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Phase 1 - S2 Metabolism, Endocrinology, Haematology > Lipid transport > Flashcards

Lipid transport Flashcards

1
Q

what are the 5 lipoprotein transporters

A 
chylomicrons
VLDL
IDL
LDL
HDL
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2
Q

true or false: lipids are hydrophilic

A

false - they’re hydrophobic which makes them difficult to transport in the blood

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3
Q

how are fatty acids transported in the blood

A

by being carried by albumin

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4
Q

how are 98% of lipids transported

A

in lipoprotein particles

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5
Q

describe phospholipid molecules

A
  • they have a hydrophobic tail made up of 2 fatty acids
  • glycerol backbone
  • phosphate
  • polar hydrophilic head attached to the phosphate
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6
Q

what part of the phospholipid classifies it

A

the hydrophilic head which can be either choline or inositol

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7
Q

what shape of phospholipids carry aqueous cargo

A

liposome

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8
Q

what shape of phospholipids carry hydrophobic cargo

A

micelle

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9
Q

where is most of the bodys cholesterol obtained

A

from synthesis in the liver

small amount comes from the diet

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10
Q

what is cholesterol used for

A
  • for stability in membranes
  • precursor to steroid hormones
  • precursor to bile acids
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11
Q

give 4 examples of steroid hormones

A

oestrogen
testosterone
aldosterone
cortisol

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12
Q

how is cholesterol transported around the body

A

it is converted into cholesterol esters but LCAT enzymes

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13
Q

what are apolipoproteins

A

proteins found either passing through the phospholipid membrane (peripheral) or on the surface (integral) of lipoproteins

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14
Q

what are the functions of apolipoproteins

A
  • allows lipoprotein molecule to form by allowing packaging of the water insoluble contents
  • act as cofactors for enzymes to break down lipids
  • act as ligands to receptors to take up cargo
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15
Q

what does the density of lipoproteins depend on

A

the amount of apolipoproteins on their surface

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16
Q

in a flotation ultracentrifugation which lipoprotein migrates the furthest

A

HDL

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17
Q

for more dense lipoproteins what happens to the size of their diameter

A

It decreases

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18
Q

what apolipoprotein is added to chylomicrons before they enter the lymphatic system

A

apoB-48

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19
Q

when chylomicrons enter the left subclavian vein what other apoproteins are added

A

apoC and apoE

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20
Q

what does the addition of apoC to chylomicrons allow

A

the binding to lipoprotein lipase on adipocytes and muscle allowing the chylomicrons to release their fat

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21
Q

what do chylomicrons mostly contain

A

dietary fat

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22
Q

what do VLDL contain

A

TAGs synthesised by the liver

23
Q

what happens to chylomicrons when the TAG content is reduced to 20%

A

the apoC dissociates and the chylomicron becomes a chylomicron remnant

24
Q

what happens to chylomicron remnants

A

they return to the liver and the apoE allows it to bind to LDL receptors on hepatocytes to be taken up by receptor mediated endocytosis

25
Q

where is VLDL synthesised

A

in the liver

26
Q

what apoproteins bind to VLDL

A

apoB100, apoC and apoE

27
Q

how do VLDL become depleted

A

they bind to LPL in the muscle and adipose cells

28
Q

what happens to the fatty acids taken up by muscle and adipose cells

A

muscle - used in energy production

adipose - resynthesised to TAGs and stored

29
Q

how are IDLs formed

A

when the TAG content of VLDL drops to 30%

30
Q

how are LDL formed

A

when the TAG content of IDL depletes to 10% and so loses its apoC and apoE

31
Q

what happens to IDL particles

A
  • can be taken up by the liver

- or can rebind to LPL to be further depleted

32
Q

what is the cholesterol content in LDLs like

A

very high

33
Q

what is the function of LDL

A

provide cholesterol from thee liver to tissues

34
Q

how are LDLs taken up by cells

A

attach to LDL receptor then taken up by receptor mediated endocytosis

35
Q

why aren’t LDLs efficiently cleared up by the liver

A

as Liver LDL receptors have a high affinity for apoE which the LDL doesn’t have

36
Q

why do LDLs become oxidisied

A

they have a long half life so are more susceptible to oxidative damage by free radicals

37
Q

outline receptor mediated endocytosis for LDLs

A
  • LDLs have the apoB100 as a ligand which binds to LDL receptors on cells requiring cholesterol
  • complex is taken up by endocytosis
  • fuse with lysosomes for digestion as release of cholesterol and fatty acids
38
Q

how are nascent HDLs synthesised

A
  • by the liver and intestine in low TAG levels
  • bud off from chylomicrons and VLDL as they’re digested by LPL
  • from apoA1 can aquire cholesterol and phospholipids to form the HDL
39
Q

how are the nascent HDLs filled

A
  • they can accumulate phospholipids and cholesterol from cells lining blood vessels
  • core progressively fills
  • this doesn’t require enzymes
40
Q

what do HDLs do

A

remove cholesterol from cells and returns it to the liver

41
Q

what do HDLs reduce the likelihood of

A

foam cell and atherosclerotic plaque formation

42
Q

what protein facilitates the transfer of cholesterol to HDLs

A

ABCA1

43
Q

what happens to the cholesterol when it enters HDLs

A

it is converted into cholesterol esters by LCAT

44
Q

as well as the liver where else might HDLs deliver cholesterol to

A

steriodogenic cells as they have a scavenger receptor to allow this

45
Q

what protein allows the exchange of cholesterol ester for TAG between HDLs and VLDLs

A

cholesterol exchange transfer protein

46
Q

what is hyperlipoproteinaemia

A

where there is raised plasma levels of one or more lipoproteins classes

47
Q

what causes hyperlipoproteinaemia

A
  • over production

- under removal

48
Q

what causes type I, IIa and III of hyperlipoproteinaemia

A

I - defective lipoprotein lipase
IIa - defective LDL receptor
III - defective apoE

49
Q

what are the clinical signs of hypercholesterolaemia

A
  • xanthelasma - yellow patches on eyelids
  • tendon xanthoma - nodules on tendons
  • corneal arcus - white circle around eye
50
Q

what does raised LDL level cause

A
  • engulfed by macrophages forming foam cells which accumulate in intima to give fatty streak
  • develops into atherosclerotic plaque
  • grows and reduces lumen
  • this can rupture to trigger a thrombosis
51
Q

what are the treatments for hyperlipoproteinaemias

A
  • reduce cholesterol and saturated fat intake
  • increase fibre
  • increase exercise
  • reduce smoking
  • statins
  • bile salt sequestrants
52
Q

what do statins do

A

inhibit HMG-CoA reductase which is used in the production of cholesterol

53
Q

what do bile salt sequestrants do

A

bind to bile salts in the GI tract so they are egested. this means more cholesterol is needed to make bile salts

54
Q

what can cholesterol tests measure

A
  • total cholesterol level
  • non HDL level
  • LDL level
  • HDL level
  • triglyceride level
  • ratio of total cholesterol to HDL

Phase 1 - S2 Metabolism, Endocrinology, Haematology (22 decks)

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