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MEH > Lecture 4 > Flashcards

Lecture 4 Flashcards

1
Q

What are some types of lipids?

A
  • triacylglycerol (di/monoacylglycerol)
  • fatty acids
  • cholesterol (cholesterol esters)
  • phospholipids
  • vitamins ADEK
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2
Q

Why are lipids hard to transport?

A

They are hydrophobic/lipophilic so it is a problem for them to travel in the blood.

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3
Q

How are lipids transported in blood?

A

Bound to carriers

  • 2% are bound to albumin (has limited capacity)
  • 98% carried as lipoprotein particles
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4
Q

What are some typical plasma lipid concentration ranges?

A

Triacylglycerol: up to 2mmol/L
Cholesterol: <5mmol/L

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5
Q

How is the phospholipid classed?

A

By the polar head group. (Polar head group linked to phosphate head, it is hydrophilic)

E.g. choline attached to phosphate = phosphatidylcholine
E.g. inositol attached to phosphate = phosphatidylinositol

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6
Q

What is the structure of a phospholipid?

A

Polar Head: hydrophilic (phosphate and polar head group)

Nonpolar tails: hydrophobic (fatty acid tails)
-2 TAILS (saturated/unsaturated-double bond:kink, allows fluidity)

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7
Q

What structures can phospholipids form?

A
  • bilayer sheet (membrane)
  • liposomes (bilayer in a spherical structure-carry things)
  • micelles (lipoprotein: single phospholipid layer)
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8
Q

Where do you obtain cholesterol from?

A

Sometimes from the diet.

Mostly synthesised in liver. (If we don’t get our 1g of cholesterol in a day, we can just synthesise it ourselves)

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9
Q

Why is cholesterol important?

A
  • moderates fluidity of membrane
  • precursor of steroid hormones (cortisol, oestrogen, testosterone, aldosterone: all synthesised from cholesterol)
  • precursor of bile acids/salts
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10
Q

How is cholesterol transported?

A

As cholesterol ester.
Addition of fatty acid to a hydroxyl group, eliminating water.

Enzyme:

  • LCAT (lecithin cholesterol acyltransferase)
  • Acyl-coenzymeA cholesterol acyltransferase
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11
Q

What it a lipoprotein?

A

Micelles consisting of a single phospholipid sphere, inside is cargo (triacylglyercol/cholesterol ester/vitamins ADEK)

-apolipoproteins attached (apoproteins)

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12
Q

What are some types of apoproteins?

A

Peripheral: associated with surface of lipoprotein particle. (ApoC/apoE)

Integral: within the phospholipid membrane (apoA/apoB)

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13
Q

What are the 5 classes of lipoproteins?

A
  • chylomicrons (main carrier of triacylglyerol-dietary fat)
  • VLDL (very low density lipoproteins- transports fats made in the liver)
  • IDL (intermediate density lipoproteins)
  • LDL (low density lipoproteins)
  • HDL (high density lipoproteins)
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14
Q

What are the main carriers of triacylglycerol?

A

Chylomicrons

VLDL’s

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15
Q

What are the main carriers of cholesterol esters?

A

IDL’s
LDL’s
HDL’s

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16
Q

What 3 lipoproteins are related/convert?

A

VLDL’s convert to IDL’s and then LDL’s over time.

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17
Q

How do you separate lipoproteins?

A
  • flotation ultracentrifugation (HDL are most dense so furthest at the bottom-have the smallest diameter)
  • particle diameter is inversely proportional to density (as density increases, diameter decreases)
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18
Q

What are the roles of apolipoproteins?

A

Structural: package water insoluable lipid

Functional: co-factor for enzymes (can bind enzyme)
-ligands for cell surface receptors

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19
Q

How many classes of apoproteins are there?

A

6 major classes

A,B,C,D,E,H

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20
Q

What is the role of chylomicrons and how are they metabolised?

A

Transport dietary fat (triacylglycerol)

  • apoB-48 added before entering lymphatic system.
  • travel to thoracic duct, empties into left subclavian vein where apoC and apoE are added once in blood
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21
Q

Why is the addition of apoC important on chylomicrons?

A

It binds lipoprotein lipase (LPL) on capillary walls of adipocytes and muscle
-allows degredation of cargo releasing triacylglycerols inside them (TAG’s can be used as energy in muscle/stored in adipocytes)

  • when triacylglycerol content reduced to 20%, apoC dissociates leaving a CHYLOMICRON REMNANT (which returns to the liver)
  • chylomicron remnants return to liver
22
Q

Why is the addition of apoE to chylomicrons important?

A

Once the chylomicron remnants return to the liver

  • LDL receptors on hepatocytes bind to apoE
  • chylomicron remnant is taken into hepatocyte via receptor mediated endocytosis
  • contents released and metabolised by liver via lysosomes (fatty acids, glycerol, cholesterol)
23
Q

What is the function of LPL? (Lipoprotein lipase)

A

To release and degrade triacylglycerides to fatty acids and glycerol from the lipoprotein. (Chylomicron/VLDL)

They can then be used in muscles as energy, or recombined to form TAG stores in adipose tissue.

24
Q

How is VLDL transported ?

A

VLDL transports fat made by liver (TAG & cholesterol made in liver) to other tissues.

-apoB100 added to VLDL, as well as apoC & apoE added from HDL’s in the blood
-VLDL binds to LPL on endothelial cells in muscle and adipose tissue and becomes depleted of TAG
(Muscle: fatty acids for energy)
(Adipose: fattty acids for resynthesis or TAG and stored)

25
Q

Where do VLDL’s go if content is above 30%?

A

-LPL dissociates from VLDL and complex can return to liver

26
Q

What are the main function of IDL/LDL particles?

A

LDL

  • provide cholesterol from liver to peripheral tissues
  • peripheral cells express LDL receptors and take up LDL via receptor mediated endocytosis, LDL’s can also be reuptaken by liver via same mechanism to release cholesterol/TAG’s
  • responsible for formation of atherosclerotic plaques in atherosclerosis
27
Q

What happens when a VLDL starts to deplete past 30%?

A

Below 30%:

  • Formation of IDL particle (short lived)
  • IDL particles can be depleted further by rebinding to LPL/taken back to liver
  • if IDL becomes depleted to 10% of original content
  • IDL loses apoC & apoE becoming an LDL (high cholesterol content)
28
Q

What is special about LDL’s?

A
  • Have a very long half life, making them more susceptible to oxidative damage via lipid peroxidation
  • oxidised LDL taken up by macrophages forming FOAM cells, contributing to atherosclerotic plaques
  • don’t have apoC/apoE so not efficiently cleared by the liver,as hepatocytes have LDL receptor which bind to apoE
29
Q

Why do LDL enter cells?

A

Receptor mediated endocytosis.

  • cells requiring cholesterol express LDL receptors
  • apoB100 on LDL acts as ligand for those receptors
  • endocytosis forming and endocytic vesicle
  • vesicle fuses with lysosome and contents degraded
  • the LDL receptor is degraded or recycled back to cell surface
30
Q

What is HDL metabolism? (Good cholesterol)

A
  • synthesised by liver OR bud off from chylomicrons/VLDL OR formed from apoA-1
  • empty/low levels of TAG
30
Q

What does apoA-1 do?

A

-they can acquire cholesterol + phospholipid from other lipoproteins and cell membranes to form HDL’s

32
Q

What is the function of HDL?

A

Remove extra cholesterol that cells may have (reverse cholesterol uptake)

  • accumulate phospholipids and cholesterol
  • particle becomes more globular
  • doesn’t require enzymes
33
Q

What is reverse cholesterol transport?

A
  • HDL’s remove cholesterol
  • important for blood vessels as reduces likelihood of foam cells and plaque formation
  • ABCA1 protein within cell allows transfer of cholesterol into the HDL particles
  • cholesterol converted to cholesterol ester via LCAT
34
Q

What is considered ‘good/bad’ cholesterol?

