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S2B2 Cardiology > Lipoproteins > Flashcards

Lipoproteins Flashcards

1
Q
  1. Describe the molecules on the inside of a VLDL
  2. Describe the molecules on the coat of a VLDL
A
  1. completely hydrophobic (TAGs and cholesteryl esters) on the interior
  2. amphipathic (cholesterol and phospholipid) on the coat
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2
Q
  1. The proteins associated with lipoproteins are called ________
  2. What are the main roles of these proteins?
A
  1. Apoproteins
  2. Enzyme action or regulation of enzymes
    Particle recognition for specific receptors
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3
Q
  1. Rank the following major lipoproteins order of protein content percentage:
    Chylomicron VLDL LDL & HDL
  2. What is the major lipid type associated with each major lipoprotein
A
  1. Chylomicron < VLDL < LDL < HDL
  2. Chylomicron - TAG
    VLDL - TAG
    LDL - cholesterol
    HDL - phospholipid
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4
Q
  1. Where does the density of IDL lie compared to the other major lipoproteins
  2. What are the HDL sub-classes?
  3. What are remnants and from which major lipoproteins are they derived?
A
  1. IDL density lies between VLDL and LDL
  2. Nascent HDL (preB HDL)
    HDL2
    HDL3
  3. Derived from chylomicrons and VLDL
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5
Q
  1. Lp(a) is a modified _______
  2. What are the main components of Lp(a)?
A
  1. a modified LDL
  2. B-100 with apoprotein(a) bound via disulfide
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6
Q

Apoprotein(a) structurally resembles ________ and (lacks / contains) activity of its resemblance

A

structurally resmebles plasminogen, but lacks plasminogen activity

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7
Q

How does Lp(a) affect LDL uptake by the LDL receptor?

A

Lp(a) prevents LDL uptake

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8
Q
  1. How does Lp(a) affect fibrinolysis
  2. How does Lp(a) affect tPA-mediated clot lysis?
  3. How does apo(a) affect tPA-mediated clot lysis?
A
  1. Lp(a) interferes with fibrinolysis by competing with authentic plasminogen
  2. Lp(a) inhibits tPA-mediated clot lysis
  3. Apo(a) inhibits tPA-mediated clot lysis
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9
Q
  1. Are Lp(a) levels an independent risk factor for cardiovascular disease?
  2. Are Lp(a) levels genetically determined? Can they respond to dietary treatment?
    3.
A
  1. Yes, Lp(a) levels are an indpendent risk factor for cardiovascular
  2. Lp(a) levels are genetically determined and do not respond to dietary treatment
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10
Q
  1. What gene is Apo(a) is derived from?
  2. What gene is it thought this evolved from
A
  1. From the LPA gene
  2. It is thought the LPA gene evolved from the plasminogen gene (PLG)
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11
Q

A-I

  1. What lipoproteins does this associate with?
  2. What is its known function?
A
  1. HDL and Chylomicrons
  2. structura, and activates LCAT
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12
Q

A-II

  1. What lipoproteins does this associate with?
  2. What is its known function?
A
  1. HDL and Chylomicrons
  2. Structural
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13
Q

A-IV

  1. What lipoproteins does this associate with?
  2. What is its known function?
A
  1. HDL and Chylomicrons
  2. unknown
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14
Q

A-V

  1. What lipoproteins does this associate with?
  2. What is its known function?
A
  1. VLDL and Chylomicrons
  2. promotes LPL activity
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15
Q

B-48

  1. What lipoproteins does this associate with?
  2. What is its known function?
A
  1. Chylomicrons
  2. Structural
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16
Q

B-100

  1. What lipoproteins does this associate with?
  2. What is its known function?
A
  1. VLDL, IDL, LDL, and Lp(a)
  2. structural, and binds to the LDL receptor
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17
Q

C-I

  1. What lipoproteins does this associate with?
  2. What is its known function?
A
  1. Chylomicrons, VLDL, and HDL
  2. unknown
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18
Q

C-II

  1. What lipoproteins does this associate with?
  2. What is its known function?
A
  1. Chylomicrons, VLDL, and HDL
  2. LPL cofactor
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19
Q

C-III

  1. What lipoproteins does this associate with?
  2. What is its known function?
A
  1. Chylomicrons, VLDL, and HDL
  2. inhibits lipoprotein binding to receptors
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20
Q

D

  1. What lipoproteins does this associate with?
  2. What is its known function?
A
  1. HDL
  2. unknown
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21
Q

E

  1. What lipoproteins does this associate with?
  2. What is its known function?
A
  1. Chylomicrons, VLDL, IDL, and HDL
  2. binds to LDL receptor (B100 and apoproteinE both do this)
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22
Q

