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Metabolism > Lipoprotein handling > Flashcards

Lipoprotein handling Flashcards

1
Q

what is triglyceride made out of

A

3 fatty acids and glycerol

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2
Q

how is a triglyceride made

A
  • made by esterification
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3
Q

why use free fatty acids as an energy store

A
  • they are the major fuel for metabolism
  • they are the immediate source of energy
  • there oxidation produces a higher ATP than the oxidation of carbohydrates and proteins
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4
Q

How are triglycerides transported in the blood

A
  • triglycerides are hydrophobic therefore they are no readily transported in the blood
  • packaged into lipoproteins - these use cholesterol and proteins
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5
Q

where is TAG stored

A
  • Liver and adipose tissue
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6
Q

what is the purpose of lipogenesis

A

converts acetyl-CoA to fatty acids

- via lipogenesis and triglyceride synthesis energy can be efficiently stored in the form of fats

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7
Q

whereas does lipogenesis take place

A
  • adipose tissue
  • liver
  • cytosol of cells
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8
Q

what do lipoproteins do

A
  • the transport of TAG, cholesterol and phospholipids between different organs and tissues.
  • they also trnsport some vitamins
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9
Q

what are lipoproteins made by

A

hepatocytes and enterocytes

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10
Q

what is the inner core of the lipoproteins made form

A

inner core is hydrophobic

- cholesterol esters and TAG and located in the core

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11
Q

what is the outer core of lipoproteins made out of

A
  • phospholipids
  • free cholesterol
  • apoproteins (these different between lipoprotein)
  • outer core is hydrophilic
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12
Q

what are two different types of apoprotein s

A

embedded (apoB) or loosely bound (apoC)

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13
Q

what do apoproteins do

A

they determine the role of lipoproteins (cellular interaction)

  • they activate and inhibit enzymes in lipoprotein metabolism
  • Ligands for the cellular apoB/E (LDL) receptors and scavenger receptors
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14
Q

what receptors are responsible for LDL clearance

A

ApoB/E receptors & scavenger receptors are responsible for LDL clearance

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15
Q

what are the 5 major types of lipoproteins

A 
chylomicrons 
VLDL
IDL
LDL
HDL
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16
Q

what is the order of apopprotiens from least dense to most dense

A 
chylomicrons 
VLDL
IDL
LDL
HDL
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17
Q

what is the main component of chylomicrons and what apoprotein does it have

A

TAG

B48 A C E

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18
Q

what is the main component of VLDL and what apoprotein does it have

A

TAG

B100 A C E

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19
Q

what is the main component of IDL and what apoprotein does it have

A

TAG and cholesterol

B100 E

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20
Q

what is the main component of LDL and what apoprotein does it have

A

Cholesterol

B100

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21
Q

what is the main component of HDL and what apoprotein does it have

A

Protein

AI AII C E

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22
Q

What does Apo B100 do

A
  • it controls the metabolism of LDL

- it is truncated from apoB48

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23
Q

what does APO B48 do

A

controls chylomicrons

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24
Q

what does APOE do

A
  • controls receptor binding of remnant particles
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25
Q

what does Apo C do

A

it acts as an enzyme inhibitor

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26
Q

what happens to chylomicrons

A
  • chymicrons originate from the enterocytes
  • chylomicrons are then converted to IDL it can then be converted to TAG by lipoprotein lipase
  • or it can then be converted back to the liver
  • or it can be converted to LDL
27
Q

what happens to LDL

A
  • LDL is even converted to cholesterol to cells or it is converted back to the liver
28
Q

what happens to HDL

A

HDL is produced by the liver , it then picks up excess cholesterol from the peripheral tissue to the liver for disposal

29
Q

what colour is someones blood who has just eaten fat blood plasma

A

Dietary fat goes into blood plasma and this makes it more cloudy

30
Q

describe how chylomicrons are used

A
  • Gut loads both the fatty acids and cholesterol into the lipoproteins called chylomicrons
  • They contain Apo protein B48
  • The chylomicrons then flow through the circulation
31
Q

what do chylomicrons interact with

A
  • interact with peripheral tissue, this contains lipoprotein lipase this allows the chlyomicrons to deposit the contents of the chylomicrons into the tissue
  • it also interacts with HDL, they swap the app proteins, this increases the levels of Apo protein CII and increases the level of app protein E
    the Apo protein E targets it from disposable therefore the liver takes it out of circulation
32
Q

what do lipoprotein lipase do

A
  • They interact with chylomicrons and VLDL

- Breaks it into free fatty acids and glycerol and these can be taken up by cells and used to store fat

33
Q

what app protein activates lipoprotein lipase

A

Apo Protein C2

34
Q

what happens after you eat a meal to lipoprotein lipase

A
  • after a meal LPL activity is high in adipose tissue
  • therefore most fatty acid from TAG is chylomicrons are targeted to adipose tissue for etherification and storage
  • the remnants are then metabolised by the liver
35
Q

what is the half life of chylomicrons

A

less than 1 hour

36
Q

what happens duration starvation to lipoprotein lipase

A
  • LPL activity is high in muscle
  • therefore FA derived from TAG in VLDL and is mainly fed into oxidation therefore it makes acetyl- CoA and enters the TCA cycle
37
Q

what does ApoA do

A
  • efflux of cholesterol from peripheral cells and the influx of cholesterol into hepatocytes
38
Q

What does ApoB do

A

ApoB100 and ApoB/E receptors cause cellular uptake of LDL - it is derived from liver and forms part of LDL
- Apo B48 is derived from the gut and is found in chylomicrons

39
Q

what does ApoC do

A
  • made in the liver
  • it is the peripheral activator of LPL
  • transferred between lipoproteins
40
Q

what does ApoE do

A
  • stabilises VLDL, ILDL and remnant particles causes cellular uptake
  • ligand for the Apo B/E receptor
41
Q

what makes up the fatty acids in the diet

A
  • most fatty acids are supplied by the diet
  • 90% is in the form of triglyceride
  • cholesterol
  • cholesterol ester
  • phospholipids
  • free fatty acid
42
Q

what are dietary TAG lipoproteins packaged into

A

chylomicrons

43
Q

how is liver derived TAG released

A
  • it is releases as VLDL
44
Q

where is lipoprotein lipase situated (lipoprotein metabolism)

A
  • it is situated on the endothelium adjacent to target cells
  • it is the gatekeeper of lipoprotein metabolism
45
Q

describe what happens to low density lipoproteins

A
  • after their secretion VLDL acquires cholesterol easter and apoproteins ApoC and ApoE from HCL
  • They are hydrolysed by LPL and this makes VLDL remnants called IDL
  • the conformation of ApoB100 and ApoE in VLDL prevents them binding to the LDL (APOB/E) recemport
  • in remnants ApoE assumes a conformation that allows them to bind to the LDL receptor
  • there is a liver enzyme (hepatic TAG lipase_ this makes IDL transform into the rich LDL
  • LDL only contains one type of apoprotein which is ApoB100
  • It therefore lacks ApoE so this means that it remains in the circulation for longer and is eventually taken up by the liver or peripheral tissues
46
Q

what does cholesterol do

A
  • it is an essential component of cell membranes
  • storied
  • bile synthesis
47
Q

what regulates cholesterol

A

HMG-CoA reductase

48
Q

what regulates the expression of HMG-CoA reductase and the LDL receptor

A

SREBP - this regulates the expression of HMG-CoA reductase and the LDL receptor

49
Q

how does LDL uptake occur

A
  • occurs when intracellular cholesterol levels delicate
  • LDL uptake occurs by the LDL ApoB/E receptor on the plasma membrane
  • this causes the formation of cholesterol being release and esterified within the cell
50
Q

what can HDL do

A
  • it can exchange components with other lipoproteins and are in the liver and intestine
51
Q

what structures are HDL

A
  • they are formed as discoid, lipid poor particles containing mainly ApoA1
52
Q

what does HDL do and how does it do it

A
  • HDL transports cholesterol from peripheral tissues to the liver for disposal via bile
  • HDL binds to the scavenger receptors and transfers cholesterol into the cell membrane
  • the redundant parts of HDL then take part in the next transport

also
- HDL scavenges free cholesterol from cell membranes via ABCA1 transporter (a membrane protein) and esterfieis it to cholesterol esters

53
Q

is LDL or HDL a risk to cardiovascular disease

A
  • LDL is a risk for cardiovascular disease whereas HDL is cardio protective
54
Q

what can elevate HDL

A
  • moderate alcohol consumption

- regulate aerobic exercise leads to elevated HDL levels

55
Q

what is high TAG levels linked to

A
  • atherosclerosis
  • stroke
  • CHD
56
Q

what is more at risk high LDL levels or high TAG levels

A
  • high LDL levels
57
Q

what does smoking and diabetes do to LDL

A
  • oxidised LDL which is generated by smoking and diabetes cause the formation of atherosclerotic plaques
58
Q

how does oxidised LDL cause plaques to form

A
  • oxidised LDL binds to scavenger receptors rather than the LDL receptor in macrophages
  • scavenge receptors are not feedback regulated by cholesterol, this causes macrophages to become lipid laden and form foam cells
  • this leads to the formation of fatty streaks in the arterial wall leading to plaque formation
59
Q

what is an LDL treatment

A
  • statins
60
Q

what do statins do

A
  • comeptivie inhibitor of HMG=CoA reductase

- this lowers in cell cholesterol and therefore takes up more LDL

61
Q

what is the mechanism of action of LDL cholestryamine

A
  • binds bile acids in the gut preventing enterohepatic circulation
62
Q

what are the LDL cholestryamine eadverse effects

A
  • gastrointestinal adverse effects

- nausea, abdominal boating, alteration of bowel habit flatulence

63
Q

what is the lipid lowering effect of LDL cholestryamine

A
  • 8-15% reduced in LDL, little or not effect on HDL cholesterol
  • results in a rise of TAG concentration
64
Q

what is the long term safety of LDL cholestryamine

A
  • not systemically absorbed - therefore safety is good

- supplements of fat soluble vitamins may be required

Metabolism (26 decks)

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