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DEN 7101F - Human Structure and Function > Exam 3 - Lipoproteins > Flashcards

Exam 3 - Lipoproteins Flashcards

1
Q

Ideal healthy level of total cholesterol

A

<200 mg/dl

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2
Q

Ideal healthy level of LDL - cholesterol

A

<100 mg/dl

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3
Q

Ideal healthy level of HDL - cholesterol

A

> 60 mg/dl

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4
Q

Ideal healthy level of triglycerides

A

<150 mg/dl

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5
Q

Most abundant lipids in the body

A
  • triglycerides
  • phospholipids
  • cholesterol
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6
Q

Which lipid is a major source of energy for cells?

A

Triglycerides

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7
Q

Major lipid component of cell membranes

A

Phospholipids

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8
Q

Majority of cholesterol is made in the:

A

Liver

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9
Q

Function of cholesterol

A
  • cell growth
  • cell division
  • membrane repair
  • steroid/hormone production
  • bile salts
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10
Q

Triglycerides structure

A

3 fatty acids to glycerol via ester linkage

high density energy store

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11
Q

Phospholipids structure

A

2 fatty acids linked to glycerol backbone, with phosphate/polar head group

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12
Q

Cholesterol is made into a cholesterol ester via what enzyme?

A

LCAT (lecithin cholesterol acyltransferase)

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13
Q

Cholesterol from the diet is only found in:

A

Animal fat

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14
Q

Cholesterol biosynthesis occurs primarily in the liver using:

A

Acetyl-CoA

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15
Q

Degradation of cholesterol only occurs in the:

A

Liver

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16
Q

What forms of metabolic fuel are found in the blood?

A
  • glucose
  • fatty acids
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17
Q

After eating, glucose becomes ____ and excess gets converted into ____

A

oxidized; glycogen

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18
Q

What form of fuel is used during fasting?

A

Fatty acids

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19
Q

Metabolic fuels are used ____

A

Inversely

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20
Q

____% of fatty acid is present as free fatty acid form (unesterified)

A

2-5% (95% in the form of fatty acid esters)

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21
Q

Free fatty acids are derived from:

A
  • intracellular hydrolysis of triglycerides in hepatic or adipose cells
  • lipoprotein lipase acting on circulating lipoproteins
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22
Q

During a fed state, insulin inhibits ______ and stimulates ____ and ____

A

hormone-sensitive lipase; triglyceride synthesis and LPL

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23
Q

Insulin during fed state results in:

A

Storage of triglycerides (don’t need to use fatty acids as fuel if glucose is present)

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24
Q

During fasting, there is a drop in ____ which activates _____ (enzyme). ____ are hydrolyzed in adipocytes

A

Insulin; hormone sensitive lipase; Triglycerides

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25
Q

Hormone sensitive lipase function

A

Make fatty acids available to cells/tissues that need it (in presence of insulin)

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26
Q

Function of lipoprotein lipase

A

Removes fatty acids off of lipoproteins so they can be mobilized/stored in the fat cell

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27
Q

True or false: lipids can be transported without aid in the bloodstream

A

False - they are insoluble so they need to be associated with lipoproteins for transport

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28
Q

Lipoprotein structure

A
  • spherical soluble particle
  • nonpolar lipids in core (TG and cholesterol esters)
  • polar aspects toward aqueous phase
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29
Q

Where are apoproteins located with respect to the lipoprotein?

A

On the outside (outermost) in aqueous phase

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30
Q

What are apoproteins?

A

Proteins associated with lipoproteins

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31
Q

Functions of apoproteins

A
  • structural role
  • binding sites for receptors
  • activators or co-enzymes for lipid metabolism
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32
Q

____ direct the fate of lipoproteins

A

Apoproteins

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33
Q

What are the different classifications of lipoproteins?

A
  • Chylomicrons
  • VLDL
  • IDL
  • LDL
  • HDL
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34
Q

Which lipoprotein has the highest density? Why?