J

  1. What lipoproteins does this associate with?
  2. What is its known function?
A
  1. HDL
  2. unknown
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23
Q

L

  1. What lipoproteins does this associate with?
  2. What is its known function?
A
  1. HDL
  2. unknown
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24
Q

M

  1. What lipoproteins does this associate with?
  2. What is its known function?
A
  1. HDL
  2. unknown
25
Q

(a)

  1. What lipoproteins does this associate with?
  2. What is its known function?
A
  1. Lp(a)
  2. unknown
26
Q
  1. Which apoproteins are associated with chylomicrons?
A
  1. A-I, A-II, A-IV
    B-48
    C-II, C-II
    apo(E)
27
Q
  1. What apoproteins are associated with VLDL?
A
  1. B-100
    C-II, C-III
    apo(E)
28
Q
  1. IDL is a remnant of which liprotein?
  2. what apoproteins associate with IDL
A
  1. IDL is a VLDL remnant
  2. B-100 and apo(E)
29
Q
  1. What apoproteins are associated with LDL?
A
  1. B-100
30
Q
  1. Which apoproteins are associated with HDL?
A
  1. A-I, A-II, A-IV
    C-I, C-II, C-III
    apo(E)
31
Q
  1. Which apoproteins are associated with Lp(a)?
A
  1. B-100
    apo(a)
32
Q
  1. How many alleles does apo(E) have? name them
  2. Compare each allele’s affinity to the LDL receptor
  3. What allele is dysbetalipoproteinemia associated with? why?
  4. What allele is hyperocholesterolemia and CHD associated with? why?
  5. Which Apo(E) allele is associated with increased incidence of late-onset Alzheimer’s?
A
  1. 3 alleles: E2, E3, and E4
  2. E2 has least affinity
    E3 has neutral affinity (reference point)
    E4 has enhanced affinity
  3. E2, due to less efficient clearance of VLDL and chylomicrons
  4. E4, due to increased down regulation of LDL receptor
  5. E4 is associated with increased incidence of late-onset Alzheimer’s
33
Q
  1. What is the broad function of lipoproteins?
  2. What is the primary function of chylomicrons?
  3. What is the primary function of VLDL?
  4. What is the primary function of HDL?
  5. List the intermeidate lipoproteins that arise from metabolism of chylomicrons and VLDL
A
  1. Lipoproteins - transport lipids
  2. Chylomicrons - carry lipids from digestion
  3. VLDL - carry lipids synthesized in the liver
  4. HDL - reservoir of apoproteins and cholesterol reverse transport
  5. chylomicron and VLDL remnants, IDL, LDL, HDL2, and HDL3
34
Q
  1. What does LCAT stand for?
  2. From what molecules does LCAT transfer fatty acids?
  3. Where is LCAT synthesized?
  4. What lipoprotein does LCAT associate with?
  5. What apoprotein is responsible for activating LCAT?
A
  1. Lecithin cholesterol acyltransferase
  2. LCAT transfers fatty acid from sn-2 position of phosphatidylcholine (AKA LECITHIN) to cholesterol
  3. synthesized in the liver
  4. associates with HDL
  5. apoA-1 activates LCAT
35
Q
  1. What does CETP stand for?
  2. Where is CETP synthesized and secreted?
  3. Which lipoprotein does CETP associate with?
  4. What is CETP’s primary function?
A
  1. CETP - Cholesteryl ester transfer protein
  2. CETP is synthesized in liver and secreted into plasma
  3. CETP associates with HDL
  4. CETP transfers cholesteryl ester from HDL to VLDL, IDL, and LDL
36
Q
  1. What does PLTP stand for?
  2. Where does the protein reside?
  3. What is PLTP’s primary function?
A
  1. PLTP - Phospholipid transfer protein
  2. Plasma
  3. PLTP facilitates transfer of phospholipid from all the lipoproteins to HDL
37
Q
  1. What does LPL stand for?
  2. Where is LPL located and how does it maintain its position?
  3. Is LPL expressed by the adult liver?
  4. What is the primary function of LPL?
  5. What hormone stimulates LPL synthesis and transfer?
  6. Which tissue-specific LPL has a relatively large Km?
  7. Which tissue specific LPL has a relatively small Km?
  8. Which tissue has the highest concentration of LPL?