A

LDL carrying cholesterol is bad- leads to atherosclerosis formation
HDL carrying cholesterol is good- removes excess cholesterol from cells and returns it back to the liver

35
Q

What happens to mature HDL’s?

A
  • taken up by liver via receptors
  • cells requiring additional cholesterol e.g. steroidogenic cells to make steroid hormones, utilise SCAVENGER receptor (SR-B1) to obtain cholesterol from HDL’s
  • the excess cholesterol once entered into the liver, can be used to make bile
36
Q

How do HDL’s contain TAG?

A

They can exchange a cholesterol ester for TAG with VLDL/LDL via cholesterol exchange transfer protein (CETP)

37
Q

What causes hyperlipoproteinaemias and what are they?

A 
Raised plasma level of one or more lipoprotein classes.
Caused by:
-over-production
-under-removal
Defects in:
-enzymes
-receptors
-apoproteins
38
Q

How many classes of hyperlipoproteinaemias?

A

6 main classes

39
Q

What are some clinical signs of hypercholesterolaemia and what is it?

A

High level of cholesterol in blood- causing deposits of cholesterol to form

  • Yellow patches on eyelid (Xanthelasma)
  • Nodules on tendon (tendon xanthoma)
  • Corneal arcus- white Circe around eye. Common in elderly, not in young so could indicate hyperchoesterolaemia
40
Q

Formation of atherosclerosis?

A

Raised serum LDL

  • oxidised LDL: lipid inside becomes oxidised (due to longer half life)
  • oxidised LDL particle is recognised by macrophages and engulfed
  • macrophages become laden with lipid forming FOAM CELLS
  • foam cells accumulate in the intima (innermost layer) of the blood vessel walls forming a fatty streak
  • fatty streaks can evolve into an atherosclerotic plaque
  • plaques can grow and restrict lumen
41
Q

Symptoms of atherosclerosis?

A

In coronary artery:
-angina (plaque blocking blood flow, lack of oxygen to myocardium)
Plaque ruptures
-thrombus forms (clot) activating platelets, block entire artery
(In coronary artery= MI, in brain artery = Stroke)

-promotes smooth muscle growth so tunica media gets larger also

42
Q

How do you treat hyperlipoproteinaemia?

A

1st approach:

  • diet (reduce cholesterol & saturated lipids, increase fibre intake)
  • lifestyle (increases exercise & stop smoking- remove oxidative stress)

2nd approach:

  • Statins ( reduce synthesis of cholesterol, by inhibiting HMG-CoA) e.g.atorvastatin
  • bile salt sequestrants (bind bile salts in GI tract: forces liver to make more bile acids using more cholesterol) e.g.colestipol
43
Q

How do statins work?

A

Inhibit HMG-CoA reductase
-catalyses HMG-CoA to mevalonate

Acetyl-CoA > HMG-CoA > mevalonate&raquo_space;>squalene»>cholesterol

44
Q

Why do you get side effects when using statins?

A

Because the statin blocks the synthesis of cholesterol strongly and early on so the other metabolites produced in the synthesis are also not produced.

45
Q

What is the desired non-HDL cholesterol concentration?

A

4 mmol/L or less

46
Q

What is the ideal LDL-cholesterol levels?

A

3 mmol/L or less

47
Q

What is the ideal HDL cholesterol conc?

A

Over 1/1.2 mmol/L

48
Q

Ideal triacylglycerol concentration?

A

Less than 2 mmol/L

49
Q

How is apoB-48 derived from apoB-100?

A

RNA editing.
ApoB-100 is the full size
-RNA from apoB-100 is edited to produce an early stop codon= 48% of original size

50
Q

How can you distinguish between chylomicrons and VLDL’s?

A

Chylomicrons contain apoB-48

VLDL’s contain apoB-100

51
Q

Why do chylomicrons enter the lymphatic system and enter the blood at the left subclavian artery?

A

To bypass fast metabolism by the liver.

MEH (22 decks)

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