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Cardio 1 > Biochem Lipoproteins > Flashcards

Biochem Lipoproteins Flashcards

1
Q

Lipoproteins are ___ water soluble

A

Poorly

*so a transport mechanism is needed

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2
Q

General structure of lipoproteins

A
  1. Completely hydrophobic molecules inside (triacylglycerols and cholesteryl esters)
  2. Amphipathic molecules form the coat (cholesterol and phospholipids)
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3
Q

Proteins associated with lipoproteins are called ___ which play important roles in the metabolism of lipoproteins through____

A

Apoproteins

  • enzymatic
  • particle recognition for specific receptors
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4
Q

Major lipoproteins in order of least to most dense and the major lipid in each.
*less dense=___ protein content

A
  1. Chylomicron-triacylglycerol
  2. VLDL-triacylglycerol
  3. LDL-cholesterol
  4. HDL-phospholipid
    * less
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5
Q

The least dense and largest lipoproteins are ___. They contain the most ___ and the least ___

A

Chylomicrons
Triacylglycerols
Protein

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6
Q

The most dense and smallest lipoproteins are ___ which contain the most ___ and the least ___

A

HDL
Protein
Lipid

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7
Q

Subclasses of HDL

A
  1. Nascent HDL (pre beta HDL)
  2. HDL2
  3. HDL3
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8
Q

Lipoprotein remnants:

A

Chylomicron remnants

VLDL remnants

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9
Q

Lp(a), lipoprotein (a) is a modified ___

A

LDL

B-100 with apoprotein (a) covalently bound via a disulfide bond

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10
Q

Apoprotein(a) structurally resembles ___, but has no ___ activity (___)

A

Plasminogen
Plasminogen
(Plasminogen activation to plasmin, which is fibrinolytic)

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11
Q 
Lipoprotein(a) prevents \_\_\_. 
It interferes with \_\_\_ by \_\_\_. 
Both Lipoprotein(a) and apoprotein(a) inhibit \_\_\_
A
  • LDL uptake
  • fibrinolysis by competing with authentic plasminogen
  • tPA-mediated clot lysis
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12
Q

Lipoprotein(a) levels are an independent risk factor for ____ and are ____, and do not respond to ___

A

Cardiovascular disease
Genetically determined
Dietary treatment

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13
Q

Apoprotein(a) is derived from what gene? This gene is thought to have evolved from the ___ gene

A

LPA

Plasminogen (PLG)

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14
Q

Apoproteins to know:
Lipoproteins involved
Function

A
  • A: HDL, chylomicron, structural
  • B-48: intestine, chylomicron, structural
  • B-100: liver, VLDL, IDL, LDL, Lp(a), structural, binds to LDL receptor
  • C-II: chylomicrons, VLDL, HDL, LPL cofactor
  • E: chylomicrons, VLDL, HDL, binds to LDL receptor
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15
Q

Which apoproteins bind to LDL receptor?

A

B-100

E

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16
Q

Which apoproteins are structural?

A

A
B-48
B-100

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17
Q

Lipoproteins and their apoproteins:

Chylomicrons

A

A
B-48
C-II
E

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18
Q

Lipoproteins and their apoproteins:

VLDL

A

B-100
C-II
E

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19
Q

Lipoproteins and their apoproteins:

IDL

A

B-100

E

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20
Q

Lipoproteins and their apoproteins:

LDL

A

B-100

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21
Q

Lipoproteins and their apoproteins:

HDL

A

A
C-II
E

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22
Q

Lipoproteins and their apoproteins:

Lp(a)

A

B-100-apo(a)

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23
Q

Apoprotein E has 3 different alleles

A

E2, E3, E4

E3 has a greater affinity for the LDL receptor than E2. E4 has the greatest.

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24
Q

E2 allele for apoprotein E is associated with ___ due to ____.
E4 is associated with ___ due to ___

A
  • familial dysbetalipoprotenemia due to less efficient clearance of VLDL and chylomicrons
  • hypercholesterolemia and CHD due to increased down regulation of the LDL receptor
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25
Q

Persons with Apo E4 have an increased incidence of ___

A

Late onset Alzheimer’s disease

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26
Q

Function of lipoproteins is ___

Specifically?

