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Module 103: The Heart, Lungs and Blood > Theme 3: Lecture 5 - Introduction to lipids > Flashcards

Theme 3: Lecture 5 - Introduction to lipids Flashcards

1
Q

What are the functions of lipids

A
  • Phospholipids & cholesterol: cell membranes
  • Triglyceride is a key energy store
  • Steroids and fatty acids play regulatory roles as hormones, vitamins and bile acids
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2
Q

How does creatine phosphate store energy

A

Creatine takes the high energy phosphate bond from ATP and stores it to rephosphorylate ADP at a later time when the cell needs the extra energy

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3
Q

What can Acetyl CoA be turned into

A
  • Cholesterol (blocked by statins)
  • Citric acid cycle to produce ATP
  • Fatty acids, stored energy (fatty acids can also be converted back into acetyl CoA)
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4
Q

Fatty acid synthesis equation

A

Acetly-CoA + ATP + e- (ATP) -> fatty acid + CO2 + CoA

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5
Q

Describe fatty acid synthesis

A

Leads to fatty acids with even-number of carbons

Consumes ATP

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6
Q

Beta oxidation equation

A

fatty acid -> Acetyl CoA + e- (ATP)

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7
Q

Describe beta oxidation

A
  • Fat Mobilization: Shortens fatty acid by 2 carbons at a time
  • Produces ATP + Acetyl-CoA
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8
Q

Describe the structure of fatty acids

A
  • Simple straight carbon chains + COOH

- In humans, most are 16-20 carbons long

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9
Q

What does it mean if it’s an essential fatty acid

A

It can’t be made in the body, has to be taken in by the diet

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10
Q

What is a triglyceride’s official name

A

Triacyl-glyceride

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11
Q

What is cholesterol an essential component of

A

cell membranes

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12
Q

What is cholesterol a precursor to

A
  • Bile acids
  • Steroid hormones
  • Vitamin D
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13
Q

Sources of cholesterol

A
  • Diet

- Made in liver (with a big emphasis on recycling)

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14
Q

How are cholesterol esters made

A

A cholesterol molecule is esterified by a long chain fatty acid

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15
Q

What are cholesterol esters broken down by

A

by lipases to free cholesterol and fatty acids

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16
Q

State cholesterol esters’ interaction with water

A

Hydrophobic

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17
Q

State cholesterol’s interaction with water

A

Amphipathic

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18
Q

What is cortisol

A

hormone secreted by the adrenal cortex

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19
Q

Structure of acetate

A

CH3COO-

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20
Q

Describe acetate

A
  • Main energy production precursor for everything that happens in citrate cycle
  • Can’t be transported in the plasma in this form so is transported by co enzyme A
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21
Q

What are ketone bodies

A
  • Soluble chemicals

- Major energy source during fasting esp for brain and heart

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22
Q

How are ketone bodies made

A

-Made from acetyl-CoaA during fasting by the liver

-

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23
Q

How long do ketone bodies last

A

5 hours

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24
Q

Name the 3 ketone bodies

A
  • Acetoacetic acid
  • Beta-hydroxybutyric acid
  • Acetone
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25
Q

Which ketone bodies are useful

A

Acetoacetic acid & beta-hydroxybutyric acid

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26
Q

Which ketone body is the waste product

A

Acetone

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27
Q

How is acetone made

A

spontaneously by decarboxylation

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28
Q

How is acetone eliminated

A

by the kidney

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29
Q

Are most naturally occurring unsaturated fatty acids cis or trans

A

cis

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30
Q

Describe unsaturated fatty acids

A
  • have a lower boiling point so more liquid at body temperature
  • increase fluidity of cell membranes
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31
Q

Why do molecules that have a cis carbon carbon double bond have a lower melting point

A
  • The cis double bond creates a kink that saturated and trans unsaturated fat slack
  • This kink lowers melting point by interfering with stacking and solidification
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32
Q

What are the two naming systems for unsaturated fatty acids

A
  • Omega classification

- Alpha classification

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33
Q

Describe the omega naming system for unsaturated fatty acids

A
  • Start at the methyl end and count the position of the double bonds in relation to that end
  • Linoleic acid would be omega 6, 9
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34
Q

Describe the alpha naming system for unsaturated fatty acids

A
  • State the number of carbons
  • State the number of double bonds
  • Start at the carboxyl end and count the position of the double bonds in relation to that end
  • Linoleic acid would be 18:2 delta 9, 12
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35
Q

What do saturated fats increase

A

LDL

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36
Q

Which fats are bad for you

A
  • Saturated fats

- Trans unsaturated fats

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37
Q

Why are cis unsaturated fats not bad for you

A
  • They have a lower melting point because of the kink

- Therefore less likely to form a big globular fat and solidify

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38
Q

Where do the 4 lipid transport pathways transport lipids to

A

-From gut (digestive tract) to liver & periphery
Periphery for lipids = muscle and adipose tissue
-From liver to periphery
-From periphery to liver
-From liver into digestive tract

39
Q

What is the exogenous pathway

A

Transport from the gut to the liver (and periphery)

40
Q

What are exogenous lipids

A

Lipids from the diet i.e. outside the body

41
Q

How are lipids transported by the exogenous pathway

A
  • Lipids from diet packaged by small intestine into “chylomicrons”
  • increased lipids in plasma after a fatty meal
  • Chylomicrons taken up by liver (or by periphery)
42
Q

