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Semester 2 - MEH > 4. Lipid Transport > Flashcards

4. Lipid Transport Flashcards

1
Q

What are the different types of lipids?

A 
Triacylglycerol 
Fatty acids
Cholesterol
Phospholipids
Vitamins A,D,E,K
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2
Q

What are the two types of triacylglycerol?

A

Diacylglycerol

Monoacylglycerol

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3
Q

What is the main feature of lipids, what problem does it pose and how can it be solved?

A

• Hydrophobic molecules insoluble in water = Problem for transport in blood!
• Solution- transported in blood bound to carriers
• ~ 2% of lipids (mostly fatty acids) carried bound to albumin but this has a limited capacity (~ 3 mmol/L)
• ~ 98% of lipids are carried as lipoprotein particles consisting of
phospholipid, cholesterol, cholesterol esters, proteins & TAG

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4
Q

What is the total concentration range for lipids?

A

4000 - 8500 mg/L

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5
Q

Describe the structure of phospholipids

A

Polar, hydrophilic head connected via phosphate to glycerol which is connected to non polar, hydrophobic tail.

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6
Q

How are phospholipids classified??

A

Classified according to their polar head group e.g.
Choline
Choline —-> phosphatidylcholine
Inositol—-> phosphatidylinositol

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7
Q

How is cholesterol obtained ?

A

Some cholesterol obtained from diet, but most synthesised in liver - daily intake of 1g of cholesterol

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8
Q

What is the function of cholesterol ?

A 
• essential component of membranes( modulates fluidity) 
• precursor of steroid hormones:
> Cortisol 
> Aldosterone 
> Testosterone 
> Oestrogen
• Precursor of bile acids
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9
Q

How is cholesterol transported in the body

A

Transported around body ascholesterol Ester

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10
Q

Describe the structure of lipoproteins

A
  • All mature lipoproteins found in normal human plasma are spherical particles that consist of a surface coat (shell) and a hydrophobic core.
  • The surface coat contains the phospholipids, cholesterol and apolipoproteins.
  • The hydrophobic core contains triacylglycerols and cholesterol esters and Fat soluble vitamins (A,D,E&K).
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11
Q

What is the function of lipoproteins?

A

The primary function of these lipoproteins is to transport insoluble lipid molecules in the bloodstream.

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12
Q

List the 5 distinct types of lipoproteins

A
  • Chylomicrons
  • VLDL (Very Low Density Lipoproteins)
  • IDL (Intermediate Density Lipoproteins)
  • LDL (Low Density Lipoproteins
  • HDL (High Density Lipoproteins)
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13
Q

Which lipoproteins are the main carriers of fat?

A

Chylomicron

VLDL

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14
Q

Which lipoproteins are the main carriers of cholesterol esters?

A

IDL
LDL
HDL

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15
Q

What do each lipoproteins contain?

A

Each contains variable content of apolipoprotein, triglyceride, cholesterol and cholesterol ester

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16
Q

how does the density of lipoproteins relates to their protein composition and size

A

The more dense the lipoprotein the higher the percentage of proteins present and the smaller the diameter. The HDL has the highest density but the smallest size whilst the VLDL has the lowest density but the largest size.

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17
Q

How is the density of lipoproteins obtained?

A

Density obtained by flotation ultracentrifugation

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18
Q

What are Apolipoproteins?

A 
Apolipoporteins are the protein components of lipoproteins.
Each class of lipoprotein particle has a particular complement of associated proteins (apolipoproteins)
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19
Q

Give classes of Apolipoproteins

A
  • Six major classes (A,B,C,D,E & H)

* apoB (VLDL,IDL &LDL) and apoAI (HDL) important

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20
Q

How can Apolipoproteins be positioned in the phospholipid bilayer?

A

Apolipoproteins can be integral passing through

phospholipid bilayer or peripheral “resting” on top

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21
Q

What are the 2 functions of Apolipoproteins?

A 
1. Structural:
Packaging water insoluble lipid
2. Functional:
Co-factor for enzymes
Ligands for cell surface receptors
22
Q

What is the function of Chylomicrons?

A

Transport dietary triacylglycerol from the intestine

to tissues such as adipose tissue.

23
Q

What is the function of VLDL?