A

HDL - lowest amount of triglycerides and smallest

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35
Q

Largest lipoprotein

A

Chylomicron (also least dense)

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36
Q

Density of lipoproteins is based on:

A

Buoyant density compared to physiological saline

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37
Q

Larger lipoprotein particles means that there is:

A
  • higher content of triglycerides
  • lower density
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38
Q

Smaller lipoprotein particles means there is:

A
  • less triglycerides
  • greater relative mass of protein
  • enriched in cholesterol esters
  • greater density
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39
Q

Lipoproteins on gel electrophoresis - what is significant about chylomicrons?

A

Trapped at origin (much larger in size so they get stuck)

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40
Q

Apoproteins can be exchanged between different lipoproteins except for:

A

Apo B100 and Apo B48

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41
Q

True or false: Apo B100 and Apo B48 can exist on the same lipoprotein particle

A

False - only one or the other

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42
Q

Between different lipoproteins, protein content can vary such as:

A

Number and types of proteins associated with them

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43
Q

Besides proteins, what else can be exchanged between lipoproteins?

A
  • Surface phospholipids and cholesterol
  • cholesterol esters and TGs (but needs cholesterol ester transfer protein)
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44
Q

Source of chylomicrons

A

Gut/intestine

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45
Q

Chylomicrons - apoproteins associated

A
  • B48
  • CII
  • E
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46
Q

Function of chylomicrons

A
  • transport dietary triglycerides
  • FFA goes to adipose/muscle
  • cholesterol esters goes to liver as remnants
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47
Q

Source of VLDL

A

Liver

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48
Q

VLDL - apoproteins associated

A
  • B100
  • CII
  • E
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49
Q

VLDL function

A
  • transports endogenous triglycerides
  • FFA goes to adipose/muscle
  • cholesterol esters go to LDL
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50
Q

Source of LDL

A

Blood (remnant of VLDL)

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51
Q

LDL apoproteins associated

A

B100

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52
Q

LDL function

A
  • transports cholesterol (from VLDL) to peripheral tissues
  • cholesterol esters go to liver and peripheral cells
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53
Q

Source of HDL

54
Q

HDL - apoproteins associated

55
Q

HDL function

A
  • reverse cholesterol transport
  • removes used cholesterol from tissues and brings to liver
  • donates apolipoproteins to CM and VLDL
56
Q

Apoprotein A1 site of action

A

Blood, plasma membrane

57
Q

Function of apoprotein A1

A
  • activates LCAT and CETP
  • binds to apo A1 receptors on cells that require cholesterol extraction (HDL)
58
Q

Apoprotein B48 site of action

A

Gut (chylomicrons)

59
Q

Apoprotein B48 function

A
  • structural
  • export of chylomicrons from intestinal cells (enterocytes)
60
Q

Apoprotein B100 site of action

A

Various cells (VLDL and LDL)

61
Q

Apoprotein B100 function

A
  • structural
  • ligand for LDL receptor
  • export of liver VLDL
62
Q

Apoprotein CII site of action

A

Capillary walls

63
Q

Apoprotein CII function

A

Activates lipoprotein lipase (LPL)

64
Q

Apoprotein E site of action

65
Q

Apoprotein function

A

Receptor ligand - clears remnants, IDL, and HDL

66
Q

ApoB100 and ApoB48 are from the same gene - which one is larger?

A

ApoB100 (it is the entire gene, ApoB48 is 48% the size of B100)

67
Q

Which apoprotein is produced exclusively by the intestine?

68
Q

ApoB48 formation is a result of:

A
  • Tissue-specific expression of editase, a cytidine deaminase
  • changes cytidine into uracil, glutamine codon CAG becomes UAG stop codon at position 6666

mRNA-editing enzyme activity

69
Q

____ are absent in a fasting state

A

Chylomicrons

once you consume the dietary fats you ingested, they are gone

70
Q

Chylomicrons are assembled in:

A

Intestinal mucosal cells

71
Q

How do chylomicrons form and enter the bloodstream?

