MMT: lipoprotein metabolism Flashcards

1
Q

What is the exogenous lipoprotein?

A

Chylomicrons

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2
Q

Once chylomicrons donate their TGs, where do they go?

A

Back to the liver

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3
Q

What is the endogenous lipoprotein?

A

VLDL

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4
Q

What happens to VLDL remnants?

A

They return to the liver as LDL or deposit in extrahepatic tissues as LDL

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5
Q

Which lipoprotein is involved in reverse cholesterol transport?

A

HDL

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6
Q

Arrange lipoproteins in terms of size (large to small).

A
  1. Chylomicrons
  2. VLDL
  3. IDL
  4. LDL
  5. HDL
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7
Q

The density of lipoproteins is largely due to…

A

Protein; high density have the most protein and least TGs

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8
Q

What does ApoA-I do?

A

Activates LCAT that helps but cholesterol into HDL

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9
Q

Where is ApoA-I found?

A

HDL

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10
Q

Where is ApoA-II found?

A

HDL

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11
Q

Where is ApoA IV found?

A

Chylomicrons and HDL

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12
Q

Where is ApoB-48 found?

A

Chylomicrons

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13
Q

Where is ApoB-100 found?

A

VLDL and LDL

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14
Q

Where is ApoC-I found?

A

VLDL and HDL

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15
Q

Where is ApoC-II found?

A

Chylomicrons, VLDL, HDL

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16
Q

Where is ApoC-III found?

A

Chylomicrons, VLDL, HDL

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17
Q

What does ApoC-III do?

A

Inhibits LPL

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18
Q

Where is ApoD found?

A

HDL

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19
Q

Where is ApoE found?

A

Chylomicrons, VLDL, HDL

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20
Q

What does ApoE do?

A

Trigger clearance of VLDL and chylomicron remnants

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21
Q

Which apolipoprotein is associated with Abetalipoproteinemia?

A

ApoB

22
Q

Where does chylomicron acquire ApoE and ApoC-II?

A

HDL

23
Q

Where is VLDL synthesized?

A

Liver

24
Q

What does VLDL do?

A

Transport TGs and cholesterol from the liver to other tissues

25
Q

How does VLDL acquire ApoC-II and ApoE?

A

From HDL

26
Q

What is abetalipoproteinemia?

A

A condition caused by MTP defect that results in ApoB proteins not being released from ER and added to chylomicrons and VLDL

27
Q

What are symptoms of abetalipoproteinemia?

A

Lipid malabsorption, caloric deficiency, lipid soluble vitamin deficiency

28
Q

What is lost in the conversion of VLDL to IDL?

A

ApoC-II

29
Q

Hepatic lipase can interact with…? What is lost in this process?

A

IDL; ApoE

30
Q

Describe the life cycle of LDL.

A
  1. ApoB-100 on LDL interacts with LDLR on hepatocyte or peripheral tissue
  2. LDL is endocytosed and put in an endosome, where it separates from the LDLR
  3. LDL combines with a lysosome, and it is degraded
  4. Cholesterol is deposited in tissue
  5. Receptor is recycled
31
Q

In hepatocytes, what regulates degradation of LDLR?

A

PCSK9

32
Q

How does PCSK9 work?

A

It binds to the receptor and causes it to stay in the endosome after endocytosis, causing it to be degraded as opposed to recycled

33
Q

What is SREBP?

A

A transcription factor for lipids

34
Q

What is Lp(a)?

A

A lipoprotein that can bind to ApoB-100 and increase risk of cardiovascular disease

35
Q

What lipoprotein is involved in reverse cholesterol transport?

A

HDL

36
Q

Nascent HDL originates from…

A

Liver and small intestine

37
Q

What proteins are found on HDL?

A

ApoA-I, ApoC-II, ApoE, LCAT, and ABCA1

38
Q

What does LCAT do?

A

Convert cholesterol to cholesterol esters to pack them into HDL

39
Q

What activates LCAT?

A

ApoA-I

40
Q

What receptor allows cholesterol to be transferred into hepatocytes?

A

SR-B1

41
Q

What is CETP?

A

Transfers lipids from HDL to VLDL

42
Q

Type I hyperlipidemia: cause, what is in excess?

A

Cause: LPL or ApoC-II deficiency
Excess: chylomicrons

43
Q

Type IIa hyperlipidemia: cause, what is in excess?

A

Cause: LDL receptor deficiency or ApoB100 defect
Excess: LDL

44
Q

Type IIb hyperlipidemia: cause, what is in excess?

A

Cause: decreased LDL receptor or increased ApoB-100
Excess: LDL and VLDL

45
Q

Type III hyperlipidemia: cause, what is in excess?

A

Cause: ApoE deficiency
Excess: chylomicron remnants and IDL

46
Q

Type IV hyperlipidemia: cause, what is in excess?

A

Overproduction of VLDL
Excess: VLDL

47
Q

Type V hyperlipidemia: cause, what is in excess?

A

Cause: increased VLDL production and decreased LPL
Excess: chylomicrons and VLDL

48
Q

A patient has pancreatitis, cloudy plasma with a creamy top layer, hepatosplenomegaly, and eruptive xanthomas. What familial hyperlipidemia do they have?

A

Type I

49
Q

How do we diagnose type I hyperlipidemia?

A

TG count

50
Q

A patient has tendinous xanthomas and atherosclerosis. What hyperlipidemia do they have?

A

Type IIa

51
Q

A patient has palmar xanthomas and tuberoeruptive xanthoma. What familial hyperlipidemia do they have?

A

Type III