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The Science of Lipidology: Lipid Metabolism, Pathogenesis of Atherosclerosis and Genetic Disorders > Module 1: Deck 1/Questions 1-7 > Flashcards

Module 1: Deck 1/Questions 1-7 Flashcards

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1
Q

What are the four major lipoprotein particles? 4

A
  1. chylomicrons 2. very low density lipoproteins 3. low density lipoproteins 4. high density lipoproteins
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2
Q

What are the largest lipoproteins?

A

chylomicrons

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3
Q

What characterized chylomicronemia syndrome? 5

A
  1. abdominal pain 2. hepatosplenomegaly 3. pancreatitis 4. eruptive xanthomas 5. lipemia retinalis
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4
Q

Conditions that exacerbate hypertriglyceridemia? 7

A
  1. poorly controlled DM 2. excessive alcohol intake 3. atherogenic diets 4. hypothyroidism 5. nephrotic syndrome 6. HIV 7. other insulin resistance states
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5
Q

Commonly implicated drugs associated with hypertriglyceridemia? 5

A
  1. estrogens 2. tamoxifen 3. glucocorticoids 4. HIV drug therapies 5. isotretinoin
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6
Q

How are Chylomicrons formed? 1

A
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7
Q

How are chylomicrons formed? 2

A
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8
Q

Following ingestion of a fatty meal, dietary lipid are emulsified by (1) into mixed (2) which are hydrolyzed by (3) in the (4). About 50% of luminal cholesterol, the majority of which is (5) in origin, is absorbed into (6) each day. Absorption of free cholesterol and non-cholesterol plant sterols is facilitated by (7). Luminal TG are broken down into (8). These (9) are then absorbed from the (10) into the (11). The enterocyte, free cholesterol is esterfied into (12) by (13).

A
  1. bile salts
  2. micelles
  3. pancreatic lipases
  4. Proximal small intestine
  5. biliary
  6. enterocytes
  7. Niemann-Pcik C1-Like 1 (NPC1L1) protein
  8. 2 monotriglyceride and fatty acids
  9. fatty acids
  10. lumen
  11. enterocyte
  12. cholesteryl esters
  13. acyl-coenzyme A (CoA): cholesterol acyltransferase-2 (ACAT-2).
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9
Q

The great majority of absorbed plant sterold are transported back into the (1) by the ATP binding cassette transporter (2). Fatty acids combine with (3) to form triglycerides. (4) combines with cholesteryl esters; triglycerides that are incorporated via microsomal triglyceride transfer protein, apolipoprotein A-I, and apolipoprotein A-IV to form (5), that are secreted into the (6) and subsequently, into the (7).

A
  1. intestinal lumen
  2. G5/G8 protein
  3. glycerol
  4. ApoB-48
  5. nascent chylomicrons
  6. intestinal lymphatics
  7. systemic circulation
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10
Q

Nascent chylomicrons are formed from what ? 3

A

Triglycerides that are incorporated via microsomal triglyceride transfer protein, apolipoprotein A-I, and apolipoprotein A-IV to form

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11
Q

G5/G8 protein is what kind of transporter?

A

ATP binding cassette transporter

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12
Q

Following nascent chylomicrons are are secreted into the circulation, their premature clearance is prevented by?

A

Apo B-48

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13
Q

Apo B-48 facilitates the binding of what? and prevents what?

A
  1. lipids to chylomicrons
  2. receptor-mediated hepatic re-uptake
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14
Q

Once the circulation, nascent chylomicrons acquire apos (4) from what?

A
  1. Apos C-I, C-II, C-III and E
  2. From HDL particles
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15
Q

What is the most important enzyme in the catabolism of chylomicrons?

A

lipoprotein lipase

(LPL)

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16
Q

What facilitates the interactoin between LPL and TG carrying lipoproteins?

A

ApoE

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17
Q

How does Apo E facilitate the interaction b/w LPL and TG carrying lipoproteins?

A

presumably by

  1. slowing the movement of these lipoproteins along the capillary endothelium and
  2. ehancing their interaction with the endothelial cell proteoglycans
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18
Q

LPL’s ability to hydrolyze chylomicrons is facilitaed by co factors? 2

A

Apo C-II and Apo A-V

(Apo C-III is an inhibitor of LPL)

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19
Q

Following free fatty acid release from chylomicrons, (1), rich in (2) are formed.

A
  1. chylomicron remnants
  2. esterfied cholesterol and Apo E
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20
Q

How does chylomicron remnant uptake occur?

2

A
  1. via receptor mediated endocytosis through the interaction of apo E with the chylomicron remnant receptor (also known as the LDL receptor-like protein (LRP)) or
  2. via the hepatocyte LDL receptor.
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21
Q

What component is required for the hepatic assembly of VLDL particles?

A

microsomal TG transfer protein

22
Q

The liver produces VLDL particles that provide an additonal source of circulating fatty acids and deliver cholestrerol, via catabolism of LDL particles, to what?

A

peripheral tissues

23
Q

VLDL assembly requires what? 3

A
  1. cholesteryl esters
  2. TG
  3. Apo B-100
24
Q

How does the process of VLDLassembly begin?