A
  1. LPL - Lipoprotein lipase
  2. LPL is anchored to the surface of capillary endothelial cells of adipose, skeletal msucle and heart muscle.
    It is non-covalently anchored via heparan sulfate.
  3. No
  4. LPL catalyzes stepwise hydrolysis of TAG to glycerol and 3 NEFA
  5. Insulin
  6. adipose tissue LPL has a relatively large km
  7. Heart tissue LPL has a relatively small Km
  8. Heart tissue has the highest concentration of LPL
38
Q
  1. What does HL stand for?
  2. Where is it located and how is it anchored?
  3. What is the primary function of HL
A
  1. HL - Hepatic Lipase
  2. on sinusoidal surface of liver cells, non-covalently bound to heparan sulfate glycoproteins
  3. HL hydrolyzes both TAG and phospholipids
39
Q
  1. What does ABC stand for?
  2. What are the two main types of ABC proteins and where are they located?
  3. What is their main function? and what significant purpose does this yeild?
A
  1. ATP-Binding Cassette transporter
  2. ABCA1 and ABCG1, they are plasma membrane proteins
  3. main function is to move cholesterol from the inner leaflet of the membrane to the outer leaflet using ATP hydrolysis. makes cholesterol avaialble for transfer to HDL
40
Q
  1. Where is the LDL receptor located?
  2. What is the receptor specifc to?
  3. What tissues is of primary importance to remove LDL?
  4. What happens when LDL binds to LDL receptor?
  5. What regulates synthesis of the LDL receptor?
A
  1. LDL receptor is located in plasma membrane in clathrin-coated pits
  2. specific to B-100 and/or apoE
  3. Liver tissue, adrenals and gonads are also important
  4. LDL is internalized and its contents are further metabolized
  5. cholesterol (will be covered later)
41
Q
  1. Where is PCSK9 synthesized and what is its destination?
  2. What is its main function?
  3. What happens to LDL receptor when PCSK9 is absent?
A
  1. PCSK9 is synthesized in the liver and secreted into the blood, where it can bind to an LDL recetpor
  2. controls proteolysis of internalized LDL receptor by targeting the receptor for lysosomes
  3. in absence of PCSK9
42
Q
  1. What does LRP stand for?
  2. How is it similar to LDL receptor, how is it different?
  3. In what tissues is LRP abundant
  4. What substrate does LRP recognize?
  5. Does intracellular cholesterol concentration affect LRP synthesis?
A
  1. LDL-receptor related protein
  2. similar structure, but not as specific for lipoproteins
  3. abundant in liver, brain, and placenta
  4. recognizes apoE
  5. no
43
Q
  1. What does SR-B1 stand for?
  2. where is SR-B1 expressed?
  3. what is its main function
  4. what is SR-B1 binding thought to result in?
A
  1. Scavenger receptor B1
  2. in the liver (and other cells)
  3. binds HDL via apoA-I; cholesteryl esters are transferred from HDL to liver
  4. thought to result in internalization of HDL
44
Q
  1. Where are chylomicrons formed?
  2. Where are lipids assembled
  3. Where are apoproteins synthesized?
  4. Where are chylomicrons assembled?
  5. What is the fate of nascent chlomicrons, and what are their identities?
A
  1. Chylomicrons are formed in intestinal epithelial cells
  2. lipids are assembled in the ER
  3. apoproteins are synthesized on RER
  4. chylomicrons are assembled in the golgi
  5. nascent chylomicrons are secreted to the lymph
    (apoA proteins and apoB48)
45
Q
  1. What apoproteins do chylomicrons accumulate in the bloodstream?
  2. where do they accumulate these from?
A
  1. they accumulate apoC and apoE
  2. apoC and apoE come from circulating HDL
46
Q
  1. what is apoC-II required for?
  2. what is apoC-III thought to inhibit? how?
A
  1. apoC-II is required for LPL activity
  2. apoC-III is thought to inhibit premature removal of chylomicrons from circulation by inhibiting binding to receptors (such as LDL receptor or LRP)
47
Q

