumen

80
Q

Name the 3 steps to atherosclerosis.

A
  • Fatty Streak
  • Fibrous Plaque
  • Complicated Lesion
81
Q

What happens during fatty streak?

A
  • LDL particles slip in endothelial cells, stuck under lining
  • Immune macrophages break down LDL particles
82
Q

What are foam cells?

A

Unhealthy macrophages

83
Q

What happens during fibrous plaque?

A

Foam cells increase, inflammation increases, fibrous accumulation -> hard

84
Q

What happens during complicated lesion?

A

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
Q

What is thrombosis?

A

Blood clot

86
Q

Name the 4 ways LDLs can be damaged.

A
  • Inflammation (oxidation)
  • Smoking
  • Glycation, blood glucose increase (type II diabetes)
  • The longer they are in transit (we need GOOD receptors)
87
Q

Why is it important to prevent LDL damage?

A

IF they are damaged they are more likely to invade arterial walls.

88
Q

Name the 5 risk factors of atherosclerosis.

A
  • High energy
  • High fat
  • High alcohol
  • Low complex CHO/fibre
  • Low/High vitamins/minerals
89
Q

Name 2 factors that increase LDL.

A 
Saturated fats (animal fats)
Trans fats (hydrogenation)
90
Q

Name 2 factors that decrease LDL.

A 
Monounsaturated fats (mediterranean diet)
Omega 3s
91
Q

Why can high CHO diets increase LDL?

A

excess CHO is synthesized into saturated FAs which increase LDL

92
Q

What should we measure for atherosclerosis disease risk?

A

NUMBER of LDL particles

93
Q

Name 5 treatment options for someone with high cholesterol.

A
  • Increase MUFA and PUFA, decrease Sat fats
  • Phytosterols
  • Statins
  • Ezetimide
  • Lovaza
94
Q

Name the two types of cholesterol reducing pharmaceuticals.

A
  • Cholesterol absorption inhibitors

- Cholesterol synthesis inhibitors

95
Q

Why is it better to decrease trans fats and sat fats than to eat less cholesterol?

A

Decreasing cholesterol intake has little effect on cholesterol status since liver monitors intake and will produce more

96
Q

When energy yielding nutrients are consumed in excess, which one(s) can lead to storage of fat?

A

Fat, carbohydrate and protein

97
Q

Define lipoprotein.

A

A cluster of lipids wrapped with proteins circulating in plasma.

98
Q

Name some approaches to decrease CVD.

A
  • 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
Q

What should fat intake be for toddlers?

100
Q

How much n-3 and n-6 PUFAs?

A

n6: 5 to 10% (12-17 grams)
n3: 0.6 to 1.2% (1.1-1.6 grams)

101
Q

How do we get omega 3 eggs?

A

Feed chickens flaxseed

102
Q

Why don’t we feed cows flaxseed? What do we do instead?

A

Rumen metabolizes omega-3

Add fish oil or flax oil (not good taste)

103
Q

What do consumers want their fat substitutes to be?

A

Mouthfeel, flavour, low in E, non toxic, no side effects

104
Q

What do manufacturers want their fat substitutes to be?

A

Stable in mfg and storage, non-toxic (consumers, envr.)

105
Q

Name the 5 fat substitutes.

A
  • Oatrim
  • Maltodextrin
  • Simplesse
  • Olestra
  • Salatrim, Caprenin
106
Q

How does Oatrim work?

A

oat-fibre based, healthy, didn’t catch on

107
Q

How does Maltodextrin work?

A

Core of starches, corn, melts when sprinkled

108
Q

How does Simplesse work?

A

Egg protein or whey + air, microparticulated protein

109
Q

How does Olestra work?

A

Sucrose polyesther instead of glycerol triesther, not absorbed, no calories

110
Q

How does Salatrim, Caprenin work?

A

Structured lipids with SCFAs, or poorly absorbed FAs

111
Q

How do anti-absorption drugs work?

A

Will go down by 30% roughly, but needs a good diet

Pancreatic lipase inhibitor

1) Nutrition & Health (21 decks)

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