A

Transport of triacylglycerol synthesised in liver to adipose tissue for storage.

24
Q

What is the function of IDL?

A

Short-lived precursor of LDL. Transport of cholesterol synthesised in the liver to tissues.

25
Q

What is the function of LDL?

A

Transport of cholesterol synthesised in liver to tissues.

26
Q

What is the function of HDL?

A

Transport of excess cholesterol from cells to liver for disposal as bile salts and to cells requiring additional cholesterol

27
Q

Describe Chylomicron Metabolism

A

1) Chylomicrons loaded in small intestine with cholestero, fat and vitamins and apoB-48 added before entering lymphatic system
2) Travel to thoracic duct which empties into left subclavian vein and acquire 2 new apoproteins (apoC and apoE) once in blood.
3) apoC binds to lipoprotein lipase (LPL) on adipocytes and muscle. Released fatty acids enter cells depleting
chylomicron of its fat content.
4) When triglyceride reduced to ~ 20%, apoC dissociates and chylomicron becomes a chylomicron remnant
5) Chylomicron remnants return to liver. LDL receptor on
hepatocytes binds apoE & chylomicron remnant taken up by receptor mediated endocytosis . Lysosomes release remaining contents for use in metabolism

28
Q

Describe VLDL metabolism

A

• VLDL made in liver for purpose of transporting
triacylglycerol (TAG) to other tissues.
• Apolipoprotein apoB100 added during formation and
apoC and apoE added from HDL particles in blood.
• VLDL binds to lipoprotein lipase (LPL) on endothelial cells in muscle and adipose and starts to become depleted of triacylglycerol
• In muscle the released fatty acids are taken up and used for energy production
• In adipose the fatty acids are used for re-synthesis of
triacylglycerol and stored as fat

29
Q

Describe IDL & LDL formation

A

• VLDL –> IDL –> LDL
• As triacylglycerol content of VLDL particles drops some, VLDL particles dissociates from the LPL enzyme
complex and return to liver
• If VLDL content depletes to ~30%, the particle becomes a short-lived IDL particle.
• IDL particles can also be taken up by liver for lysosomal degradation or rebind to LPL enzyme to further deplete in TAG content
• Upon depletion to ~ 10%, IDL loses apoC & apoE and becomes an LDL particle (high cholesterol content)

30
Q

How does LDL contribute to atherosclerosis?

A
  • Half life of LDL in blood is much longer than VLDL or IDL making LDL more susceptible to oxidative damage(lipid peroxidation)
  • Oxidised LDL taken up by macrophages that can transform to foam cells and contribute to formation of atherosclerotic plaques
31
Q

What is the function of LDL?

A
  • Primary function of LDL is to provide cholesterol from liver to peripheral tissues.
  • Peripheral cells express LDL receptor and take up LDL via process of receptor mediated endocytosis and Lysosomal degradation of the LDL releases Cholesterol, Fatty acid and Glycerol
32
Q

Why are LDLs not efficiently cleared by the liver?

A

LDL do not have apoC or apoE so are not efficiently

cleared by liver (Liver LDL-Receptor has a high affinity for apoE).

33
Q

Exaplain how LDL enters cells and what happens once inside

A

• Cells requiring cholesterol express LDL receptors on plasma membrane
• apoB-100 on LDL acts as a ligand for these receptors
• Receptor/LDL complex taken into cell by endocytosis into endosomes
• Fuse with lysosomes for digestion to release
cholesterol and fatty acids
• LDL –Receptor expression controlled by cholesterol concentration in cell

34
Q

How is HDL synthesised and where?

A
  • Nascent HDL synthesised by liver and intestine (low TAG levels)
  • HDL particles can also “bud off” from chylomicrons and VLDL as they aredigested by LPL
  • Free apoA-I can also acquire cholesterol and phospholipid from other lipoproteins and cell membranes to form nascent-like HDL
35
Q

How does HDL mature? Are enzymes required?

A
  • Nascent HDL accumulate phospholipids and cholesterol from cells lining blood vessels
  • Hollow core progressively fills and particle takes on more globular shape
  • Transfer of lipids to HDL does not require enzyme activity
36
Q

Why is HDL considered good cholesterol?

