Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Metabolism > Lipid transport in blood > Flashcards

Lipid transport in blood Flashcards

1
Q

overview process of fuel storage (basic)

A
  • energy providing foods are consumed in greater quantities than needed at the time
  • excess energy is stored
  • CHO stored as glycogen, but store limited as liver glycogen dissapears overnight
  • long term fuel store is lipid as TAG
  • lipid storage is not limited = we get fat
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what fuel store is limited

A

CHO as glycogen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what fuel store isnt limited

A

lipid as TAG

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what is TAG

A

triacylglycerol

  • glycerol phosphate
  • 3 x fatty acids
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

where does TAG synthesis occur

A

in nearly all cells

but mostly in the liver, SI and adipose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what is glycerol phosphate

A

active form of glycerol and comes from glycolysis.

the phosphate group leaves once TAG is formed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

state of TAG

A

completely hydrophobic and therefore will NOT circulate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

how are TAGs made hydrophillic

A

addition of apoproteins and other lipids such as plp c and VLDL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

plp c

A

phospholipid cholesterol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

VLDL

A

very low density lipoprotein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

lipoprotein structure

A

outer shell:
- singles layer of phospholipids, cholesterol and apoproteins

inner shell:
- TAG and cholesterol esters

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what are the hydrophilic parts of lipoprotein

A

phospholipids
cholestorol
apoproteins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what are the hydrophobic parts of lipoprotein

A

TAG

cholesterol esters

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

state of phospholipids

A

hydrophilic, charged and polar

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

state of cholesterol

A

hydrophillic and polar

NOT charged

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

purpose of lipoprotein

A

allows lipid, which is insoluble in water, to be transported as a lipoprotein complex

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

role of apoproteins

A
  • don’t function on their own
  • structural role as they are onthe outside of lipoprptein bc hydrophillic
  • recognised by receptors on cell surfaces
  • activate certain enzymes in lipid metabolism
  • important for transport and storage
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

classes of lipoproteins

A

chylomicrons
VLDL
LDL
HDL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

how do classes of lipoproteins vary

A

more fat = lower density

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

chylomicrons

A
  • largest and lowest density lipoprotein

- carry mainly TAG

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

VLDL

A
  • very low density lipoprotein

- carries mainly endogenous fat/TAG

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

LDL

A
  • low density lipoprotein
  • carries mainly cholesterol to the tissue
  • BAD CHOLESTEROL
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

HDL

A
  • high density lipoprotien
  • carries mainly cholesterol, from the tissue to the liver
  • cholesterol is taken to liver for excretion
  • GOOD CHOLESTEROL
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

what apoproteins are found on chylomicrons

A

apo B48
found in the intestine; fat that we eat
48 AA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

what apoproteins are found on VLDL

A

apo B-100

100 AA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

what apoproteins are found on LDL

A

apo B-100

100 AA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

B-100

A
  • apoprotein found on VLDL and LDL
  • important for receptor recognition
  • 100 AA
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

B-48

A
  • apoprotein found on chylomicrons
  • structural role
  • 48 AA
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

apo-E

A
  • apoprotein on chylomicron remnants
  • important for receptor recognition
  • or from HDL
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

apo C-11

A

activates LPL

- on chylomicrons

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

apo A-1

A

activates LCAT

- on HDL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

How do apoproteins work as destination-targeting signals

A
  • bind to specific receptors on the surface of cells
  • binding leads to uptake of the lipoprotein bound to apo
  • uptake is receptor-mediated endocytosis
    = individual lipoproteins are taken up only by designated cells for specificty
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

what is the uptake method for lipoproteins in to cells

A

receptor-mediated endocytosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

LPL

A

lipoprotein lipase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

apoproteins that activate enzymes

A

apo C-11 on chylomicrons activates LPL
= removes fatty acids from TAG
apo A-1 on HDL activates LCAT
= forms cholesterol in peripheral cells and phospholipd on HDL itself, and carries as ester to the liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

current average fat intakes

A

~80g per day

needs to be reduced by 30%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

what activates LPL

A
  • apo C-11

- insulin in absorptive state

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Transport of lipid from the gut: exogenous fat

A
  • fat eaten
  • TAG from SI joins with apo-E and apo C-11 from HDL in cirucaltion to form chylomicron for cirucaltion
  • LPL on capillary lining is activated by apo C-11 and insulin in absorptive state, and hydrolyses TAG
  • TAG cannot move across membrane, but FA can
  • FA cross to adipose where re-esterified using GP from glycolysis
  • glycerol from TAG is inactive, and goes to liver where glyerol kinase activates it
  • of the remaining chylomicron:
    - apo C-11 returns to HDL
    - apo E binds to recepto on liver causes chylomicron remnant to be internalised and reused
39
Q