A

To transport lipid molecules

  • chylomicrons carry lipids from digestion
  • VLDL carry lipids from liver
  • HDL serve as a reservoir of apoproteins and for cholesterol “reverse transport”
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27
Q

These lipoproteins arise as intermediates in the metabolism of chylomicrons and VLDL

A

Chylomicron and VLDL remnants
IDL
LDL
HDL2 and HDL3

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28
Q

Chylomicron are formed in ___ from digestion of ____. Lipids are assembled in the ___. Apoproteins are synthesized in ___. Chylomicrons are assembled in ___.
Nascent chylomicrons are secreted into lymph - including what?

A 
Intestinal epithelial cells
ER
Rough ER
Golgi
apoA proteins and apoB-48
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29
Q

When chylomicrons enter the blood stream they accumulate ___ and ___ from the ___

A

apoC and apoE from circulating HDL

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30
Q

ApoC-II is required for ___. ApoC-III is thought to inhibit ____ by ___

A

LPL activity

Premature removal of chylomicrons from circulation by inhibiting binding to receptors, such as LDL and LRP

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31
Q

LPL removed 80-90% of the ___
Where?
As this is removed chylomicrons become __
What else happens?

A

Triacylglycerols

  • adipose, skeletal muscle, heart
  • smaller
  • surface molecules are transferred to HDL (cholesterol, apoA, apoC, and phospholipid-requires PLTP)
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32
Q

The chylomicron remnant (after LPL removes TAG) gains __ and ___ from HDL. It is then cleared from the blood by __. How?

A 
ApoE and Cholesteryl ester 
The liver (binds to LDL (B-100/E) receptor due to presence of apoE and binds to LRP)
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33
Q

Chylomicrons are only present after a meal. The half life is ___. About 80% of the lipid from chylomicrons goes to ___.
Liver uptake of remnants accounts for ___ of the chylomicron lipid

A

Less than 1 hour
Heart, adipose tissue, and muscle
20% or less

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34
Q

LCAT

Function

A

Lecithin cholesterol acyltransferase

-transfers the fatty acid from the sn-2 position of phosphatidylcholine (aka lecithin) to cholesterol

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35
Q

LCAT is synthesize in the ___ and secreted into plasma. It becomes associated with ____ and is activated by ___.

A

Liver
HDL
ApoA-1

36
Q

CETP

Function

A

Cholesteryl ester transfer protein

-facilitated transfer of cholesteryl ester from HDL to VLDL, IDL, and LDL

37
Q

CETP is synthesized in the ___ and secreted into plasma. It becomes associated with ___

A

Liver

HDL

38
Q

PLTP

Function

A

Phospholipid transfer protein

-facilitates transfer of phospholipid from VLDL, IDL, LDL, etc. to HDL

39
Q

LPL
Location
Function

A

Lipoprotein lipase

  • anchored non covalently by interaction with heparan sulfate to capillary endothelial cells of adipose, skeletal muscle, and heart muscle
  • catalyzes hydrolysis of triacylglycerol to glycerol and 3 NEFA
40
Q

LPL synthesis and the transfer of LPL to the surface of capillary endothelial cells is stimulated by ___.
LPL is NOT expressed where?

A

Insulin

Adult liver

41
Q

Relative Km of LPL in different tissues:?Where is the highest concentration of LPL?

A

Adipose: large
Heart: small
*heart

42
Q

HL
Function
Location

A

Hepatic lipase

  • hydrolyzes TAG and phospholipids
  • non covalently bound to heparan sulfate glycoproteins on the sinusoidal surface of liver cells
43
Q

ABCA1 and ABCG1
What are they?
Function?

A

ATP binding cassette transporters

  • cellular plasma membrane proteins
  • required for ATP hydrolysis, they move cholesterol from the inner to outer leaflet
44
Q

LDL (B-100/E) receptor

Where is it found?

A

-Plasma membrane receptor in clathrin coated pits

45
Q

___ is of primary importance in clearing LDL. other tissues of importance include:

A

Liver
Adrenal glands
Gonads

46
Q

Binding of LDL to LDL receptors results in ____

A

-internalization of the LDL and further metabolism of its constituents

47
Q

The proteolysis of the internalized LDL is controlled by ___, which is a protein synthesized in the ___ and secreted into the blood stream. It binds to the receptor and targets it to ____ when it becomes internalized.
In the absence of this protein, what happens to LDL?

A

PCSK9
Liver
Lysosomes
Recycled into the plasma membrane

48
Q

LRP
Specificity?
Location?
What does it recognize?

A

LDL receptor related protein

  • not as specific as LDL for lipoproteins
  • liver, brain, placenta
  • apoE
49
Q

Difference in the effect of intracellular cholesterol concentration on LRP vs LDL

A

Cholesterol concentration in the cell has a significant effect on LDL but not LRP

50
Q

SR-B1
Where?
Function?

A

Scavenger receptor B1

  • liver and other cells
  • binds to HDL via apoA-I and cholesteryl esters are transferred from HDL to liver
51
Q

VLDL and LDL are synthesized in the ___ and assembled in the ____. Their apoproteins are synthesized ___.

A

Liver
Golgi
On the RER

52
Q

In the bloodstream VLDL requires ___ from HDL

A

apoE

apoC

53
Q

TAG is removed from VLDL by ___

A

Action of LPL of peripheral tissues

54
Q

As VLDL becomes smaller, what components are transferred to HDL ?

A

apoC
Phospholipid
Some TAG in exchange for cholesteryl ester

55
Q

The VLDL ___ may be removed by the liver

A

Remnant (IDL)

56
Q

IDL binds to ____ and is internalized. Which IDL is more likely internalized?
Requirements?

A

LDL (B100/E)

  • IDL with multiple copies of apoE
  • Have to be small enough to have access to liver cell plasma membranes
57
Q

About ___% of the IDL is cleared by the liver. That which is not becomes ___

A

50
Remodeled to form LDL
-IDL becomes anchored to hepatic lipase and HL hydrolyzes the TAG and phospholipids of the IDL
-apoE is transferred to HDL

58
Q

LDL is rich in ___. It contains ___ as its apoprotein component. It has a ____ plasma half life, unlike chylomicron remnants and VLDL remnants.

A
  • Cholesteryl waters and cholesterol
  • only one molecule of apoB100
  • long (up to several days)
59
Q

LDL is cleared from the bloodstream by ____. About ___ % is cleared by the liver and the remaining is cleared by ___

A 
Receptor mediated internalization
70
-extrahepatic tissues 
1. Adrenal gland; LDL receptors
2. Macrophages; Scavenger receptors
60
Q

HDL is synthesized in the ____

A

Liver and intestine

61
Q

What is nascent HDL ?

A

Pre beta HDL
A disc shaped phospholipid rich particle with apoproteins
-from liver: A-I, A-II, E, and C
-from intestine: only A-I

62
Q

Once in circulation, HDL acquires what?

A
  • cholesterol from other lipoproteins and from cells
  • LCAT from plasma
  • CETP from plasma
  • other apoproteins from other circulating lipoproteins
63
Q

Transfer of cholesterol to HDL from the ___ of the cells plasma membrane is aided by the action of ___

A

Outer leaflet

ABCA1

64
Q

In circulation, what is one function of HDL?

A
  • reservoir for the apoproteins needed by nascent chylomicrons and nascent VLDL
  • important role in reverse cholesterol transport
65
Q

HDL3 vs HDL2

A

HDL3 is small, but becomes larger as it acquires more TAG, and becomes HDL2, which is a substrate for HL (which hydrolyzes the excess TAG and phospholipid)

66
Q

HDL3 removes ___, converting it to ___, and then transfers that to ___ and ___ in exchange for ___ and ___