A

Because it takes excess cholesterol to the liver for disposal as bile salts or to other cells that need it. Therefore, prevents buildup of cholesterol in the blood vessels so prevents atherosclerotic plaque formation

37
Q

What is the process called when HDL removes cholesterol laden cells and returns it to liver?

A

Reverse cholesterol transport

38
Q

Describe Reverse cholesterol transport

A
  • HDL have ability to remove cholesterol from cholesterol-laden cells and return it to liver
  • Important process for blood vessels as it reduces likelihood of foam cell and atherosclerotic plaque formation
  • ABCA1 protein within cell facilitates transfer of cholesterol to HDL. Cholesterol then converted to cholesterol ester by LCAT
39
Q

What is the fate of mature HDL?

A
  • Mature HDL taken up by liver via specific receptors
  • Cells requiring additional cholesterol (e.g. for steroid hormone synthesis) can also utilise scavenger receptor (SR-B1) to obtain cholesterol from HDL
  • HDL can also exchange cholesterol ester for TAG with VLDL via action of cholesterol exchange transfer protein (CETP)
40
Q

What are Hyperlipoproteinaemias?

A

Raised plasma level of one or more lipoprotein classes

41
Q

What can cause Hyperlipoproteinaemias?

A

Caused by either:

  1. Over-production
  2. Under-removal

6 main classes

42
Q

In Hyperlipoproteinaemias, what can the defect be in?

A

Defects in:
• Enzymes
• Receptors
• Apoproteins

43
Q

What is Hypercholesterolaemia?

A

High level of cholesterol in blood

44
Q

What are the visible features of Hypercholesterolaemia?

A

Cholesterol depositions in various areas of body:
• Xanthelasma - Yellow patches on eyelids
• Tendon Xanthoma - Nodules on tendon
• Corneal arcus - obvious white circle around eye. Common in older people but if present in young could be a sign of hypercholesterolaemia

45
Q

How can raised serum of LDL lead to atherosclerosis?

A

• Oxidised LDL form ROS which are recognised and engulfed by macrophages
• Lipid laden macrophages called Foam cells accumulate in intima of blood vessel walls to form a
fatty streak
• Fatty streaks can evolve into atherosclerotic plaque
• atherosclerotic plaque Grows and encroaches on the lumen of the artery
• If the atherosclerotic plaque is in the coronary arteries, it can block blood flow and lead to angina
• If the atherosclerotic plaque continues to grow, it can rupture which Triggers acute thrombosis (clot) by activating platelets and clotting cascade
• If thrombosis in coronary artery –> myocardial infarction
• If thrombosis in artery in brian –> stroke

46
Q

What is the First approach to treating hyperlipoproteinaemias?

A

Diet:
• Reduce cholesterol and saturated lipids in diet. Increase fibre intake.
Lifestyle:
• Increase exercise
• Stop smoking to reduce cardiovascular risk - also can reduce the oxidative stress on LDLs cause by smoking

47
Q

What is the second approach to treating hyperlipoproteinaemias?

A

Statins:
• Reduce cholesterol synthesis by inhibiting HMG-CoA
reductase e.g. Atorvastatin

Bile salt sequestrants:
• Bind bile salts in GI tract. Forces liver to produce more bile acids using more cholesterol e.g. Colestipol

48
Q

How can an increase in fibre levels help to treat hyperlipoproteinaemias?

A

Increased fibre is important because it helps to remove bile salts from the body in faeces instead of them to be reabsorbed.
This means that the body has to take more cholesterol out of blood to make bile salts.
This reduces the blood cholesterol levels.

49
Q

How do statins work?

A

They inhibit the enzyme HMG-CoA reductase which is used in the pathway where HMG-CoA from Acetyl CoA is converted to Mevalonate and eventually to cholesterol

50
Q

What are the ideal levels for cholesterol tests

A 
Total cholesterol: 5mmol/l or less
Non HDL cholesterol: 4mmol/l or less
LDL: 3mmol/l or less
HDL: over 1mmol/l men or 1.2mmol/l women
Total cholesterol:HDL-C ratio - Ratio above 6 considered high risk - the lower the ratio the better.
Tag: less than 2mmol/l in fasted sample

Semester 2 - MEH (23 decks)

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