Transport of lipid from the gut: endogenous fat

A

similar to the process of exogenous liver, but starts from VLDL in the liver

  • VLDL has b-100, but also picks up C-11 and E from HDL
  • LPL on capillary lining is activated by apo C-11 and hydrolyses TAG
  • TAG cannot move across membrane, but FA can
  • FA cross to adipose where re-esterified using GP from glycolysis
  • glycerol from TAG is inactive, and goes to liver where glyerol kinase activates it
  • of the remaining VLDL is becomes IDL, and apo E and C-11 return to HDL
  • IDL is now LDL with just B-100 apoprotein, consisting of mostly cholesterol
  • 50% of LDL will go to the liver via B100 receptor
  • 50% of LDL will go to periphery by B100 receptor
40
Q

what does defective b100 receptor cause

A

high blood cholesterol

41
Q

cholesterol synthesis

A

we do not need cholesterol from the diet becuase we can biosynthesis it
- if diet provides cholesterol, biosynthesis is reduced and number of b100 receptors on cell surface

42
Q

control of cholesterol synthesis

A
  • nucleus makes LDL receptors
  • B-100 on LDL binds to receptor and whole of LDL is internalised
  • lysosome forms and cholesterol is released along with proteins from LDL
  • cholesterol release effects the nucles to stop synthesis of enzymes used to synthesis cholesterol
    = balance between diet and biosynthesis
  • vegans rely on biosynthesis
43
Q

who relies on cholesterol biosynthesis

A

vegans

44
Q

LDL receptors

A
  • very important
  • recognises B-100 on LDL
  • remove LDL and hence cholesterol from circulation
    = receptor mediated endocytosis
45
Q

LDL receptor deficiency

A

= familia hypercholesterolemia

  • very high blood cholesterol levels
  • premature death from atherosclerosis (8yrs!!)
46
Q

how is cholestoerl synthesised (biochem prcess)

A
  • acetyl CoA + acetoacetyl CoA -> HMG-CoA
  • HMG-CoA -> mevalonate = rate limiting step
    needs HMG-CoA reductase
  • mevaolonate -> cholestorel
47
Q

what is the rate limiting step of cholesterol synthesis

A
  • HMG-CoA -> mevalonate = rate limiting step

needs HMG-CoA reductase

48
Q

enzyme needed for cholesterol synthesis

A

HMG-CoA reductase

49
Q

how is cholesterol reduced therapeutically

A

statins

50
Q

how do statins work

A

statins ihibit HMG-CoA reductase, and therefore decreases cholesterol synthesis in cells

  • this allows liver and periphery to take up more cholesterol from the circulation
  • 0.5g/day is removed from circuation by liver in the form of bile salts
51
Q

what does removal of cholsterol from circulation by liver from

A

bile salts

52
Q

alternative approaches for reducing total LDL cholesterol

A
  • inhibitors of cholesterol absorption
  • bile acid sequestering agents
    = prevent reabsorption from the intestine
53
Q

LCAT

A

lecithine cholesterol acyltransferase
- transfers acyl group (FA) from lecithine and puts it on cholesterol

LCAT AKA PCAT
lecithine = phosphatidylcholine

54
Q

descirbe HDL

A
  • high density lipoprotein
  • HLD are good cholesterol
  • made in SI and liver
  • flat and hollow inside
  • comes with Apo- A1
55
Q

role of HDL in cholesterol transport

A
  • HDL goes to peripheral cells to remove cholesterol
  • LCAT is activated by apo-A1 on HDL
  • LCAT removes a FA from lecithine to bind to cholesterol and transport from periphery to HDL
  • cholesterol ester is formed and buried inside HDL bc neutral
  • Most cholesterol ester then taken to liver for excretion
  • some CE is offloaded to VLDL to allow HDL to continue removal of cholesterol
  • this is becuase build up of CE in HDL inhibits LCAT
56
Q

CETP

A

cholsterol ester transfer protein

57
Q

what does CETP do

A

CETP allows the offloading of CE to other lipoproteins

  • HDL transfers CE to LDL, IDL and VLDL
  • IDL and LDL deliver contents to extrahepatic tissues but a proprtion retun to liver using LDL receptor
  • transfer of CE between lipoproteins is reversible
  • without CEPT, LCAT would be inhibited by CE
  • inhibition of LCAT would stop efficent removal of cholsterol from circulatin
58
Q

IDL

A

intermediate density lipoprotein

59
Q

what is the recepto though which HDL delivers cholesterol directly to the liver

A

SR-B1

60
Q

normal cholestero levels

A

~5

61
Q

high serum cholesterol is

A

bad

62
Q

high HDL is

A

good

63
Q

accumulation of high cholesterol in lymphatic organs and premature CV disease =

A

Tangier diease

64
Q

what is Tangier disease

A

accumulation of high cholesterol in lymphatic organs and premature CV disease =

65
Q

what causes Tangier disease

A
  • deficiency of gene coding for ABCA-1 transferase

- ABC-1 is needed to transport cholesterol out of cells to HDL and enables macrophages to unload cholesterol