A
  • hydrolysis of triglycerides into fatty acids
  • Fatty acids cross cell membrane of enterocytes
  • fatty acids are reassembled into TGs inside the intestinal cell and packaged into chylomicron
  • Chylomicron enters lacteal
  • Enters lymphatic system
  • then enters blood via thoracic duct
72
Q

As chylomicrons circulate in the blood, they acquire apoproteins:

A

A, CII and E

73
Q

Triglyceride content of chylomicrons

74
Q

True or false: chylomicrons can vary in size

A

True - size of particles depends on the amount of triglyceride available (based on dietary intake)

75
Q

Triglyceride composition of chylomicron closely resembles:

A

Dietary intake

76
Q

VLDL triglyceride content

A

55% (also contains significant amount of cholesterol and CE)

77
Q

Nascent VLDL contains which apoprotein?

A

B100 (major structural apoprotein)

78
Q

___ acts upon VLDL in order to liberate FFA

79
Q

Lipolysis created _____ VLDL remnants

A

smaller, more cholesterol ester-rich

80
Q

VLDL assembly occurs in what kind of cells?

A

Hepatocytes (through uptake of recycled plasma lipoproteins)

81
Q

Three sources of fatty acids for VLDL assembly

A
  • plasma FFA that dissociate from albumin
  • from TG-rich lipoproteins that have undergone receptor-mediated endocytosis
  • synthesis in liver de novo
82
Q

VLDL secretory particles are released into:

A

the space of Disse

83
Q

50% of VLDL is lipolytically converted into:

A

IDL and LDL

84
Q

IDL is enriched in:

A

Cholesterol esters

85
Q

LDL is ____-rich

A

Cholesterol

86
Q

95% of protein in LDL is:

87
Q

LDL contributes to ____ of the cholesterol found in plasma

88
Q

Best single predictor of increased risk of atherosclerosis

A

High level of plasma LDL or apoB100

89
Q

Lipoprotein lipase - site of action and activator

A

Site of action: capillary walls
Activator: Apo CII

90
Q

ACAT (acyl-CoA cholesterol acyltransferase) - site of action and activator

A

Site of action: inside cells
Activator: free choles

91
Q

ACAT function

A

cholesterol ester storage

92
Q

LCAT (lectin cholesterol acyltransferase) site of action and activator

A

Site of action: blood
Activator: Apo A1

93
Q

LCAT function

A

Cholesterol extraction from cells (HDL carries CE for liver clearance to bile acids)

94
Q

CETP - site of action and activator

A

Site of action: plasma membrane
Activator: apo A1 (choles included)

95
Q

CETP function

A

flips cholesterol and lecithin to outer layer of lipid bilayer for LCAT action in blood

96
Q

Apo CII activates lipoprotein lipase which breaks down _____ into ____ and _____

A

Triglycerides; free fatty acids and glycerol backbone

FFA goes to muscle and adipose, glycerol goes to liver

97
Q

LPL is attached to inner wall of capillary via:

A

Polysaccharide chain

98
Q

Review endogenous and exogenous pathways on slides

99
Q

When HDL goes back to the liver it is:

100
Q

Cholesterol is excreted as ____ or ____ from HDL

A

bile salts; repackaged in VLDL

101
Q

Cholesterol synthesis in the liver is regulated by:

A

Cholesterol arriving through HDL

102
Q

Lipoprotein clearance involves irreversible removal from ____

103
Q

Chylomicrons half life

A

1 hour - cleared by liver E receptor

104
Q

Large VLDL half life

A

Minutes; 50% cleared by liver, 50% to IDL/LDL

105
Q

Small VLDL/IDL half life

A

1-2 hours, converted to LDL

106
Q

LDL half life

107
Q

Why does LDL have a longer half life?

