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MEH > 2.2 Lipid Transport > Flashcards

2.2 Lipid Transport Flashcards

1
Q

What are the main 5 groups of lipids?

A 
Triacylglycerols
Fatty acids
Cholesterol
Phospholipids
Vitamins A D E K
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2
Q

Why are lipids bound to carriers in blood?

A

As they are hydrophobic

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3
Q

What fatty acids are bound to albumin?

A

Few, only 2% of lipids, which are fatty acids released from adipose tissue during lipolysis. Go on to supply muscle.

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4
Q

What carriers transport the majority of lipids?

A

98% of lipids are carried as lipoprotein particles consisting of phospholipid, cholesterol, cholesterol esters, proteins & TAG

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5
Q

What are the typical plasma concentration ranges for lipids?

A 
Triacylglycerol 0-2.0 mmol/L 
phospholipids ~2.5 mmol/L 
total cholesterol <5.0 mmol/L 
cholesterol esters ~3.5 mmol/L 
Free fatty acids 0.3-0.8 mmol/L
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6
Q

Describe the structure of phospholipids

A

Hydrophilic polar head (glycerol, may include other molecules such as choline, phosphate or inositol)
Hydrophobic non-polar fatty acid tails.

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7
Q

What three shapes do phospholipids form in hydrophilic polar solutions?

A

Liposome
Micelle
Bilayer sheet

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8
Q

How do we obtain cholesterol?

A

Diet

Synthesised in liver

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9
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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10
Q

How is cholesterol transported around the body?

A

Cholesterol transported as cholesterol ester. It is Esterified with fatty acid. Enzyme catalysing this reaction is LCAT lecithin cholesterol acyltransferase.

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11
Q

Describe the structure of lipoproteins

A

Phospholipid monolayer with small amount of cholesterol. Peripheral apoproteins lie on the outer surface (apoC and apoE). Integral apoproteins are embedded in the phospholipid mono layer (apoA and apoB). A lipid cargo is carried at the core of the lipoprotein. Cargo consists of TAGs, cholesterol ester and vitamins A D E and K.

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12
Q

What are the structural roles of apoproteins?

A

Packaging non-water soluble lipid molecules into soluble form as multi-molecular particles. Apoproteins contain hydrophilic regions that can interact with water and hydrophobic regions that can interact with lipid molecules.

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13
Q

What are the functional roles of apoproteins

A

Involved in activation of enzymes by acting as a cofactor.

Recognition of cell surface receptors/ ligands for cell surface receptors.

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14
Q

How do lipoproteins vary?

A

Contain different types of lipids
Have different apoproteins composition
Density

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15
Q

How can different classes of lipoproteins be separated?

A

By ultracentrifugation or electrophoresis

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16
Q

What are the 5 different types of lipoproteins?

A 
Chylomicrons ( and chylomicron remnants) 
VLDL
IDL
LDL
HDL
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17
Q

What is the function of chylomicrons?

A

Transport dietary TAGs from the intestine to the tissues such as adipose tissue

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18
Q

What is the function of VLDL?

A

To transport TAGs synthesised in the liver to adipose tissue for storage.

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19
Q

What is the function of IDL?

A

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

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20
Q

What is the function of LDL?

A

Transport of cholesterol synthesised in the liver to tissues. An evolved IDL.

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21
Q

What is the function of HDL?

A

Transport excess tissue cholesterol to liver for disposal as bile salts an to cells requiring additional cholesterol

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22
Q

What are classed as good cholesterol?

A

Chylomicrons and VLDL

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23
Q

What are classed as bad cholesterol?

A

IDL
LDL
HDL

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24
Q

How do we obtain the density of lipoproteins?

A

By ultracentrifugation.

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25
Q

Describe the pattern of diameter in lipoproteins?

A

Particle diameter is inversely proportional to density. Hence VLDL are the largest, and HDL are the smallest.

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26
Q

How does the presence of chylomicrons change the appearance of centrifuged blood?

A

Superior plasma layer appears creamy (not clear and transparent.

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27
Q

What can chylomicrons be expected to appear in the blood?

A

4 to 6 hours after a meal

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28
Q

What lipoproteins contain apoB?

A

VLDL
IDL
LDL

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29
Q

What lipoproteins contain apoA?

A

HDL

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30
Q

What apoproteins distinguishes between chylomicrons and VLDL?

A

ApoB-48.

Chylomicrons loaded in small intestine and apoB-48 added before entering lymphatic system

31
Q

What apoproteins do chylomicrons acquire after entering the blood?

A

ApoC and apoE

Chylomicrons travel to thoracic duct which empties into left subclavian vein and acquire 2 new apoproteins (apoC and apoE) once in blood.

32
Q

What is the function of apoC?

A

apoC binds lipoprotein lipase (LPL) on adipocytes and

muscle.

33
Q

What is the function of lipoprotein lipase (LPL)?

A

Hydrolysed TAGs in lipoprotein particles to fatty acids and glycerol. Fatty acids are then taken up by tissues for beta oxidation and glycerol is taken up by the liver. Depletes chylomicrons of fat content

34
Q

How is a chylomicrons remnant formed?

A

When apoC binds to lipoprotein lipase, TAGs inside the chylomicrons are hydrolysed. When triglyceride reduced to ~ 20%, apoC dissociates and
chylomicron becomes a chylomicron remnant

35
Q

What is the function of apoE?

A

To bind to the LDL receptor on hepatocytes so that chylomicron remnant can by taken up by receptor mediated endocytosis.

36
Q

What happens to chylomicron remnants in the blood stream?

A

Chylomicron remnants return to liver. LDL receptor on
hepatocytes binds apoE & chylomicron remnant taken up by receptor mediated endocytosis . Lysosomes degrade chylomicron remnants and release remaining contents for use in metabolism

37
Q

How do lipids enter the blood stream from the small intestine.

A
  1. Hydrolysed by pancreatic lipases into fatty acids and glycerol. Fatty acids absorbed into intestinal epithelial cells
  2. Fatty acids re-esterified into TAGs using glycerol phosphate produced from glycerol metabolism in epithelial cells.
  3. TAGs packaged into chylomicrons which enter lymphatic system.
  4. Chylomicrons enter blood stream from the thoracic duct into the left subclavian vein.
38
Q

What is lipoprotein lipase?

A

Enzyme that hydrolyses triacylglycerol in lipoproteins
Requires ApoC-II as cofactor
Found attached to surface of endothelial cells in capillaries of muscle and adipose tissue.

39
Q

How is synthesis of lipoprotein lipase increased?

A

By insulin.

40
Q

Where are VLDL made?

A

In the liver.

41
Q

What apoproteins are present in VLDL?

A

Apolipoprotein apoB100 added during formation and

apoC and apoE are later added from HDL particles in blood.

42
Q

How are IDL formed?

A

VLDL binds to lipoprotein lipase (LPL) on endothelial cells in muscle and adipose and starts to become depleted of triacylglycerol

If VLDL content depletes to ~30%, the particle
becomes a short-lived IDL particle.

43
Q

What happens after VDLV had binded to lipoprotein lipase?

A

VLDL starts becoming depleted of TAGs. As triacylglycerol content of VLDL particles drops some, VLDL particles dissociates from the LPL enzyme complex and return to liver

44
Q

What happens to the fatty acids released from VLDL after binding to lipoprotein lipase?

A

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

45
Q

How is a LDL particle made?

A

IDL particles can also be taken up by liver 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).

46
Q

Why are oxidised LDL harmful?

A

Oxidised LDL are recognised and engulfed by macrophages. Lipid laden macrophages called foam cells accumulate in the intima of blood vessel walls to form fatty streaks. These fatty streaks can evolve to form atherosclerotic plaques. The atherosclerotic plaques can grow and obstruct the lumen of the artery causing an angina. If they rupture this will trigger thrombosis. And possibly result in a stroke or myocardial infarction.

47
Q

Describe the structure of blood vessel walls.

A

Most inner layer = tunica intima (endothelium, subendothelial layer and internal elastic layer)

Middle layer = tunica media (smooth muscle fibres)

Out layer = tunica externa. ( collagen fibres)

48
Q

How do tissues obtain cholesterol from LDLs?

A

Peripheral cells express LDL receptors which bind to the apoB-100 protein of the LDLs and take up LDL via
process of receptor mediated endocytosis. LDL then subjected to lysosomal digestion.

49
Q

Why is the half life of LDL in blood is much longer than VLDL or IDL?

A

As LDLs do not have apoC or apoE which can be recognised by liver cells, and therefore aren’t cleared efficiently by the liver. This makes LDLs more susceptible to oxidative damage

50
Q

Which lipoproteins are more susceptible to oxidative damage?

A

LDLs

51
Q

What is familial hypercholesterolaemia?

A

Absence (homozygous) or deficiency (heterozygous) of functional LDL receptors. Elevated levels of LDL and cholesterol in plasma. Homozygotes develop extensive atherosclerosis in early life, heterozygotes develop atherosclerosis in later life.

52
Q

What apoproteins on LDLs acts as a ligand for LDL receptors?

A

apoB-100

53
Q

What controls LDL receptor expression by the cell?

A

Cholesterol concentration in the cell.

54
Q

How does HDL vary from other lipoproteins?

A

Brings lipids to the liver from the tissues, rather than to the tissues from the liver.

55
Q

Where is HDL synthesised?

