Lipoprotein Metabolism Flashcards

(48 cards)

1
Q

2 places where lipids are synthesized

A

Liver and intestine

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2
Q

How are triglycerides transported in plasma

A

Lipoproteins

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3
Q

Classifications of the lipoproteins

A

All same components, just different %

Chylomicrons - most fat, least protein
HDL- least fat, most protein

HDL is smallest and most dense

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4
Q

Give other names for the following

  1. VLDL
  2. LDL
  3. HDL
A
  1. Pre beta lipoprotein
  2. Beta lipoprotein
  3. Alpha lipoprotein
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5
Q

What is an apoprotein

Function

A

Protein component of a lipoprotein

Mostly present on the surface; act as surface receptors

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6
Q

Name where each of the following apoproteins are present:

  1. Apo A-1
  2. Apo B-48
  3. Apo B-100
  4. Apo C-II
  5. Apo E
A
  1. LCAT
  2. Chylomicrons
  3. VLDL and LDL
  4. Lipoprotein lipase activator
  5. IDL and chylomicrons
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7
Q

Difference between structure of Apo B-48 and Apo B-100

A

They are both from the same B gene, 48 is only 48% transcribed and 100 is 100% transcribed

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8
Q

List the lipoproteins in order of which has the highest cholesterol to lowest cholesterol

List them from highest TAG to lowest TAG

A

LDL, HDL, VLDL, chylomicrons

Chylomicrons, VLDL, LDL, HDL

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9
Q

HDL

  1. Generated by
  2. Function
A
  1. Liver and intestine

2. Delivers cholesterol to the liver for elimination

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10
Q

LDL

  1. Generated by
  2. Function
A
  1. VLDL

2. Deliver cholesterol to peripheral tissues

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11
Q

VLDL

  1. Generated by
  2. Function
A
  1. Liver

2. Deliver de novo TAG to peripheral tissues

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12
Q

Chylomicrons

  1. Generated by
  2. Function
A
  1. Intestine

2. Deliver dietary TAG to peripheral tissues

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13
Q

How does an immature chylomicron become mature

What is the only component that an immature already has

A

Acquires Apo C-II and Apo E from HDL

Immature chylomicron has Apo B48

~immature VLDL has Apo 100 and also has to acquire apo C-II and apo E

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14
Q

Immature chylomicrons are produced from

A

Dietary lipids

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15
Q

Once chylomicron is mature it enters circulation where it is acted on by

A

Lipoprotein lipase (in muscle/adipose)

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16
Q

Lipoprotein lipase converts chylomicron to chylomicron remnant. In this process, what does it release

A

Glycerol to liver (which can form DHAP), FFAs, and Apo C-II (which is returned back to HDL)

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17
Q

What is required in order for packaging of lipoprotein

A

MTP

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18
Q

When will serum be milky?

A

After a high fat meal, chylomicrons will temporarily cause serum to become milky

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19
Q

Chylomicron remnant is taken up by liver by

A

Apo E receptors

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20
Q

Lipoprotein lipase works on which lipoproteins

A

VLDL and chylomicrons

21
Q

If chylomicrons are still in your blood after not eating for ~5+ hours, what does that indicate

A

MTP or Apo B-48 are defective

22
Q

Lipoprotein lipase:

