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MEH * > 2.2 - Lipid Transport > Flashcards

2.2 - Lipid Transport Flashcards

1
Q

How are lipids transported in the blood?

A

Insoluble in water = must therefore be carried in the plasma in association with protein.
Most is carried as highly specialised non - covalent assemblies known as lipoprotein particles. The remaining 2% are bound non covalently to albumin (generally are fatty acids released from adipose during lipolysis and used as a fuel by tissue).

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2
Q

What are plasma lipoprotein particles??

A

Multi molecular complexes that contain variable amounts of different lipids.
Primary function is to transport water insoluble lipid molecules in the blood stream. Several classes of lipoproteins are found. .

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3
Q

What are protein components?

A 
Specific proteins (apoproteins) that have functional as well as structural roles. 
Structurally = packaging non polar lipid into soluble particles. 
Functionally = activation of enzymes or recognition of cell surface receptors
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4
Q

How is a lipoprotein shaped?

A

Circular = stable.

Surface coat and hydrophobic core (triglycerole, cholesterol ester and fat soluble vitamin a)

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5
Q

What are the 5 lipoprotein classes and how do they vary in their transport function?

A

1) chylomicrons - transport dietary triglycerol from intestines to tissue
2) VLDL - transport of triacylglycerol synthesised in liver to adipose tissue for storage
3) IDL - short lived precursor for LDL. Transport of cholesterol synthesised in the liver to tissue.
4) LDL - transport of cholesterol synthesised in the liver to tissue
5) HDL - transport of excess tissue cholesterol to liver for disposal as bile salts and to cells requiring additional cholesterol.

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6
Q

What is the role of lipoprotein lipase?

A

The enzyme responsible for removing the core triglycerols from lipoproteins. It is found attached to the inner surface of capillaries in tissues such as adipose and muscle.

Insulin increases synthesis of enzyme in tissue. Triglycerols become fatty acid and glycerol.

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7
Q

What is the role of lecithin: cholesterol acyltransferase (LCAT)?

A

Convert surface lipid into core lipid to maintain stability in the lipoprotein since lipoprotein lipase removes core lipid = alters ratio.
Helps maintain lipoprotein structure.

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8
Q

Where do chylomicrons enter the Blood stream from the lymphatic system?

A

Thoracic duct which empties into the left subclavian vein.

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9
Q

What is cholesterol a precursor of?

A
  • steroid hormones e.g. testosterone, oestrogen, cortisol and aldosterone
  • bile acids
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10
Q

How is cholesterol transported around the body?

A

As a cholesterol ester

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11
Q

Above what level of cholesterol in the plasma can lead to cardiac failure?

A

5 mmol/l

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12
Q

What’s the difference between a liposome and a Micelle?

A

Liposome = bilayered spherical structures with a central cavity environment

Micelle = monolayered with lipohphilic environments

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13
Q

How do VLDL break down?

A

VLDLs deplete into IDL which deplete into LDLs

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14
Q

What are apolipoproteins and where are the main ones found?

A

Each class of lipoprotein particle has a complement of associated proteins

ApoB = in VLDL, IDL and LDL

ApoAl = in HDL

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15
Q

How are chylomicrons metabolised?

A
  • loaded into small intestine and apoB-48 added before entering lymphatic system
  • travel to thoracic duct which empties into left subclavian vein and acquire apoC and apoE in the blood
  • apoC binds with lipoprotein lipase (LPL) on adipocytes and muscle. Released fatty acids enter cells depleting chylomicrons of its fat content.
  • when fat content gets low apoC dissociates and chylomicrons becomes chylomicron remnant
  • chylomicron remnants return to over. LDL receptor on hepatocytes binds apoE and remnant is taken up by receptor mediated endocytosis. Lysosomes release remaining contents for use in metabolism
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16
Q

Why would an LDL recognise apoB but not apob-48?

A

As apoB-48 is only 48% the size of apoB so will not be recognised as the missing segment has a section that will be recognised by the LDL.

17
Q

What is the role of lipoprotein lipase?

A

Hydrolysed triacylglycerol in lipoproteins.

Found attached to surface of endothelial cells in capillaries.

18
Q

How are VLDL metabolised?

A
  • ApoB is 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 stores as fat.
19
Q

How are IDL and LDLs metabolised?

A
  • as triglycerol content of VLDL particle drops some, VLDL particles dissociate from the LPL enzyme complex and returns to the liver.
  • if VLDL content deplete to around 30%, the particle becomes a short lived IDL particle
  • IDL particles can be taken up to liver to remind to LPL enzyme to further deplete TAG content
  • upon depletion to around 10%, IDL loses apoC and apoE and becomes an LDL
20
Q

What is the function of LDL and what is its clinical relevance?

A

Function

  • To provide cholesterol fro the liver to peripheral tissues
  • Peripheral cells express LDL receptor and take up LDL via a process of receptor mediated endocytosis
  • Also, don’t have ApoC or apoE so aren’t effectively cleared by liver (liver LDL receptor has a high affinity for apoE)

Clinical relevance

  • half life of LDL is longer than VLDL or IDL = more susceptible to oxidative damage
  • oxidised LDL taken up by macrophages that can transform to foam cells and contribute to formation of atherosclerotic plaques.
21
Q

How do LDLs enter cells?

A

Receptor mediated endocytosis

  • cells needing cholesterol have LDL receptors on plasma membrane
  • apoB acts as a ligand
  • taken in by cell through endocytosis and fuse with lysosomes for digestion to release cholesterol and fatty acids
22
Q

How are HDLs metabolised?

A

Synthesis

  • synthesised by liver and intestine (low TAG levels)
  • HDL particles can also bud off from chylomicrons and VLDL as they are digested by LPL
  • free apoA can also acquire cholesterol and phospholipids from other lipoproteins and cell membranes to for nascent like HDL.

Maturation
- HDL accumulates phospholipids and cholesterol from cells lining blood vessels = core fills and it tajes a more globular shape

Reverse cholesterol transport
- remove cholesterol from cells and return to liver = reduces likelihood of foam cells and atherosclerotic plaques forming

Fate of mature HDL

  • taken up by liver by specific receptors
  • cells requiring additional cholesterol can also utilise scavenger receptor to obtain cholesterol from HDL
  • HDL can also exchange cholesterol ester for TAG with VLDL via action of cholesterol exchange transfer protein.
23
Q

What are hyperlipoproteinaemias and what are their causes?

A

Hyperlipoproteinaemias
- raised plasma level of one or more lipoprotein classes

Caused by defective

1) lipoprotein lipase
2) LDL receptor
3) apoprotein E

24
Q

What are the clinical signs of hypercholesterolaemias?

A
  • xathelasma = yellow patches on eyelids
  • tendon xanthoma = nodules on tendon
  • corneal Argus = obvious white circle around eye. Not normal in young people.
25
Q

What do foams cells accumulate to form?

A

Foam cells accumulate in the intima of blood vessel walls to form a fatty streak which then evolves into an atherosclerotic plaque.

26
Q

What is the treatment of hyperlipoproteinaemias?

A

Diet
- reduce cholesterol and saturated lipids in diet

Lifestyle

  • exercise
  • stop smoking to reduce cardiovascular risk

If no response = DRUGS.

  • statins reduce cholesterol synthesis via acetyl coA pathway by inhibiting HMG- CoA reductase
  • bile salt sequestrants = bind bile salts in GI tract = forces liver to produce more bile acids using more cholesterol.
27
Q

Why is there a greater need for HDL cholesterol in women?

A

As need to synthesise more hormones

MEH * (21 decks)

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