What is the endogenous pathway

A

Transport from the liver to the periphery

43
Q

Where are peripheral lipids stored

A

in muscle and adipose tissue

44
Q

What are endogenous lipids

A

Lipids made by the body i.e. from inside

45
Q

How are lipids transported by the endogenous pathway

A

Lipids from liver are packaged into VLDLs

46
Q

What is the reverse cholesterol transport pathway

A

Transport from periphery to the liver

47
Q

What is the reverse cholesterol transport pathway important in

A

recycling of lipids

48
Q

When does the reverse cholesterol transport pathway occur

A

When lipid supplies in the liver are being exhausted

49
Q

What indicates reverse path activity

A

HDL in blood

50
Q

Which transport pathway is bile production in

A

Transport from liver into gut (and gall bladder)

51
Q

How does cholesterol help with bile production

A

It is converted into bile acids

52
Q

Where do bile acids go after being deposited in the gut

A

Most are reabsorbed by the gut and returned to the liver and recycled

53
Q

Why are enzymes and receptors needed in the lipid transport pathways

A

to move fats in and out of blood vessels

54
Q

Give an example of an enzyme used in lipid transport pathways

A

lipoprotein lipase

55
Q

What does lipoprotein lipase do

A
  • It is a cell surface-linked enzyme in capillary walls
  • Metabolises TG to fatty acids + glycerol because TG cannot go through cell membranes
  • In order to remove triglycerides from VLDL and to move the TG across the capillary membrane, TG must first be metabolised via lipoprotein lipase
56
Q

What are lipoprotein particles

A

plasma soluble particles which can carry lipids

57
Q

Why do lipids need to be packaged to be transported in the body

A

They aren’t plasma soluble

58
Q

What are apolipoprotein particles

A

Proteins in lipoprotein particles that can hold lipids

59
Q

What are apolipoprotein particles’ relationship with water

A

They are amphipathic

60
Q

Example of a apolipoprotein particle

A

Apolipoprotein E (apoE)

61
Q

What density are triglycerides

A

very low density

62
Q

What density is cholesterol

A

midway between TGs and proteins

63
Q

Are bigger lipoprotein particles lower or higher in density

A

lower in density

64
Q

Why is LDL the most dangerous lipoprotein

A
  • LDL contents get incorporated into atheromas
  • LDL in blood may be “storage” for cholesterol that “cannot be stored elsewhere”
  • Excess LDL accumulates in atheromas
65
Q

Where does LDL come from

A

LDL is eventually “left-over” after periphery absorbs endogenous TG from VLDL from liver

66
Q

When does HDL appear

A

when cholesterol is being used up

67
Q

What does HDL do

A

lipid transport from fat cells to liver (reverse cholesterol transport)

68
Q

What does VLDL signify

A

risk of atheroma

69
Q

What does VLDL do

A

Used to transport endogenous cholesterol and TG from Liver to adipose and muscle

70
Q

What is left after TG is removed by periphery from VLDL

71
Q

What is IDL

A
  • Intermediate density lipoprotein
  • IDL is intermediate step in pathway where VLDL becomes LDL
  • Results from VLDL losing TG to periphery
  • IDL will become LDL
72
Q

What is IDL a sign of

73
Q

When are chylomicron levels high

A

after fat containing meals

74
Q

Are chylomicrons associated with CV risk

75
Q

What do chylomicrons do

A

carry lipids from gut to periphery (for exogenous lipids)

76
Q

Which cells release insulin

A

Beta cells in pancreas

77
Q

Which cells release glucagon

A

alpha cells in pancreas

78
Q

What causes type 1 diabetes

A

no insulin made

79
Q

What causes type 2 diabetes

A

absent or decreased response to insulin by target cells but insulin is still being made

80
Q

What causes type 2 diabetes mellitus

A

obesity and genetic predisposition

81
Q

What is hypercholesterolaemia

A
  • Too much cholesterol in the blood
  • A subclass of hyperlipidaemias
  • High fasting levels of plasma cholesterol
82
Q

What is hyperlipidaemia

A

Too much lipid in the blood

83
Q

Example of hypercholesterolaemia

A

familial hypercholesterolaemia

84
Q

What does hypercholesterolaemia cause

A

increased risk of arteriosclerosis

85
Q

What is arteriosclerosis

A

arteries become thick and stiff, sometimes restricting blood flow

86
Q

What causes hypercholesterolaemia

A

combination of environmental and genetic factors

87
Q

What are statins

A

Drugs used to treat hypercholesterolaemia

88
Q

How do statins work

A

Block endogenous cholesterol synthesis by blocking HMG-CoA Reductase (the entry step into cholesterol synthesis)

89
Q

Give and example of a statin

A

simvastatin

90
Q

What are statins prescribed for

A

CAD prophylaxis

91
Q

What is metabolic syndrome

A

a group of risk factors that occur together, leading to increased risk for CAD, stroke, and type 2 diabetes

92
Q

What are the causes for metabolic syndrome

A
  • Insulin resistance
  • Central obesity (waist circumference)
  • high blood pressure
93
Q

What does increased HDL mean

A
  • More recycling of cholesterol

- Lower CV risk

Module 103: The Heart, Lungs and Blood (51 decks)

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