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Biochemistry Block 3 > Lipoprotein Metabolism > Flashcards

Lipoprotein Metabolism Flashcards

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

A

Apo C-II

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
Q

VLDL

  1. Assembled where?
  2. Cholesterol or cholesterol ester
  3. What type of apoprotein
  4. Where does it go once synthesized
A
  1. Liver cells
  2. Cholesterol
  3. Apo B-100 (essential for removal of LDL)
  4. Blood
26
Q

Main lipid component of both chylomicrons and VLDL

A

TAG

27
Q

Function of ACAT

A

Converts cholesterol to cholesterol ester

28
Q
  1. Decreased cholesterol in the cell activates what two things?
  2. Inhibits what?
A
  1. LDL receptor gene expression, HMG CoA reductase
  2. ACAT

~opposite for increased cholesterol in cells

29
Q

Deficiency of LDL receptor causes?

A

Increase in plasma LDL, thus an increase in plasma cholesterol

(LDL receptor aids in cellular uptake/ degradation of LDL)

30
Q

When the pH of the endosomes (vesicles containing LDL) fall what happens to LDL?

After this happens, what happens to the remnant of LDL?

A

LDL separates from its receptor-CURL

Transferred to lysosome for degradation

31
Q

What happens to free cholesterol if it is not utilized?

A

It becomes esterified by ACAT and stored as cholesterol ester

32
Q

What is woolmans disease?

A

Inability to hydrolyse lysosomal cholesterol esters by cholesterol esterase

33
Q

What is Niemann-Pick disease?

A

Inability to transport unesterified cholesterol out of the lysosomes

34
Q

What is familial hypercholesterolemia (type II hyperlipidemia) what does it cause

A

LDL receptor deficiency (genetic or dietary); raises LDL level

35
Q

Name 3 enzymes activated by free cholesterol

A

ACAT, LCAT, and PCAT

36
Q

Function of scavenger receptor Class A (SR-A)

A

Endocytosis of chemically modified LDL in which lipid component or ApoB has been oxidized

37
Q

VLDL and CM require what two lipoproteins?

Where do they get them from

A

Apo C-II and Apo E

HDL

38
Q

Function of nascent HDL

What enzyme functions to do this

A

Take up unesterified cholesterol and esterify them

LCAT

39
Q

What activates LCAT activity

A

Apo A1

40
Q

What binds to HDL to facilitate uptake of cholesteryl esters?

How does it bind to HDL

A

SR-B1

Via Apo A

41
Q

SR-B1 synthesis is upregulated for ?

A

Steroidogenesis

42
Q

LCAT

  1. Bound to?
  2. Function
  3. What does it promote?
A
  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
Q

HDL and IDL make an exchange. What is the exchange

What is needed in order to make this exchange

A

HDL gives cholesteryl esters to IDL
IDL gives TAG and phospholipids to HDL

CETP

44
Q

Tangier disease:

  1. Caused by
  2. Will cause
  3. How does it present
A
  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
Q

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
A
  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
Q

Type IIA Hyperlipidemia

  1. Defect in?
  2. Biochemical findings?
  3. Features?
A
  1. LDL receptor
  2. Increased LDL and increased cholesterol
  3. High risk of atherosclerosis, xanthomas of achilles tendon
47
Q

Type IV Hyperlipidemia

  1. Defect in?
  2. Biochemical findings?
  3. Features?
A
  1. Insulin deficiency
  2. LPL will be inactive, increased TAG
  3. Most common hyperlipidemia, associated with obesity, DM, and alcoholism
48
Q

Abetalipoproteinemia/Bassen-Kornzweig syndrome

  1. Defect in which protein?
  2. This protein is necessary for?
  3. Deficiency leads to lack of
  4. Characterized by
A
  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

Biochemistry Block 3 (11 decks)

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