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U8 MCP > Blood Lipoproteins Lec 2 > Flashcards

Blood Lipoproteins Lec 2 Flashcards

1
Q

What are the lipoprotein complexes?

A 
Chylomicrons
very low density lipoproteins (VLDL)
intermediate density lipoproteins (IDLs)
low density lipoproteins (LDLs)
hight density lipoproteins (HDLs)
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2
Q

What is the purpose of lipoproteins?

A

to protect their hydrophobic cargo from aqueous env. while shuttling from tissue to tissue

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3
Q

What is in the core of the lipoprotein (the hydrophobic core)?

A

Triacylglycerol (TAG)

cholesterol esters

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4
Q

how is the density determined for lipoproteins?

A

protein to lipid ratio–ex: chylomicrons contain the highest % of lipid (primarily TAG) and the lowest % protein

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5
Q

When performing electrophoresis which lipoprotein particle is going to travel the furthest and which the least?

A

Furthest—HDL

Least– chylomicron

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6
Q

When performing ultracentrifugation which lipoprotein will sit on top and which will be at bottom?

A

Top- chylomicrons

bottome- HDL3

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7
Q

What are some of the functions of apoliproteins?

A

sites for cell surface receptors
enzyme activators involved in lipoprotein metabolism
some–structural components of the lipoprotein

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8
Q

Apo A-I-where is it synthesized and whats its function?

A

Liver and intestine

Structural protein in HDL

Activates LCAT- Transfers FA from lecithin to cholesterol to generate CE

Involved in RCT–transfer of cell cholesterol by ABCA1 to nascent HDL and delivery to liver

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9
Q

What is LCAT and what activates it?

A

transfers a FA from lecithin to cholesterol to generate CE–activity involved in maturation of HDL

Apo A-I activates it

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10
Q

Apo A-II where is it synthesized and whats its function?

A

Liver

Structural protein- HDL

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11
Q

Apo B-100 where is it synthesized and whats its function?

A

Liver
Structural protein-VLDL/LDL
VLDL assembly
LDLR binding

measurements of api B-100 in plasma reflect particle number and higher levels are associated with CVD

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12
Q

Apo B-48 where is it synthesized and whats its function?

A

Intestine

Chylomicron formation and secretion

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13
Q

Apo C-I where is it synthesized and whats its function?

A

Liver

LCAT activator–transfers FA from lecithin to cholesterol to generate CE–maturation of HDL

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14
Q

Apo C-II where is it synthesized and whats its function?

A

Liver

LPL activator

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15
Q

Apo C-III where is it synthesized and whats its function?

A

Liver

LPL inhibitor

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16
Q

Apo E (E2, E3, E4) where are they synthesized and whats their function?

A

Recognition by LDL and CM remnant receptors–mediates the hepatic uptake of CM and VLDL remnants as well as IDL

Responsible for clearance of intestinal derived LPs after a meal and for the clearance of VLDL and IDL before they are covered to LDL

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17
Q

What Apo E is a risk for dysbetalipoproteinemia (type III hyperlipidemia) ? and what is seen in the plasma?

A

Apo E2–characterized by elevation of CM and VLDL remnants in the plasma

18
Q

Apo(a) where is it synthesized and whats its function?

A

Liver

modulates thrombosis/thrombolysis

19
Q

Where are the enzymes involved in the synthesis of the TAG, cholesterol and phospholipids found for chylomicron metabolism?

A

Smooth ER–> microsomal triglyceride transfer protein (MTP)–loads Apo B-48 with lipid

20
Q

What enzyme loads Apo B-48 with lipid?

A

microsomal triglyceride transfer protein (MTP)

21
Q

When the nascent chylomicron reaches the blood it receives what?

A

Apo-E and Apo-C

22
Q

What does Apo-C II come in contact with in the blood and what does this cause?

A

LPL–activation

-hydrolyzes TAG–yielding fatty acids/glycerol

23
Q

What occurs after the FAs are formed and all thats left is a chylomicron remnant?

A

Remnant taken up by liver by Apo-E binding to specific lipoprotein receptors followed by endocytosis/lysosomal hydrolytic enzymes degrading remnant components to cholesterol/AAs/FAs

24
Q

Where does Apo C-II bind to the LPL?

A

The C terminal domain–provides specificity

25
Q

In the fed state (elevated insulin) adipose tissue does what and muscle tissue does what? what occurs in the fasted state?

A

Adipose tissue–LPL expression is increased
Muscle– LPL is decreased

Fed– Adipose LPL decreased
Muscle–LPL increased

26
Q

When pts have deficiency of LPL or Apo C-II what occurs and what are the pts at risk of?

A

Type 1 hyperlipoproteinemia/familial LPL deficiency

Accumulation of chylomicron TAG in plasma

Higher risk for pancreatitis

27
Q

What Nascent particles are present on VLDLs after they are produced by the liver?

A

Apo B-100

28
Q

What do HDL particles supply to VLDLs?

A

Apo E and Apo C-II

29
Q

What does cholesterol ester exchange protein (CETP) facilitate?

A

Exchange of TAGs from VLDL to HDL for cholesterol esters

Greater concentration of TAG contacting lipoprotein parcels in blood the greater the exchange

30
Q

How does nonalcoholic fatty liver (hepatic steatosis) occur?

A

conditions where there is an imbalance btwn TAG synthesis and secretion of VLDL

31
Q

What do pts with homozygous E2 deficiency have?

What occurs in these pts?

A

can’t clear chylomicrons or IDL–this is type III hyperlipoproteinemia

hypercholesterolemia and premature atherosclerosis

32
Q

Apo E-4 is related to what dz?

A

Alzheimer’s

33
Q

If cholesterol is not needed right away what occurs and how does it occur?

A

Cholesterol is estterified by Acyl CoA: cholesterol acyl transferase(ACAT)

get increased ACAT activity with increased intracellular cholesterol

+ fatty acid to C3–replaces OH to form cholesterol ester

34
Q

What is the function of the LDL particle?

A

to provide cholesterol to the peripheral tissues and return it to the liver

35
Q

What do LDL receptors recognize on the LDL particles?

A

Apo B- 100 and Apo E

36
Q

What is type II hyperlipidemia/familial hypercholerolemia?

A

Deficiency of LDL receptor–causing elevated plasma LDL-cholesterol

37
Q

What causes the conformational change causing release of LDL from it receptor?

A

ph dependent conformational change at region 2 of the LDL receptor

38
Q

Where and how are HDLs formed?

A

formed in blood by addition of lipids to api A-1 which is synthesized in the liver and intestine and secreted in the blood

39
Q

What does HDL supply?

A

circulating supplier of api C-II and Apo E

40
Q

What is Tangier disease?

A

rare deficiency in ABCA1–leading to absence of HDL particles because of degradation of lipid-free apo A-I

41
Q

What is reverse cholesterol transport?

A

Transfer of cholesterol from peripheral cell to HDL–from HDL to liver for bile acid/salt synthesis

U8 MCP (10 decks)

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