Lecture 68 Flashcards

1
Q

How do free fatty acids (such as those released from adipose stores during fasting) travel in the bloodstream?

A

Bound to Albumin

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2
Q

How many long chain FAs can bind to one albumin protein?

A

10

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3
Q

What happens to the majority of free FAs traveling in the bloodstream?

A

They are delivered to the liver where they are repackaged as triglyceride and incorporated into VLDL for delivery to other tissues.

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4
Q

What is the secondary structure of Apolipoproteins on the surface of lipoprotein particles?

A

Amphipathic alpha helices

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5
Q

Sizes of Lipoproteins:

A
Chylomicron: <0.95 g/ml
VLDL: 0.95-1.01 g/ml
IDL: 1.01-1.02 g/ml
LDL: 1.02-1.06 g/ml
HDL: 1.06-1.2 g/ml
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6
Q

Composition of Lipoproteins:

A

Chylomicron: 92% TG
VLDL: 50% TG
LDL: 36% CE and 10% Ch
HDL: 15% CE and 4% Ch

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7
Q

Chylomicrons (location, function, apolipoproteins)

A

Produced in intestinal enterocytes. Carrier of dietary fat (triglycerides) and cholesterol. Synthesized with ApoB-48; picks up ApoC-II and ApoE from HDL

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8
Q

VLDL (location, function, apolipoproteins)

A

Produced in the liver. Carrier of triglyceride and cholesterol to extra-hepatic tissues. Synthesized with ApoB-100; picks up ApoC-II and ApoE from HDL.

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9
Q

LDL (location, function, apolipoproteins)

A

Produced from VLDL after loss of triglyceride. Primary carrier of cholesterol and cholesterol esters to peripheral tissues or to liver for excretion.

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10
Q

HDL (location, function, apolipoprotines)

A

Active in reverse cholesterol transport. Produced in liver and intestine. Exchanges lipid and apolipoproteins between particles. Uses ApoA-I, ApoC-II and ApoE

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11
Q

What are the two major structural apolipoproteins and where are they found?

A

ApoB (VLDL, IDL, LDL, chylomicrons)

ApoA-I (HDL)

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12
Q

What are the variation in ApoB and where are they found?

A

ApoB-100: VLDL and LDL

ApoB-48: Chylomicrons

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13
Q

Which apolipoprotein activates lipoprotein lipase (LPL) on the surface of endothelial cells?

A

ApoC-II

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14
Q

How is the chylomicron remnant taken up by the liver?

A

via the ApoE receptor.

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15
Q

What happens to the glycerol released from the hydrolysis of triglycerides via LPL?

A

It is transported to the liver where it is

  1. used to make triglycerides for BLDL production
  2. Enters glycolytic or gluconeogenic pathways
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16
Q

Name 4 ways the liver can produce triglycerides

A
  1. de novo lipogenesis

2. repackaging of fatty acids that were taken up from adipose stores, chylomicron remnants or LDL

17
Q

Describe the regulation of Lipoprotein Lipase (LPL)

A

During fasting:

  • expression of LpL is down-regulated in adipose tissue
  • expression of LpL is maintained in heart and other tissues

In the fed state:
-insulin and feeding stimulate LPL expression in adipose

18
Q

Which apolipoprotein interacts with the LDL receptor?

A

ApoB-100

19
Q

What happens to LDL after it is taken up by the LDL receptor?

A

It is delivered to the lysosome, where it is hydrolyzed to yield cholesterol, glycerol, fatty acids and AAs.
-LDL receptors are returned to the plasma membrane and re-used.

20
Q

What is the leading cause of mortality worldwide?

A

Atherosclerosis of coronary and peripheral vasculature

21
Q

Which enzyme exchanges cholesterol esters and triglycerides between HDL to LDL?

A

CETP (Cholesterol Ester Transfer Protein)

22
Q

Which enzyme transfers cholesterol to the outer leaflet of the plasma membrane?

A

ATP-binding cassette protein (ABC-A1)

23
Q

Which enzyme converts cholesterol to cholesterol esters in HDL? Why is this beneficial?

A

LCAT (Lecithin: cholesterol acyl transferase)

-Prevents reuptake of cholesterol by the cell and allows HDL to hold more cholesterol

24
Q

What is Tangier disease?

A

Mutation in ABC-A1 transporter –> high intracellular cholesterol levels –> higher risk for coronary heart disease

25
Q

Which Apoprotein activates LCAT?

A

ApoA-I

26
Q

What happens to LDL containing oxidatively modified cholesterol?

A
  • taken up by macrophages via scavenger receptors
  • formation of foam cells
  • accumulation of foam cells in subendothelial space of blood vessels
  • fatty streak causes a lesion in the endothelial layer of the blood vessel
  • vessel ruptures and thrombus forms