A

when apo B-100 is translocated to the endoplasmic reticulum and interacts with microsomal TG transfer protein (MTP)

25
Q

MTP-driven lipidation gives rise to (1) which is retained in the (2) through interaction with chaperones if not further processed to become (3)

A
  1. pre-VLDL
  2. ER
  3. VLDL2
26
Q

Lipid poor VLDL2 exits the ER and is ether converted to (1) in the (2) through addition of (3) or is (4)

A
  1. large TG rich VLDL1
  2. Golgi apparatus
  3. TG
  4. secreted
27
Q

(1) and (2) are involved in lipoprotein catabolism but not VLDL assembly.

A
  1. hepatic lipase
  2. endothelial lipase
28
Q

The LDL receptor is involved in the clearnace of (1)

A
  1. apoB containing lipoproteins
29
Q

The expression of apoB100 is regulated by what?

A

proteolytic degradation

30
Q

As with chylomicrons, the activity of lipoprotein lipase (LPL) is facilitated by what? (2)

A

Co factors apo C-II and Apo A-V

31
Q

Where is lipase maturation factor found and what is it involved in?

A

LMF1 is a protein residing in the endoplasmic retitulum and is involvedin the maturation and transport of LPL though the secretory pathway.

32
Q

What is the primary enzyme involvedin the chylomicron and VLDL catabolism?

A

LPL

33
Q

What is the predominent cofactor that promotes LPL activity? What else acts synergistically with this? (possibly by facilitating the interaction between LPL and TG ricj lipoproteins)

A
  1. Apo C-II
  2. Apo A-V
34
Q

What does GPIHP1 do?

A

promotes vascular adherence of LPL and Tg rich lipoproteins to vascular endothelium. (acts as a stablizing platform for LPL)

35
Q

What is Apo C-III gene synthesis and expression stimulated by?

3

A
  1. glucose via hepatic nuclear factor 4-alpha
  2. and the carbohydrate response binding element protein.
  3. plasma fatty acids
36
Q

What does Apo C-III inhibit? (1-3)

What specifically do these metabolic derangements often accompany? (4)

A
  1. the activity of lipoprotein lipase
  2. hepatic uptake of the VLDL and chylomicrons remnants
  3. increases VLDL assembly
  4. poorly controlled DM 2
37
Q

Loss of function mutations in apo C-III were shown to be associated with what? 2

A

lower TG levels and a reduced ASCVD risk

This is generally accepted for ANGPLT4 loss of function mutations as well.

38
Q

Where is angiopoietin-like protein 3 (ANGPTL3) expressed predominantly?

Under the control of what?

It has been shown to inhibit what?

A
  1. liver
  2. peroxisome proliferator activated receptors
  3. LPL activity
39
Q

Where is ANGPTL4 synthesized (3) and where is it secereted?

Under the control of what?

A
  1. liver, heart, muscle
  2. liver X receptor
40
Q

What does angiopoietin-like protein 4 inhibit?

A

TG clearance

41
Q

ANGPTL4 is a noncompetitive inhibitor of LPL that acts, at least in part, by how?

A

dissociating catalytically active LPL dimers in to inactive LPL monomers

42
Q

Lipoprotein maturation factor 1 (LMF1) resides in the ER and is essential to the folding and assembly of several lipases, including ? (3)

A
  1. LPL
  2. hepatic lipase
  3. endothelial lipase
43
Q

What are mutations in LMF1 associated with? 2

A

lipase deficiency and hypertriglyceridemia

44
Q

What is a disorder associated with severe hypertriglyceridemia, hyperchylomicronemia and pancreatitis and is a rare autosomal recessive disorder that presents in childhood or early adolescence and is associated with loss of function mutations in genes regulating the catabolism of TG rich proteins?

What are these enzymes that these genes affect (TG rich lipoproteins)? 6

A

Monogenic hypertriglyceridemia

  1. LPL
  2. apo-C II
  3. Apo A-V
  4. LMF1
  5. GPIHBP1
  6. GDP1
45
Q

What is ABCA1?

what does it do?

A
  1. a cholesterol efflux regulatory protein
  2. mediates the efflux of cholesterol to lipid poor apolipoproteins
46
Q

What is GHIHBP1?

A

is the protein that acts as a stablizing platform for LPL as it interacts with TG rich lipoproteins.

47
Q

A proposed mechanism for elevated TG levels as a marker for increased ASCVD risk is?

A

LIke LDL particles, remnant particles deliver their cholesterol cargo to the arterial wall.

48
Q

Remnant cholesterol is a measure of what?

Fasting state and then non fasting state

A

the cholesterol content of VLDL particles and intermediate density lipoprotein particels in the fasting state

and of the VLDL particles and IDL plus chylomicron remnants in the non fasting state when one calculates LDL-C using the Friedewalk equation.

49
Q

How is remnant cholesterol calculated?

A

RC = TC - HDLC - LDLC

50
Q

Why specifically are TG particles atheroslcerotic?

A

because they are larger than LDL particles, they can deliver 5-20 times more cholesterol per particle

In addition, unlike LDL particles, which require oxidation or other modification to be taken up by arterial wall macrophages, remnant particles do not require oxidation and are taken up in an unregulated fashion.

51
Q

What does the unregulated uptake of TG in the arterial wall promote?

A

foam cell formation and atherosclerotic progression

52
Q

Why does estogen estrogen increase TG?

A

Estrogen decreases hepatic lipase activity, an effect that reduces the hydrolysis of VLDL, HDL, LDL and TG

Also it can increase hepatic TG synthesis and hepatic VLDL secretion

The Science of Lipidology: Lipid Metabolism, Pathogenesis of Atherosclerosis and Genetic Disorders (5 decks)

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