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Cardiovascular > Cholesterol and Lipid Metabolism > Flashcards

Cholesterol and Lipid Metabolism Flashcards

1
Q

describe the solubility of lipids

A

insoluble, or sparingly soluble, in water

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2
Q

what are lipids essential for?

A

membrane biogenesis

membrane integrity

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3
Q

what are the roles of lipids?

A

energy sources
precursors for hormones
signalling molecules

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4
Q

give two non polar lipids?

A

cholesterol esters

triglycerides

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5
Q

how are non polar lipids transported in the blood?

A

within lipoproteins

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6
Q

what are the types of lipoproteins?

A

high density lipoproteins (HDL)
low density lipoproteins (LDL)
very low density lipoprotein (VLDL)
chylomicrons

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7
Q

what is the difference in lipoproteins in people with CV disease?

A 
elevated LDL (or particles rich in triglycerides)
decreased HDL
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8
Q

what are the causes of the difference in lipoproteins in people with CV disease?

A

diet and lifestyle

genetic factors eg familial hypercholesterolaemia

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9
Q

what do lipoproteins consist of?

A

a hydrophobic core and a hydrophilic coat

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10
Q

describe the hydrophobic core of lipoproteins

A

contains esterified cholesterol and triglycerides

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11
Q

describe the hydrophilic coat of lipoproteins

A

a monolayer of amphipathic cholesterol, phospholipids and one, or more, apoproteins

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12
Q

which apoproteins do HDLs contain?

A

apoA1 and apoA2

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13
Q

which apoprotein do LDLs contain?

A

apoB-100

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14
Q

which apoprotein do VLDLs contain?

A

apoB-100

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15
Q

which apoprotein do chylomicrons contain?

A

apoB-48

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16
Q

what is the role of apo-B containing lipoproteins?

A

deliver triglycerides to muscle for ATP biogenesis and adipocytes for storage

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17
Q

where are chylomicrons formed?

A

intestinal cells

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18
Q

what is the role of chylomicrons?

A

transport dietary triglycerides

the exogenous pathway

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19
Q

where are VLDL particles formed?

A

liver cells

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20
Q

what is the role of VLDL particles?

A

to transport triglycerides synthesised in that organ

the endogenous pathway

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21
Q

summarise the life cycle of apo-B containing liposomes

A

assembly
intravascular metabolism (involving hydrolysis of the triglyceride core)
receptor mediated clearance

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22
Q

how are triglycerides in chylomicrons formed?

A

monoglycerides combine with free fatty acids

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23
Q

how are cholesteryl esters in chylomicrons formed?

A

cholesterol combines with NCPC1L protein and esterifies

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24
Q

how are chylomicrons assembled?

A

triglyceride combines with apoB48

MTP and lipidation are used

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25
Q

what is an enterocyte?

A

an intestinal cell

the site of chylomicron assembly

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26
Q

how do chylomicrons exit enterocytes?

A

by exocytosis following the addition of a second apoprotein (apoA1)

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27
Q

how are chylomicrons carried to the systemic circulation?

A

they enter the lymphatics and is crammed in lymph via the thoracic duct

28
Q

what is MTP?

A

microsomal triglyceride transfer protein

29
Q

where are the components that form chylomicrons derived from?

A

digestion of dietary fat and bile

30
Q

where are the fatty acids that form VLDL particles derived from?

A

adipose tissue and de novo synthesis

31
Q

describe the assembly of VLDL particles

A

MTP lipidates apoB100 forming nascent VLDL that coalesces with triglyceride droplets

32
Q

how are chylomicrons and VLDL particles activated?

A

by the transfer of apoCII from HDL particles

33
Q

what is lipoprotein lipase (LPL)?

A

a lipolytic enzyme associated with the endothelium of capillaries in adipose and muscle tissue

34
Q

how are apoB containing lipoproteins metabolised?

A

ApoCII facilitates binding of the lipoproteins to LPL which hydrolysis core triglycerides to free fatty acids and glycerol which enters tissues

35
Q

what are the particles depleted of triglycerides but still containing cholesteryl esters termed?

A

chylomicron and VLDL remnants

36
Q

what is the role of LPL?

A

causes the particles to become relatively enriched in cholesterol due to triglyceride metabolism

37
Q

what is apoE?

A

a high affinity ligand for receptor mediated clearance

38
Q

what happens once the apoB containing lipoproteins dissociate from LPL?

A

apoCII is transferred to HDL particles in exchange for apoE
remnants return to the liver and are further metabolised by hepatic lipase
all apoB48 remnants and half apo100 remnants are cleared by receptor mediated endocytosis into hepatocytes

39
Q

what happens to the remaining apoB100 containing remnants?

A

they lose further triglyceride through hepatic lipase, become smaller and enriched in cholesteryl ester and via intermediate density lipoproteins become LDL particles lacking apoE and retaining solely apoB100

40
Q

what is the clearance of LDL particles crucially dependant upon?

A

the LDL receptor expressed by the liver and other tissues

clearance by the liver is most important

41
Q

how does cellular uptake of LDL particles occur?

A

receptor-mediated endocytosis

42
Q

how is cholesterol released in the cell?

A

at the lysosome, it is released from choleryl ester by hydrolysis

43
Q

what does released cholesterol cause?

A

inhibition of HMG-CoA reductase which is the rate limiting enzyme in de novo cholesterol synthesis
down regulation on LDL receptor expression
storage of cholesterol as cholesterol ester

44
Q

why is LDL the bad cholesterol?

A

because at the start of atherosclerosis, LDL from the blood is uptaken into the intima of the artery and oxidised into atherogenic oxidised LDL

45
Q

what initiates atherosclerosis?

A

dysfunction and injury of the lining of blood vessels

46
Q

why is HDL the good cholesterol?

A

it plays a key role in removing excess cholesterol from cells by transporting it in plasma to the liver
only the liver has the ability to eliminate cholesterol from the body

47
Q

where is HDL formed?

A

mainly in the liver

48
Q

how is HDL formed?

A

initially as apoA1 in association with a small amount of surface phospholipid and unesterified cholesterol (disc like pre-B-HDL)
this matures in the plasma to spherical a-HDL as surface cholesterol which is enzymatically converted to hydrophobic cholesterol ester that migrates to the core of the particle

49
Q

how does HDL deliver cholesterol to the liver?

A

it accepts excess cholesterol from the plasma membrane of cells and transports it via transport cholesterol tranport

50
Q

what happens once HDL reaches the liver?

A

it interacts with a receptor (scavenger receptor B1) that allows transfer of cholesterol and cholesteryl esters into hepatocytes

51
Q

what does cholesterol ester transfer protein (CETP) do?

A

in the plasma it mediates the transfer of cholesteryl esters from HDL to VLDL and LDL, indirectly returning cholesterol to the liver

52
Q

what is the classification system of primary dyslipidaemia?

A

Frederickson

53
Q

what causes primary dislipidamia?

A

a combination of diet and genetic factors

54
Q

what causes secondary dislipidaemia?

A

it is a consequence of other diseases eg type II diabetes, hypothyroidism, alcoholism, liver disease

55
Q

name examples of statins

A

simvastatin and atorvastatin

56
Q

how do statins reduce cholesterol?

A

act as competitive inhibitors of HMG-CoA reductase which is the rate limiting step in cholesterol synthesis in hepatocytes
decrease in hepatocyte cholesterol synthesis causes a compensatory increase in LDL receptor expression and enhanced clearance of LDL

57
Q

when are statins ineffective

A

in homozygous familial hypercholesterolaemia where LDL receptors are lacking

58
Q

when are fibrates used?

A

in patients with very high triglyceride levels

59
Q

name fibrates

A

bezafibrate

gemfibrozil

60
Q

how do fibrates act?

A

they are agonists of a nuclear receptor (PPARalpha) which enhances the transcription of the gene that encodes for LPL

61
Q

name bile acid binding resins

A

colestyramine
colestipol
colsevelam

62
Q

how do bile binding resins act?

A

they cause the excretion of bile salts resulting in more cholesterol to be converted to bile salts by interrupting enterohepatic recycling

63
Q

what do binding resins cause?

A

decreased absorption of triglycerides and increased LDL receptor expression

64
Q

how does ezetimibe act?

A

it inhibits NPC1L1 transport protein in enterocytes of the duodenum, reducing the absorption of cholesterol

65
Q

what does ezetimibe cause?

A

a decrease in LDL with little change in HDL

Cardiovascular (31 decks)

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