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Flipped Classroom: Lipoproteins II Flashcards

1
Q

Successively denser, having higher ratios of protein to lipid and therefore will be on top of the centrifuge tube

A

VLDLs and LDLs

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2
Q

Can also be separated on the basis of their size using electrophoretic mobility

A

Plasma lipoproteins

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3
Q

Function in the regulation of lipoprotein metabolism through their involvement in the transport and redistribution of lipids among various cells and tissues

A

Apoproteins

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4
Q

Have a role as cofactors for enzymes of lipid metabolism

A

Apoproteins

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5
Q

Apoproteins help maintian the structure of

A

Lipoproteins

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6
Q

What are the two basic phases of lipoprotein metabolism?

A

Processing and clearance

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7
Q

When lipoproteins undergo changes in composition of both surface and core components

A

Processing phase

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8
Q

Cleared from the blood via reeptor-mediated endocytosis (clearance phase)

A

Lipoproteins

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9
Q

Major protein of HDL

-activates LCAT

A

ApoA-I

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10
Q

Primarily found in HDL where it activates hepatic lipase activity

A

ApoA-II

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11
Q

Derived from ApoB-100 gene by RNA editing

-Found exclusively in chylomicrons

A

ApoB-48

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12
Q

ApoB-48 lack the

A

LDLR binding domain

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13
Q

Major protein of LDL

-Binds to LDL receptor (LDLR)

A

ApoB-100

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14
Q

Activates lipoprotein lipase (LPL)

A

ApoC-II

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15
Q

Inhibits LPL

A

ApoC-III

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16
Q

Major protein of remnant lipoproteins

A

ApoE

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17
Q

ApoE binds to

A

LRP and LDLR

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18
Q

What are the two important lipases in lipoprotein metabolism

A

Lipoprotein lipase and hepatic lipase

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19
Q

Hydrolyze triglycerides into FFAs and glycerol

A

LPL and Hepatic lipase

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20
Q

Attached by interaction with glycosaminoglycans on the endothelial cells

A

Lipoprotein Lipase (LPL)

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21
Q

Interacts with chylomicrons or VLDLs to catalyze the hydrolysis of triacylglycerides to FFAs and glycerol

A

LPL

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22
Q

Serves as a cofactor for LPL on the lipoprotein

A

ApoC-II

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23
Q

What percentage of the FFAs are taken by adipose tissue, heart, and muscle?

-rest returned to liver

A

80%

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24
Q

Primarily a phospholipase, but also possesses triglyceride hydrolase activity

A

Hepatic Lipase (HL)

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25
Q

HL is synthesized by hepatocytes and is present primarily on

A

Liver endothelial cells

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26
Q

Transported from the liver to the capillary endothelium of the adrenals, ovaries, and testes, where it functions in the release of lipids from lipoproteins for use in these organs

A

HL

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27
Q

Serves as the cofactor for HL on HDL

A

ApoA-II

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28
Q

Hydrolyzes triglycerides and possibly excess surface phospholipids in the final processing of chylomicron remnants

A

HL

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29
Q

HL completes the processing of IDL to

A

LDL

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30
Q

Participates in the conversion of HDL2 to HDL3 by the removal of triglyceride and phospholipid from

A

HDL2

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31
Q

Important for metabolizing dietary triacylglycerols and contain B48, CII, CIII, and E

A

Chylomicrons

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32
Q

Important for metabolizing liver derived triacylglycerols and contain B100 instead of B48

-also contain CII, CIII, and E

A

VLDLs

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33
Q

Formed in cicrulation by VLDL metabolism and delivers primarily cholesterol to the peripheral tissues

A

LDL

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34
Q

Contains only B100

A

LDL

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35
Q

Synthesized in the liver and reside on HDL

A

ApoC-II and III

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36
Q

Mainly stems from the liver, and chylomicrons acquire it from HDL

A

ApoE

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37
Q

Lipoprotein metabolism can be broken down into which three pathways?

A
  1. ) Exogenous
  2. ) Endogenous
  3. ) Reverse cholesterol transport
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38
Q

Deals with dietary lipids and originates in the intestine

A

Exogenous pathway

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39
Q

Deals largely with de novo synthesized lipids and originates in the liver

A

Endogenou spathway

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40
Q

Deals largely with cholesterol in the peripheral tissues

A

Reverse cholesterol transport pathway

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41
Q

Dietary lipids are taken up by intestinal epithelial cells and are released into the lymphatic system inside of chylomicrons in the

A

Exogenous pathway

42
Q

Then, on the walls of blood capillaries, triglycerides are hydrolyzed to FFAs and glycerol by

43
Q

A similar reaction is catalyzed in the walls of the liver by

44
Q

Through the removal of triglycerides by LPL in the exogenous pathway, chylomicrons become remnants and they are taken up by the

45
Q

As for the endogenous pathway, the liver exports cholesterol and cholesterol esters in

46
Q

Then, lipases remove triglycerides, thereby converting VLDL to

A

IDL and LDL

47
Q

Contains much more cholesterol than it does triglycerides

48
Q

Then, in the endogenous pathway, liver and peripheral cells endocytose the cholesterol-rich

49
Q

In the reverse cholesterol transport pathway, extrahepatic tissues export cholesterol by adding it to circulating

50
Q

This cholesterol is then delivered mainly to the

51
Q

Located at the apical membrane of enterocytes and facilitates the uptake of cholesterol across the brush border membrane

A

NPC1L1 protein

52
Q

Promotes the active transfer of cholesterol and plant sterols back into the intestinal lumen for secretion

A

ABCG5/G8 transporter

53
Q

This absorbed cholesterol is esterified by

-is then incorporated into nascent chylomicron particles

A

Acyl CoA cholesterol acyltransferase 2 (ACAT2)

54
Q

Synthesized around the ApoB-48 in the ER

A

Chylomicrons

55
Q

Dietary fatty acids are used for triglyceride synthesis in the

56
Q

Transfers triglycerides and cholesterol esters to ApoB-48

A

Microsomal Triglyceride Transfer Protein (MTP)

57
Q

The nascent chylomicrons leave the ER and are secreted through the Golgi complex to the basolateral side of the

A

Enterocyte

58
Q

In the blood, chylomicrons gain ApoC-II and III and ApoE from

59
Q

Necessary for the uptake of chylomicron remnants by the liver

A

ApoC-III and ApoE

60
Q

Chylomicron remnants (but not chylomicrons) are small enough to enter the

A

Space of Disse in the liver

61
Q

In the space of Disse in the liver, we see triglyceride removal by

62
Q

ApoE on chylomicron remnants binds to the

-Results in remnants entering hepatocytes via endocytosis

A

LDL receptor-related protein 1 (LRP1)

63
Q

The chylomicron remnants are then degraded by

64
Q

Absorption of the fat soluble vitamins A, D, E, and K occurs in the small intestine, and these vitamins are transported ot the liver by

A

Chylomicrons

65
Q

The halflife for a given chylomicron is

66
Q

Fasting blood samples are used to determine lipids in order to prevent contamination by

A

Chylomicrons

67
Q

Ancompasses the triglycerides inside all lipoprotein particles, i.e. chylomicrons, chylomicron remnants, VLDL, IDL, LDL, and HDL

A

Total triglycerides

68
Q

The nascent chylomicron enters the circulation carrying ApoB-48 and a large cargo of

A

Triacylglycerol

69
Q

It then receives ApoE and C-II from

70
Q

The chylomicrons travel around the circulatory system until they associate with

71
Q

As triacylglycerol is lost, the chylomicron shrinks and forms a

A

Chylomicron Remnant (CMR)

72
Q

The released fatty acids can be reassembled into triacylglycerol for storage as fat or oxidized to produce

73
Q

The remnant is taken up by the liver through receptor mediated endocytosis because the liver recognizes

A

ApoB-48 and ApoE

74
Q

Dietary cholesterol delivered to the liver in CMR can be repackaged in VLDLs and sent out to tissues or converted to

A

Bile salts

75
Q

Inhibits cholesterol synthesis by the liver

A

Dietary cholesterol

76
Q

The counterparts to the chylomicron and exogenous pathway is

A

VLDL and the endogenous pathway

77
Q

VLDLs are created in the liver, containing “endogenous”

A

TAGs and CEs

78
Q

The liver synthesizes a small amount of fatty acids from excess dietary carbohydrate and esterifies these fatty acids with glycerol to form

A

Triglycerides

79
Q

The liver packages triglycerides into

-released into blood

80
Q

Nascent VLDL enters the circulation containing

A

APoB-100 and some ApoE and C-II

81
Q

As ith chylomicrons, additional ApoE and ApoC-II are donated to VLDL from

82
Q

The presence of ApoC-II stimulates LPL to degrade the

A

TAGs present in VLDL

83
Q

This results in the delivery of liver-originating FFAs to adipose and other

A

Peripheral organs

84
Q

The resulting action of LPL on VLDL is its conversion to the

A

VLDL remnant (AKA IDL [intermediate density lipoprotein])

85
Q

What is the halflife of VLDL?

86
Q

Approximately half of the VLDL remnants are cleared from the circulation by the liver via

A

ApoE and its receptor

87
Q

The remaining half of IDL is remodeled to

-remains in circulation

88
Q

The conversion of IDL to LDL involves the removal of both TAGs and phospholipids and requires the action of

89
Q

As a consequence of the cumulative action of LPL and HL on these particles, the LDL particle is significantly enriched in

A

Cholesterol Esters (CEs)

90
Q

The half-life of LDL particles is long, on the order of

91
Q

The majority of lipids observed in a fasting blood sample is

A

LDL, VLDL, and IDL

92
Q

The majority of blood-borne cholesterol is from

93
Q

Throughout the body, LDL’s ApoB-100 acts as a ligand for

A

LDL receptors (LDLR)

94
Q

Approximately 2/3 of the circulating LDL is taken up by the liver via

A

ApoB-100 binding to LDL receptors

95
Q

The remaining 1/3 is taken up via ApoB-100 and the LDL receptor in

A

Peripheral tissues

96
Q

NOT the only mechanism for the clearance of LDL particles form blood

97
Q

After endocytosis of LDL, triglycerides and cholesterol esters are hydrolyzed in lissomes by

A

Lysosomal acid lipase

98
Q

What percentage of all of the LDL is taken up by the liver?

A

Approximately 70%

99
Q

Acts on LDL receptors to prevent their recycling to the plasma membrane surface and promote their degradation in lysosomes

100
Q

An integral part of the cholesterol-dependent regulation of the number of LDLRs

GI (59 decks)

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