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Kris 307 > Textbook and Required Readings (Midterm) > Flashcards

Textbook and Required Readings (Midterm) Flashcards

1
Q

What are the three principal lipid components of bile?

A

Bile salts, pancreatic lipase, and sterols

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2
Q

Which fatty acids are resistant to hydrolysis by lipase?

A

FAs linked at the sn-2 position of MGs, PLs, and CEs

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3
Q

Under what form is cholesterol present in bile?

A

Unesterified form

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4
Q

Where is biliary cholesterol absorbed?

A

At a site more proximal than diet-derived cholesterol within the small intestine

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5
Q

What are the hydrophilic components in lipoproteins?

A

Phospholipid polar head groups and cholesterol hydroxyl groups

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6
Q

What forms the core of lipoprotein molecules?

A

Hydrophobic cholesterol esters and triglycerides

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7
Q

What does the exogenous transport system transfer?

A

Transfers lipids of intestinal origin to peripheral and hepatic tissues

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8
Q

What is the relation between MTP and Apo-B?

A

MTP transfers lipids onto nascent Apo-B particles to create chylomicrons

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9
Q

What do chylomicron TG-depleted remnant particles take up? Where are they taken?

A
  • Take up CE from HDLs

- Rapidly taken up by the liver

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10
Q

What is the function of ABCA1?

A

Mediate the efflux of cellular cholesterol and phospholipids to lipid-poor HDL

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11
Q

Where is Apo E synthesized? Where is it present?

A
  • In the liver

- On all forms of lipoproteins

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12
Q

Why is Apo E important?

A

In the hepatic clearance of TG-depleted chylomicron remnants

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13
Q

Where is LDL cleared from the plasma?

A
  • Liver
  • Adipocytes
  • Smooth muscle cells
  • Fibroblasts
  • All contain the LDLR
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14
Q

As HDL becomes enriched with CE, ______ and ______ are picked up from other proteins to form spherical HDL.

A

Apo-C-II and Apo-C-III

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15
Q

What does CETP exchange?

A
  • CE from HDL2 to VLDL and CM

- TG from VLDL and CM to HDL2

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16
Q

As a result of CETP’s action, what does HDL2 convert to?

A

Reconverts to HDL3

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17
Q

What is the consequence of manipulating ER calcium?

A
  • Causes the re-distribution of a portion of intracellular UC to a pool that is NOT available to the SCAP-SREBP complex
  • Not directly accessible to the components of the cholesterol-sensing mechanism
18
Q

What kind of nuclear receptors are steroid receptors?

A

Homodimers

19
Q

What kind of nuclear receptors are RXR receptors?

A

Heterodimer

20
Q

How do co-regulators influence transcription?

A

Through chromatin remodeling with histone modifications

21
Q

What is the consequence of increased function of LXR?

A

Decreases cholesterol from the GI tract

22
Q

What are the two properties of the LDL receptor?

A
  • Allows large amounts of cholesterol to be delivered to the body
  • Keeps concentration of LDL in the blood low enough to avoid buildup (plaques)
23
Q

What is the second messenger responsible for suppressing HMGR activity?

A

Cholesterol generated from LDL within the lysosome

24
Q

What lipoproteins does LDLR bind?

A
  • Apo B-100

- Apo E

25
Q

Where is the largest amount of LDL receptors found?

A

In the liver

26
Q

How is FH related to SREBP?

A
  • Mutations in the sterol-sensing region of SCAP blocks sterol regulation in SREBP processing
  • Activates SRE responsive genes (HMGCR, LDLR) if it senses low cholesterol (as it is in FH)
27
Q

How does LXR increase fatty acid synthesis?

A

By inducing SREBP-1c

28
Q

Which SREBP is implicated in glucose metabolism?

A

SREBP-1c

29
Q

How does vitamin A regulate the expression of specific target genes?

A

Through its binding to nuclear RARs and RXRs

30
Q

Where is Apo E synthesized?

A

In the liver

31
Q

What does HDL exchange with chylomicrons in circulation?

A
  • HDL exchanges Apo E and Apo C

- CM exchange Apo A-I and Apo A-IV

32
Q

What does CETP convert?

A

HDL2 to HDL3

33
Q

What is the consequence of CETP deficiency?

A

Causes high plasma levels of HDL

34
Q

What is the consequence of Tangier disease? What is it caused by?

A
  • Nearly total absence of HDL

- Molecular lesion in ABCA1 gene

35
Q

Which genetic disorders cause elevated LDL?

A
  • FH
  • PCSK9
  • Familial defective Apo B
  • Autosomal recessive hypercholesterolemia
36
Q

Which genetic disorders cause elevated HDL?

A
  • CETP deficiency

- Hepatic lipase deficiency

37
Q

Which genetic disorders cause low HDL?

A
  • Tangier disease
  • LCAT deficiency
  • Apolipoprotein A-1 deficiency
38
Q

Which genetic disorders cause low TG or cholesterol?

A

Abetalipoproteinemia

39
Q

What is FH treated with?

A

Combination of statin and ezetimibe

40
Q

Which apolipoproteins are not present in abetalipoproteinemia? Which ones are?

A
  • No Apo-B particles are present

- Only HDLs

Kris 307 (19 decks)

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