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Tissues > T13 - Lipoprotein Metabolism > Flashcards

T13 - Lipoprotein Metabolism Flashcards

1
Q

Give an example of a hydrophilic amphipath. (2)

A

fatty acids

phospholipids

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2
Q

Give an example of a hydrophobic amphipath.

A

cholesterol

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3
Q

What is the composition of mixed micelles?

A

phospholipids

long chain fatty acids

MAGs

bile acids

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4
Q

Describe the relative orientations of the components of mixed micelles.

A

hydrophobic portions of PLs, fatty acids, and MAGs oriented toward center and surrounded by amphipathic bile acids

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5
Q

Describe the common, generic structure of all lipoproteins.

A

hydrophobic TG + CE core

trace quantities of fat-soluble vitamins

surface with amphipathic molecules (unCE + PLs) + amphipathic apolipoproteins

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6
Q

What are the two criteria by which lipoproteins are classified?

A

classification based on relative size and density

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7
Q

What is the density of plasma?

A

1.006 g/mL — slightly higher than water because of presence of proteins

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8
Q

List the relative densities of cholesterol, CE, PL, protein, and TG.

A

cholesterol/CE/PL = 1.000

TG = 0.900

protein = 1.200

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9
Q

What are the six major classes of lipoproteins?

A

HDL

LDL

VLDL

CM

IDL

CMr

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10
Q

Describe HDL.

A

small particles that are rich in protein + CE and poor in TG

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11
Q

Describe LDL.

A

less protein but mostly CE and slightly higher TG

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12
Q

Describe VLDL. (2)

A

large amounts of TG, some CE, and little protein

density below plasma density

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13
Q

Describe CM.

A

even more TG relative to CE (>10:1 ratio) and very little protein

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14
Q

Describe IDL.

A

have similar amounts of TG and CE

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15
Q
A
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16
Q

How are IDLs produced?

A

produced from metabolism of VLDL particles

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17
Q

Describe CMr.

A

remnants of chylomicrons rich in CE and TG

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18
Q

What is the alternative pathway for hepatic CM uptake if hepatic LDL receptors are nonfunctional?

A

LRP mechanism — CMr can still be cleared normally even in patients without functional LDLR (i.e. familial hypercholesterolemia)

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19
Q

What is the principal function of chylomicrons?

A

to deliver TG to peripheral tissues

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20
Q

What are the physical characteristics of VLDL? (3)

A

TG-rich but lower TG:cholesterol ratio (5:1) than that present in CMs (20:1)

VLDLs smaller than CMs (80 nm vs. 500 nm)

VLDL contains 1 copy of ApoB-100 but multiple copies of ApoAI, ApoCII, and ApoE

21
Q

Where does VLDL synthesis occur?

A

ER of hepatocytes

22
Q

Describe the steps of VLDL synthesis. (3)

A

made in ER → undergoes lipidation → secreted into blood → acquires multiple copies of ApoE + ApoCII from HDL

23
Q

Which ApoB variant does VLDL contain?

A

ApoB-100 (remember, because VLDL is made in the liver, it can only have the B-100 variant)

24
Q

What protein/enzyme does VLDL encounter as it circulates through the body?

A

encounters lipoprotein lipase (just like CMs do) and undergo breakdown such that most of the VLDL’s TGs are delivered to peripheral tissue

25
Q

What does VLDL become after interaction with lipoprotein lipase?

A

becomes a VLDL remnant = intermediate density lipoprotein (IDL)

26
Q

How are VLDL remnants cleared?

A

through two pathways:

1) 50% of the time, cleared by LDLR-mediated endocytosis in the liver
2) the other 50% of the time, VLDL remnant further metabolized into LDL, which contains a single ApoB-100

27
Q

What enzyme is responsible for the conversion of IDL to LDL?

A

hepatic lipase

28
Q

Hepatic lipase is responsible for what activity?

A

conversion of IDL into LDL

i.e. conversion of VLDL into LDL

29
Q

Where does the formation of LDL from VLDL occur?

A

vascular space

30
Q

How is LDL cleared from circulation?

A

in liver or peripheral tissue via LDLR-mediated endocytosis

31
Q

What structure on LDL serves as the ligand for LDLR-mediated endocytosis?

A

ApoB-100

32
Q

Differentiate between the rate of clearance of LDL and VLDLr.

A

VLDLr uses ApoE for uptake

LDL uses ApoB-100 for uptake

ApoB-100 has lower affinity than ApoE for LDLR

therefore, VLDLr cleared faster than LDL

33
Q

(T/F) All LDL is cleared by the liver.

A

False. 20% of the LDL is taken up by extrahepatic tissues.

34
Q

What are the values of VLDLr and LDL in a normal individual?

A

VLDLr = 10/20 mg/dl (cleared rapidly)

LDL = 90-100 mg/dl

35
Q

What is the principal composition of HDL?

A

high amounts of ApoAI with smaller amounts of ApoCII and ApoE (basically, mostly protein)

36
Q

Where is HDL synthesized?

A

in the liver and small intestines

37
Q

How is HDL initially synthesized?

A

as disc-like particles w/ unesterified cholesterol, phospholipids, and ApoA-I

38
Q

Describe the steps of HDL particle formation.

A

disc-like particle forms → unesterified cholesterol esterified to long-chain fatty acid via LCAT enzyme → esterified cholesterol forms HDL core

39
Q

Which enzyme is responsible for HDL particle formation?

A

lecithin-cholesterol acyltransferase (LCAT)

40
Q

(T/F) Cells in the body are capable of degrading sterols.

A

False. No cells in the body can degrade sterols.

41
Q

What is the only cell type that does NOT continuously synthesize cholesterol from acetyl CoA?

A

RBCs

42
Q

What are the two mechanisms by which HDL particles pick up cholesterol in peripheral tissue and deliver it back to the liver?

A

(1) CETP: cholesteryl esters in HDL transferred to CM/VLDL/LDL (all ApoB lipoproteins) via enzyme cholesterol ester transfer protein (CETP) and cleared by the liver via LDLR-mediated endocytosis
(2) SR-BI: ApoAI interacts with SR-BI (a.k.a. SCAR-B1) on hepatocyte which allows direct transfer of cholesterol esters from HDL to hepatocyte cytosol

43
Q

How is cholesterol excreted by the liver and small intestines? (2)

A

some of the cholesterol that returns to the liver is converted to bile acid and secreted into bile

alternatively, cholesterol is secreted directly into bile by ABCG5/ABCG8

44
Q

Describe the levels of CM, VLDL, HDL and LDL in fasting individuals.

A

in fasting individuals:

CM and VLDL low

HDL and LDL high

45
Q

A mutation in CETP would have what effect on HDL levels?

A

mutation in CETP → high HDL levels

46
Q

An increase in triglyceride levels has what effect on HDL levels?

A

increase in triglycerides → lower HDL levels

47
Q

Why are levels of CM and VLDL so low in fasting blood samples?

A

CM and VLDL are low in fasting blood because they’ve been taken up/cleared by the liver

48
Q

What is the effect of having a non-functional LDL receptor for the clearance of exogenously-derived lipoprotein particles?

A

No effect. LRP is a form of redundancy that can clear LDLs. LRP binds ApoE instead of ApoB. LRP, unlike LDL receptors, is not regulated and is constitutively on.

Tissues (23 decks)

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