A

Cholesterol
Cholesteryl ester
IDL and chylomicrons
Phospholipid and TAG

67
Q

___ of the liver binds HDL2 and selectively transfers cholesteryl ester to the liver cell

A

SR-B1

68
Q

Abetalipoproteinemia

Cause

A
  • Deficiency of a triglyceride transfer protein in the ER
  • liver and intestine are unable to assemble or secrete apoB-containing lipoproteins
  • chylomicrons, VLDL, and LDL are essentially absent
69
Q

Abetalipoproteinemia

Consequences

A
  • Severe fat malabsorption
  • accumulation of triglycerides in intestine and liver
  • deficiencies of fat soluble vitamins
70
Q

Abetalipoproteinemia

Untreated patients develop:

A
  • ataxia
  • retinitis pigmentosa
  • myopathy
71
Q

Abetalipoproteinemia

Clinical signs respond to treatment with ___

A

Vitamin E

72
Q

Tangier disease

Cause

A
  • deficiency of ABCA1

- cholesterol cannot be transferred from plasma membrane to nascent HDL

73
Q

Tangier disease

Consequences

A
  • HDL cannot be formed
  • decreased LDL (no transfer of CE to VLDL from HDL)
  • CE deposits in reticuloendothelial cells, bone marrow, Schwann cells
74
Q

Tangier disease

Symptoms

A
  • peripheral neuropathy
  • hepatosplenomegaly
  • lymphadenopathy
75
Q

Tangier disease has a mild tendency for ___

A

Early atherosclerosis (due to reduced LDL?)

76
Q

Familial hypercholesterolemia

Cause

A

Autosomal dominant

  • deficiency of LDL receptor
  • heterozygotes: 50% reduction in LDL receptors can double the LDL cholesterol!
  • homozygotes: rare. No functional LDL receptors
77
Q

Familial hypercholesterolemia

Consequences

A
  • accelerated CHD

- xanthomas

78
Q

Familial LCAT deficiency

Consequences

A
  • block in reverse cholesterol transport
  • limited ability of HDL to acquire cholesterol from VLDL or chylomicrons
  • elevated blood cholesterol and triglycerides
79
Q

Familial LCAT deficiency

Symptoms

A
  • free cholesterol accumulates in most tissues
  • kidney disease
  • corneal clouding
  • mild tendency for early atherosclerosis
80
Q

CETP deficiency

Consequences

A
  • benign
  • CE cannot be transferred from HDL to other lipoproteins
  • homozygotes may have 4x elevation of HDL cholesterol, while LDL is normal or low
81
Q

In CETP deficiency ___ is still possible

A

Reverse cholesterol transport

  • through transport of CE by SR-B1 receptors of the liver
  • or through endocytosis of HDL with multiple copies of apoE
82
Q

CETP deficiency is common in ___

A

Japan

83
Q

Frederickson classification of hyperlipoproteinemias

Type I

A 
Hyperchylomicronemia
Rare
Huge increase in triglycerides
Cholesterol may be slightly elevated 
Not associated with increased atherosclerosis 
-caused by deficiency of LPL and apoC-II
-treatment: low fat diet
84
Q

Frederickson classification of hyperlipoproteinemias

Type II

A 
Hypercholesterolemia 
Common 
LDL elevated 
-cause: familial hypercholesterolemia 
-secondary causes more common: obesity, diabetes
-major risk factor for atherosclerosis
85
Q

Frederickson classification of hyperlipoproteinemias

Type III

A

Dysbetalipoproteinemia
Rare
Increased triglycerides and cholesterol
-Causes: homozygotes for apoE2 (which won’t bind to hepatic apoE receptors). Chylomicron and VLDL remnants accumulate
-symptoms: xanthomas, increased risk of CHD
-treatment: diet

86
Q

Frederickson classification of hyperlipoproteinemias

Type IV

A

Hypertriglyceridemia
Common
Increased triglycerides and cholesterol
-causes: obesity, type 2 diabetes, alcoholism, progesterone-rich contraceptives, excess dietary carbs esp. sugars

87
Q

Frederickson classification of hyperlipoproteinemias

Type V

A 
Hyperlipoproteinemia
Rare
Increased triglycerides and cholesterol
-causes: increased chylomicrons and VLDL, uncontrolled diabetes, obesity, kidney disease
-treatment: diet

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