  1. Converts chylomicrons to
  2. Converts VLDL to
A
  1. Chylomicron remnant

2. IDL

23
Q

What activates lipoprotein lipase

24
Q

Chylomicrons

  1. Assembled where?
  2. Cholesterol or cholesterol ester
  3. What type of apoprotein
  4. Where does it go once synthesized
A
  1. Intestinal mucosal cells
  2. Cholesterol ester
  3. Apo B48 and Apo E
  4. Lymphatic circulation
25
VLDL 1. Assembled where? 2. Cholesterol or cholesterol ester 3. What type of apoprotein 4. Where does it go once synthesized
1. Liver cells 2. Cholesterol 3. Apo B-100 (essential for removal of LDL) 4. Blood
26
Main lipid component of both chylomicrons and VLDL
TAG
27
Function of ACAT
Converts cholesterol to cholesterol ester
28
1. Decreased cholesterol in the cell activates what two things? 2. Inhibits what?
1. LDL receptor gene expression, HMG CoA reductase 2. ACAT ~opposite for increased cholesterol in cells
29
Deficiency of LDL receptor causes?
Increase in plasma LDL, thus an increase in plasma cholesterol (LDL receptor aids in cellular uptake/ degradation of LDL)
30
When the pH of the endosomes (vesicles containing LDL) fall what happens to LDL? After this happens, what happens to the remnant of LDL?
LDL separates from its receptor-CURL Transferred to lysosome for degradation
31
What happens to free cholesterol if it is not utilized?
It becomes esterified by ACAT and stored as cholesterol ester
32
What is woolmans disease?
Inability to hydrolyse lysosomal cholesterol esters by cholesterol esterase
33
What is Niemann-Pick disease?
Inability to transport unesterified cholesterol out of the lysosomes
34
What is familial hypercholesterolemia (type II hyperlipidemia) what does it cause
LDL receptor deficiency (genetic or dietary); raises LDL level
35
Name 3 enzymes activated by free cholesterol
ACAT, LCAT, and PCAT
36
Function of scavenger receptor Class A (SR-A)
Endocytosis of chemically modified LDL in which lipid component or ApoB has been oxidized
37
VLDL and CM require what two lipoproteins? Where do they get them from
Apo C-II and Apo E HDL
38
Function of nascent HDL What enzyme functions to do this
Take up unesterified cholesterol and esterify them LCAT
39
What activates LCAT activity
Apo A1
40
What binds to HDL to facilitate uptake of cholesteryl esters? How does it bind to HDL
SR-B1 Via Apo A
41
SR-B1 synthesis is upregulated for ?
Steroidogenesis
42
LCAT 1. Bound to? 2. Function 3. What does it promote?
1. HDLs and LDLs in plasma 2. Esterifies cholesterol on surface of lipoprotein; cholesteryl ester moves to interior of lipoprotein 3. Flux of cholesterol from cell membranes into HDL
43
HDL and IDL make an exchange. What is the exchange What is needed in order to make this exchange
HDL gives cholesteryl esters to IDL IDL gives TAG and phospholipids to HDL CETP
44
Tangier disease: 1. Caused by 2. Will cause 3. How does it present
1. Defect in cholesterol transport out of cells; defects in ABC-A1 2. HDL levels will be half the normal amount 3. Build up of cholesterol in tonsils, liver, spleen, peripheral neurons; foam cells observed
45
Type I Hyperlipidemia 1. Defect in? 2. Biochemical findings? 3. Features? 4. What will it not cause 5. Mortality from this is typically caused by
1. LPL or Apo C-II deficiency 2. Increased chylomicrons and increased TAG 3. Red/orange eruptive xanthomas, fatty liver/spleen, acute pancreatitis 4. Will not lead to atherosclerosis 5. Pancreatitis
46
Type IIA Hyperlipidemia 1. Defect in? 2. Biochemical findings? 3. Features?
1. LDL receptor 2. Increased LDL and increased cholesterol 3. High risk of atherosclerosis, xanthomas of achilles tendon
47
Type IV Hyperlipidemia 1. Defect in? 2. Biochemical findings? 3. Features?
1. Insulin deficiency 2. LPL will be inactive, increased TAG 3. Most common hyperlipidemia, associated with obesity, DM, and alcoholism
48
Abetalipoproteinemia/Bassen-Kornzweig syndrome 1. Defect in which protein? 2. This protein is necessary for? 3. Deficiency leads to lack of 4. Characterized by
1. Microsomal triglyceride transfer protein gene; these synthesize of beta lipoproteins 2. Absorption of fat, cholesterol and ADEK 3. Apo B48 and Apo B100 4. Increased content of sphingomyelin and decreased content of lecithin