in chylomicron metabolism…

  1. _____ removes 80-90% of TAG, which reduces the size of the chylomicrons
  2. Where are surface molecules transferered to? identify these surface molecules
A
  1. LPL
  2. Surface molecules are transferred to HDL
    (Phospholipids *requires PLTP*, cholesterol, and apoA and apoC
48
Q
  1. What do chylomicron remnants gain from HDL?
  2. Where are chylomicron remnants cleared from the blood?
  3. What lipoprotein receptors do the remnants bind to?
A
  1. more apoE and cholesteryl ester
  2. remnants are cleared from the blood by the liver
  3. remnants bind to LDL (B100/E) receptor due to apoE presence
    also to LRP
49
Q
  1. When are chylomicrons present?
  2. what is their half life?
  3. where do most of the lipids from chylomicrons go?
  4. Where do a minority of lipids from chylomicrons go?
A
  1. Chylomicrons are only present after a meal.
  2. The half-lfie of chylomicrons is less than 1 hour
  3. ~80% of the lipids go to heart, adpose, and muscle
  4. ~20% or less are uptaken by the liver
50
Q
  1. Where (generally speaking) are VLDL and LDL synthesized?
  2. Describe where their components are synthesized
  3. Describe (specifically) where VLDL is assembled
  4. Which lipoprotein and apoproteins are secreted into the bloodstream?
  5. What does the VLDL acquire in the bloodstream, and from where?
A
  1. VLDL and LDL are synthesized in the liver
  2. Lipids are assembled in the ER; apoproteins are synthesized ON the RER
  3. VLDL is assembled in the golgi
  4. Nascent VLDL, apoB-100, and small amounts of apoE and apoCs are secreted in the bloostream
  5. In the bloodstream, VLDL acquires apoE and apoC from HDL
51
Q
  1. How are TAGs removed from VLDL
  2. As VLDL becomes smaller, whichc omponents are transferred to HDL?
  3. Where do VLDL remnants (IDL) aqcuire cholesteryl ester from?
A
  1. TAGs are removed from VLDL via action of LPL of peripheral tissues
  2. apoC apoproteins, phospholipids and some TAGs (in exchange for choelsteryl ester) are transferred to HDL
  3. VLDL remnants (IDL) acquire some cholesteryl ester from HDL
52
Q
  1. What is responsible for removing VLDL remnants (IDL) from the bloodstream, and approximately what % of IDL are cleared by this?
  2. How is IDL internalized?
    Which IDLs are more likely to be internalized?
  3. Describe what happens to the other IDL that are not removed? include the role of hepatic lipase
  4. What happens to the excess apoE?
A
  1. VLDL remnants (IDL) may be removed by the liver, which removes ~50% of IDL that is removed from the blood.
  2. IDL binds to LDL (B100/E) receptor and is internalized.
    IDLs with multiple copies of apoE are more likely internalized.
  3. The other 50% that aren’t removed from the liver are remodeled to form LDL. IDL becomes anchored to hepatic lipase (HL). HL hydrolyzes TAG & phospholipids.
  4. apoE is transferred to HDL
53
Q
  1. LDL is realtively rich in ________ and ___________
  2. What apoprotein(s) associate with LDL?
  3. Compare/contrast the plasma half-life of chylomicron remnants, VLDL remnants, and LDL
A
  1. LDL is relatively rich in cholesterol and cholesterol ester
  2. LDL contains one molecule of apoB100 as its apoprotein component
  3. chylomicron remnants and VLDL remnants have short half lives
    LDL has a LONG plasma half-life, upt o several days
54
Q

1.

A
55
Q
  1. What are scavenger receptors and what is their substrate?
  2. Name an example of a known cell that expresses scavenger receptors
  3. How does the Km of scavenger receptors to their substrate compare to the Km of LDL receptor?
A
  1. Scavenger receptors are receptors that can bind an internalize LDL (alternatively from LDL receptor)
  2. macrophages express scavenger receptors
  3. scavenger receptors have ~ 5-7x higher Km (less affinity) than the LDL receptor
56
Q
  1. Where is HDL synthesized?
  2. Describe the general composition of Nascent HDL
  3. How is the composition different based one where it is synthesized?
A
  1. HDL is synthesized in the liver and intestine
  2. Nascent HDL is disc-shaped and phospholipid rich, with apoproteins
  3. From liver: has A1, A2, E, and C-apolipoproteins
    From intestine: only has A1
57
Q
  1. List the components that HDL acquires in circulation, and where these components are obtained from
  2. describe HDL’s reservoir function for other lipoproteins
A
  1. Cholesterol - from other lipoproteins & cells; HDL docks to cells via ApoA1 or ApoE; ABCA1 helps transfer cholesterol from outer leflet to the plasma membrane of HDL
  • *CETP** & LCAT are obtained from the plasma
    2. HDL also collects other apoproteins from other lipoproteins, serves as a reservoir for apoproteins needed by nascent chylomicrons and nascent VLDL
58
Q
  1. Describe the size and lipid content of HDL3
  2. How much LCAT activity is expressed in HDL3?
  3. Describe HDL3’s role in “reverse cholesterol transport” and the transition to HDL2
A
  1. HDL3 is small and relatively lipid poor
  2. HDL3 -> High LCAT activity
  3. HDL3 removes cholesterol, converting it to cholesteryl ester (CE)
    The CE rich HDL3 transfers CE to IDL, and chylomicron remnants in exchange for phospholipid and TAG
    As HDL accumulates TAG, it becomes a larger HDL2
59
Q
  1. Describe the process of HDL2 being regenerated to HDL3
A
  1. HDL2 is a substrate for HL
    HL hydrolyzes excess TAG and PL
    Liver SR-B1 binds the HDL2 and selectively transfers the CE to the liver cell
    HDL2 decreases in size to ultimately regenerate HDL3

S2B2 Cardiology (7 decks)

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