A

In the liver and intestine. Can bud off from chylomicrons and VLDL as they are digested by lipoprotein lipase. Free apoA-I can also acquire cholesterol and phospholipid from other lipoproteins and cell membranes to form nascent-like HDL

56
Q

How do HDLs acquire lipids?

A

Nascent HDL accumulate phospholipids and cholesterol from cells lining blood vessels, reducing the likelihood of developing atherosclerotic plaque and foam cells. Hollow core progressively fills and particle takes on more globular shape. Transfer of lipids to HDL does not require enzyme activity

57
Q

What protein allows HDL to take up cholesterol from cells to be loaded into the lipoprotein?

A

ABCA1 protein.

58
Q

How is cholesterol transported in HDL.

A

Cholesterol must be converted to cholesterol ester for transportation. This is done by LCAT.

59
Q

What is the difference between a mature HDL particle and an immature HDL particle?

A

Mature HDL particle has accumulated phospholipids and cholesterol from endothelial cells and has a globular shape due to its core no longer being hollow.

60
Q

What is the fate of mature HDL particles?

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)

61
Q

What is a nascent HDL particle?

A

An empty/immature HDL particle. Has a hollow core.

62
Q

What receptor can frequently by found on steroidogenic cells to attain cholesterol?

A

The scavenger receptor (SR-B1) this receptor helps attain cholesterol for steroid hormone synthesis within these cells from HDLs.

63
Q

What is hyperlipoproteinaemias?

A

A raise plasma level of one or more lipoprotein classes caused by either over-production or under-removal. Usually result due to a defect in enzymes, receptors or apoproteins.

64
Q

What are dyslipoproteinaemias?

A

Any defect in the metabolism of plasma lipoproteins.

65
Q

How are hyperlipoproteinaemias diagnosed?

A

Measurement of fasting glucose, total cholesterol and triacylglycerol and examination of the results of plasma lipoprotein separation by electrophoresis.

66
Q

How many different types of hyperlipoproteinaemias are there?

A

6 different types.

67
Q

What health risk is commonly associated with hyperlipoproteinaemias?

A

Coronary artery disease.

68
Q

What is hypercholesterolaemia?

A

High levels of cholesterol in blood

69
Q

What are clinical signs of hypercholesterolaemia?

A

Xanthelasma - Yellow patches on eyelids

Tendon Xanthoma - Nodules on tendon

Corneal arcus - obvious white circle around eye. Common in
older people but if present if young could be a sign of hypercholesterolaemia

70
Q

How does an atherosclerotic plaque form?

A

Macrophages digest oxidised LDLs subendothelial space, below the tunica intima. The then become foam cells and accumulate to form a fatty stream in the walls of arterioles. Fatty streaks evolve into atherosclerotic plaques which promote smooth muscle growth i the tunica media, further obstructing the lumen.

71
Q

What is the first approach treatment of hyperlipoproteinaemias?

A

Diet - Reduce cholesterol and saturated lipids in
diet. Increase fibre intake as cholesterol exits body with fibre in bile salts within faeces.
Lifestyle - Increase exercise, stop smoking to reduce cardiovascular risk.

72
Q

What is the second line of treatment for hyperlipoproteinaemias?

A

Only use if there is not a sufficient response to first line treatment. Drugs.

Statins = Reduce cholesterol synthesis in the liver by inhibiting HMG-CoA reductase e.g. Atorvastatin

Bile salt sequestrants - Bind bile salts in GI tract, promoting them to be excreted in faeces.. Forces liver to produce more bile acids using more cholesterol e.g. Colestipol

73
Q

What is the mechanism of action of statins?

A

To treat hyperlipoproteinaemias ( high cholesterol)

Acetyl-coA forms Hydroxymethyl glutaryl-CoA, a precursor of cholesterol. Hydroxymethyl glutaryl-CoA is converted to mevalonate by HMG-CoA reductase.

Statins inhibit HMG-CoA reductase, and therefore stop production of cholesterol from Hydroxymethyl glutaryl-CoA

74
Q

What tests are used to measure cholesterol?

A
  1. HDL-Cholesterol (HDL-C)
    Ideally over 1mmol/L (men) and over 1.2mmol/L (women).
  2. Triglyceride (TG) Ideally < 2mmol/L in fasted sample
  3. LDL-Cholesterol (LDL-C)
    Ideally 3 mmol/L or less
  4. Non HDL-Cholesterol (total cholesterol minus HDL-cholesterol)
    Ideally 4mmol/L or less
  5. Total Cholesterol (TC)
    Ideally 5 mmol/L or less
  6. Total cholesterol:HDL-C ratio.
    Ratio above 6 considered high risk - the lower the ratio the better.

MEH (23 decks)

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