A

Loss of ApoE – loss of Apo E receptors on the liver so takes longer to clear but longer access to extrahepatic tissues

108
Q

____% of plasma LDL is cleared by the liver

109
Q

____ of plasma LDL is cleared by extrahepatic tissues

110
Q

_____ is preferentially used by extrahepatic tissues as opposed to de novo cholesterol synthesis

A

LDL cholesterol

111
Q

70% of LDL clearance is mediated by ____; remainder is by _____

A

LDL receptors; scavenger receptors (macrophages)

112
Q

LDL cholesterol is taken up into cells via ____

A

clathrin coated pits (endocytosis)

113
Q

Increased cholesterol causes inhibition of:

A
  • inhibits production of cholesterol
  • inhibits LDL receptor synthesis (less HMGCoA reductase, so less synthesis of endogenous receptors)
114
Q

Mutations in LDL receptors causes increased ____ and therefore _____

A

plasma LDL levels; accelerates progress of atherosclerosis

115
Q

What is the function of HMGCoA reductase?

A

responsible for synthesizing cholesterol

116
Q

Statin drugs decrease ____ by targeting ____

A

LDL; HMGCoA reductase

117
Q

Type 1 Hyperlipoproteinemia: defect, lipoprotein in excess, lipid elevations

A
  • defect: Decreased LPL or altered ApoCII
  • lipoprotein in excess: chylomicrons
  • lipid elevations: triglycerides
118
Q

Type 2 Hyperlipoproteinemia: defect, lipoprotein in excess, lipid elevations

A
  • defect: LDL receptor deficiency
  • lipoprotein in excess: LDL
  • lipid elevations: cholesterol
119
Q

Type 2b Hyperlipoproteinemia: defect, lipoprotein in excess, lipid elevations

A
  • defect: decreased LDL receptor, increased ApoB
  • lipoprotein in excess: LDL and VLDL
  • lipid elevations: cholesterol and triglyceridea
120
Q

Type 3 Hyperlipoproteinemia: defect, lipoprotein in excess, lipid elevations

A
  • defect: defective ApoE synthesis
  • excess: VLDL and IDL
  • lipid elevations: cholesterol and triglycerides
121
Q

Type 4 Hyperlipoproteinemia: defect, lipoprotein in excess, lipid elevations

A
  • defect: increased VLDL synthesis
  • excess: VLDL
  • elevated: triglycerides
122
Q

Type 5 Hyperlipoproteinemia: defect, lipoprotein in excess, lipid elevations

A
  • defect: increased VLDL production, decreased LPL
  • excess: VLDL and chylomicrons
  • elevated: cholesterol and triglycerides
123
Q

Corneal arcus is associated with hyperlipoproteinemia types ____ in what population?

A

2 and 3; males over 40

124
Q

Corneal arcus is predictive of:

A

increased risk of coronary artery disease

125
Q

Corneal arcus looks like:

A

Ring around cornea

126
Q

Tendon xanthoma is found in:

A

Type 2a hyperlipoproteinemia

127
Q

Increased LDL circulation can be acted on by _____ and taken up by _____. These then become ____ cells which can deposit into artery walls and cause _____ to develop

A

Oxygen radicals; scavenger receptors on macrophages; foam cells; atherosclerosis/CAD

128
Q

Common cause of accelerated atherosclerosis is:

A

Deficiency of LDL receptors

can also be inherited defect or high cholesterol/high saturated fat diet

129
Q

Foam cells are ____ filled with ____

A

Macrophages; cholesterol esters

130
Q

Oxidized LDL stimulates endothelial cells to release _____ to recruit ____ to the arterial wall

A

cytokines; monocytes

131
Q

Foam cells form a ____ as part of the atherogenic plaque

A

Fatty streak

132
Q

Elevated LDL means that there is increase in:

A
  • residence time in plasma
  • modification and oxidation of LDL

DEN 7101F - Human Structure and Function (23 decks)

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