66
Q

ABC-1 transferase

A

ATP binding casette 1

  • needed to transport cholesterol out of cells to HDL and enables macrophages to unload cholesterol
  • antiatherogenic
67
Q

antiatherogenic

A

preventing or inhibiting atherogenesis or antiatherogenic effects

68
Q

Apo-1 milano

A

mutation in Apo A1 that was recognised in a lab in Milan
- Apo A1 is needed to activate LCAT
- carriers have v low HDL so expected to have high incidence of CVD
BUT
people with Apo-1 milano have been shown to live to 100
- presumably from increased efflux of cholesterol
- possible therapeutic treatment?

69
Q

varieties of hyperlipidaemias

A
  • hypercholesterolaemia
  • hypertriglycerideaemia

effected by either genetics or diet and lifestyle

70
Q

examples of genetic hyperlipoproteinaemias

A
  • defective LDL receptor
  • lipoprotein lipase deficiency
  • deficiency of C-11
  • deficiency of apoproteins involved in remnant uptake
71
Q

effects of defective LDL receptor

A

hypercholesterolaemia

- high LDL in blood

72
Q

effects of lipoprotein lipase deficiency

A

high chylomicrons and VLDL

73
Q

effects of C-11 deficiency

A

high chylomicrons and VLDL

74
Q

effects of deficiency of apoproteins involved in remnant uptake

A
  • high chylomicron and VLDL remnant
75
Q

risk factors for secondary hyperlipoproteinaemias

A
  • obesity
  • T2D
  • dietary cholesterol
  • diestry FA (SFA)
  • alcoholism
76
Q

how does alcohol effect lipoprotein

A
  • exercise and small amounts of exercise increase HDL but lots of alcohol increases LDL
77
Q

What lifestyle factors increase HDL

A

exercise and small amounts of exercise

78
Q

difference of dietary FA

A
  • SFA vs PUFA
    n-6 PUFA lower cholesterol
    n-3 PUFA lower TAG
79
Q

what is lipoprotein a

A

Lp (a) is LDL with apo-A

80
Q

high levels of Lp(a)

A
  • high concentrations in plasma are associated with increased CHD risk
  • levels of Lp(a) are gentic but can be increased by transfat and decreased by oestrogen
  • related to plasminogen
  • Lp(a) slows the breakdown of blood clots by competeing with plasminogen
81
Q

CHD

A

coronary heart disease

82
Q

what increases Lp(a)

A

trans fats

83
Q

what decreases Lp(a)

A

oestrogen

84
Q

what is atherosclerosis

A

plaque build up
plaque is:
- complex structure involving inflammation and proliferation of smooth muscle in artery wall
- contains connective tissue and pool of holesterol rich lipid
- stars as a fatty streak from accumulation of foam cells

85
Q

what are foam cells

A

macrophages filled with lipid, mainly cholesterol

86
Q

how do foam cells effect LDL metabolism

A
  • usually LDL will go to extrahepatic cells when cholesterol is low, and to the liver for excretionwhen cholesterol is high

but, when there’s too much LDL it becomes oxidised and is no longer recognised by normal receptor
- oxidised LDL is recognised by scavenger receptor in foam cells
- scavenger regualtors are not down regulated like normal LDL receptors
= cholesterol accumulation

87
Q

what happens to stored fat

A

hormone sensitive lipase inside adipocyt is activated by glycogen in he fasting state, and inhibited by insulin in the fed state

fasting state:

  • free FA are released into bloodstream from adipocytes
  • not actually ‘free’ but they are non-esterified
88
Q

NEFA transport

A

carried adsorbed to the surface of blood protein: serum albumin

89
Q

why is serum albumin a carrier for many molecules

A

it has hydrophobic patches on its surface and so is the carrier for many molecules with hydrophobic sections

90
Q

can the brain use FFA as energy source

A

no, serum bound FFA cannot cross the blood brain barrier

91
Q

ketone bodies function

A
  • act on pancrease to stimulate insulin release
  • insulin limits muscle proteolysis and adipose lipolysis
    = conservation of muscle tissue
92
Q

ketones action during fasted state

A
  • causes insulin producting from beta cells
  • start breaking down fat which limits protein breakdown
  • concervse protein, which is the only source of glucose in fasted state
  • glucose is needed for brain
93
Q

ketones and diabetes

A

action of ketones is not good for diabetics
- during starvation, ketons usually causes insulin producting from beta cells
- this cant happen in diabetics
= ketoacidoses from accumulation of ketones = medical emergency

94
Q

What is the mechanism by which malonyl-CoA regulates fatty acid oxidation

A

inhibits fatty acid transport into mitochondria

Metabolism (11 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions