Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

MEH * > S2 Lipid Transport > Flashcards

S2 Lipid Transport Flashcards

1
Q

How are lipids transported in blood? (2 ways)

A
  • mostly carried as lipoprotein particles

* some are carried bound to albumin (has limited capacity)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

How is cholesterol obtained and transported?

A

Obtained from the diet and some is synthesised by the liver

Transported as a cholesterol ester (addition of a fatty acid)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is cholesterol a precursor for?

A
  • steroid hormones e.g. cortisol, oestrogen, aldosterone and testosterone
  • bile acids
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is the structure of lipoproteins?

A
  • phospholipid monolayer with a small amoutn of cholesterol present
  • cargo consisting of: TAG, cholesterol ester and fat soluble vitamins
  • integral and peripheral apolipoproteins
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are the five classes of lipoprotein?

A
  1. Chylomicrons
  2. VLDL - very low density lipoproteins
  3. IDL - intermediate density lipoproteins
  4. LDL - low density lipoproteins
  5. HDL - high density lipoproteins
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What do chylomicrons transport?

A

Dietary fat

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What do VLDL evolve into? And what does that then evolve into?

A

IDL

LDL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is the good and bad cholesterol?

A

Good - HDL

Bad - LDL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Which lipoproteins are the main carriers of fat?

A

Chylomicrons and VLDL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Which lipoproteins are the main carriers of cholesterol esters?

A

IDL, LDL and HDL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are apolipoproteins?

A
  • proteins associated with lipoproteins
  • there are 6 major classes - ABCDEH
  • apoB (VLDL, IDL and LDL) and apoAI (HDL) are important
  • they can be peripheral or integral
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are the two roles of apolipoproteins?

A
  1. Structural - package water insoluble lipids

2. Functional - cofactors for enzymes and ligands for cell surface receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

How does chylomicron metabolism occur?

A
  1. Chylomicrons are loaded in the s. intestine with e.g. fat, cholesterol and vitamins and apoB-48 is added
  2. Transported through in the lymph and empties in blood through left subclavian vein (apoC and apoE are added)
  3. apoC binds to lipoprotein lipase (LPL) which is on the capillary walls at muscle and adipose tissue
  4. It releases fatty acids into the cells and the chylomicron remnants return to the liver
  5. The LDL receptor on hepatocytes binds to apoE and the chylomicron remnants are taken up by receptor mediated endocytosis
  6. Lysosomes release the remaining contents for use in metabolism
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

How does VLDL metabolism occur?

A
  1. VLDL is made in the liver to transport TAG to other tissues
  2. apoB100, apoC and apoE added to VLDL
  3. VLDL binds to LPL on endothelial cells in muscle and adipose tissue and TAG is released into the tissue cells
  4. In the muscle the fatty acid are used for energy production
  5. In adipose the fatty acid are used to resynthesise TAG and store it as fat
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

How does IDL and LDL metabolism occur?

A
  1. The TAG content of VLDL occurs, some VLDL dissociates for the LPL enzyme complex and are returned to the liver
  2. If the VLDL content depletes to about 30%, the particle becomes a IDL particle
  3. IDL can be taken upon but the liver or remind to LPL to further deplete TAG content
  4. If the IDL content depletes to about 10%, IDL loses apoC and apoE and comes an LDL particle
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is the function of LDL?

A

Provide cholesterol from the liver to peripheral tissues which have LDL receptors so take up LDL via receptor mediated endocytosis

17
Q

What apolipoproteins don’t LDL have? What does this mean?

A

apoC and apoE

Not efficiently cleared by the liver as liver LDL receptor has a high affinity for apoE

18
Q

Which has the longest half life, VLDL, IDL or LDL? What does this mean clinically?

A

LDL

It is more susceptible to oxidation damage

If LDL is oxidised, macrophages take it up and transform into foam cells which contribute to atherosclerosis

19
Q

Describe receptor mediated endocytosis. And what happens if the molecule/particle is to be digested?

A

A ligand binds to receptors on the cell surface leading to endocytosis into endosomes (vesicles).

The endosome fuses with a lysosome

20
Q

What controls LDL receptor expression?

A

The cholesterol concentration in a cell

21
Q

What happens in the synthesis of HDL?

A
  1. New HDL is synthesised by the liver and intestine or can “bud off” from chylomicrons and VLDL (as digested by LPL)
  2. apoA-I can get cholesterol and phospolipid from other lipoproteins and cell membranes to form ‘new-like’ HDL
22
Q

What happens in the maturation of HDL?

A
  1. New HDL accumulates phospholipids and cholesterol from cells lining blood vessels
  2. The hollow core fills and the particle (HDL) becomes more globular
23
Q

Does transfer of lipids to HDL require enzyme activity?

A

No

24
Q

What does HDL do? Why is this good?

A

Reverse cholesterol transport

HDL can remove cholesterol from cells containing LOTS of cholesterol and return it to the liver

It reduces the likelihood of foam cell and atherosclerosis formation

25
Q

What protein facilitates transfer of cholesterol to HDL?

What then converts cholesterol to cholesterol ester?

A

ABCA1 protein

LCAT

26
Q

What is the fate of mature HDL?

A
  1. Taken up by the liver via receptors
  2. Cells that need extra cholesterol can utilise a scavenger receptor to get cholesterol from HDL
  3. HDL can exchange cholesterol ester for TAG with VLDL via cholesterol exchange transfer protein (CETP)
27
Q

What cells may need extra cholesterol?

A

Cells involved in steroid hormone synthesis

28
Q

How is cholesterol disposed of in the liver?

A

Converted into bile salts (or is transported to cells requiring additional cholesterol)

29
Q

What is the general role of VLDL, IDL and LDL?

A

VLDL - transports TAG synthesised in the liver to adipose tissue for storage

IDL - transports cholesterol synthesised in the liver to tissues (a short-lived precursor)

LDL - transport of cholesterol synthesised in the liver to tissues

30
Q

What are hyperlipoproteinaemias? What causes it?

A

Raised plasma level of lipoprotein(s)

Caused by over-production or under-removal due too defects in enzymes, receptors and apolipoproteins

31
Q

What are the clinical signs of hypercholesterolaemia?

A
  • high levels of cholesterol in the blood
  • cholesterol deposits in areas of the body
    E.g. xanthelasma- yellow patches on eyelids
    tendon xanthoma- nodules on tendon
    corneal arcus - white circle around eye (common in old people, but not young people)
32
Q

How does oxidised LDL lead to atherosclerosis?

A
  1. Oxidised LDL
  2. Macrophages recognise and engulf
  3. Macrophages containing lipid called foam cells. These accumulate in the tunica intima of blood vessel walls and form a fatty streak
  4. The fatty streak can evolve into atherosclerotic plaque
  5. This plaque can grow and block the lumen of the artery (e.g. coronary artery) and can cause angina or can rupture triggering thrombosis which block the arteries (e.g. coronary artery or brain) leading to myocardial infarction or a stroke
33
Q

How can hyperlipoproteinaemias be treated?

A
  • reduce cholesterol and saturated lipids in diet and increase fibre intake
  • increase exercise
  • stop smoking
  • use statins to reduce cholesterol synthesis
  • use bile salt sequestrants
34
Q

How do statins reduce cholesterol synthesis?

A

By inhibiting HMG-CoA reductase

35
Q

What do bile salt sequestrants do?

A

Bind bile salts in the GI tract which forces the liver to produce more bile acids, using more cholesterol in the process

36
Q

How does an increase in fibre intake treat hyperlipoproteinaemias?

A

Allows excretion of bile salts, instead of the bile salts being reabsorped and reused, so liver needs to use more cholesterol to produce more bile salts

MEH * (22 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions