Brainscape's Knowledge GenomeTM

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


See full index

Life support (Year 1) > F: CELL Lipid Transport > Flashcards

F: CELL Lipid Transport Flashcards

1
Q

How are lipids transported (generally)?

A

Transported by 3 interlinked systems:

  • Exogenous pathway - transports lipid from gut to live
  • Endogenous pathway - Transports lipids synthesised by liver to non-hepatic tissue including adipocytes
  • 3rd pathway - Lipid taken from circulation and from non-hepatic tissue back to liver
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What’s the percentage composition of types of lipids in circulation?

A
  • Triglycerides (45%)
  • Phospholipids (35%)
  • Cholesterol esters Cholesterol (15%)
  • Free Fatty Acids (5%)
    • Fatty acids (particularly polyunsaturated FAs) are ligands for transcription factors involved in energy metabolism. E.g. they play a role in regulation of insulin metabolism
    • They upregulate lipid oxidation in liver + muscle and down regulate genes involved in lipogenesis in liver and adipose tissue. Also increase expression of UCP-2 and 3 in mitochondria to increase thermogenesis

% in human plasma varies greatly with
nutritional state

All are insoluble in water

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

Describe transportation of free fatty acids

A
  • Formed from triglycerides stored in adipose tissue
  • Circulates bound to protein as Na+ salt (particularly albumin) as unbound FA acts as detergent
  • Saturation occurs at about 2mM FA molecules
  • FA enter cells by simple diffusion
  • Intracellular concentration FFA kept low
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Describe chylomicrons

A
  • Reflects meal composition
  • Low density due to high TG
  • Also contain fat soluble vitamins - A and E
    • These are important antioxidants, preventing the oxidation of lipids which are associated with heart disease
  • Life time in circulation of 1 hour (TGs 5 mins)
  • Remnants removed by the liver with involvement of Apo E
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Explain the process of how dietary lipids become chylomicrons

A
  • Enter as TGs
  • Undergo enzymatic breakdown using lipases into FAs + monoacylglycerols
  • Cross cell membrane and enter cell to reform TGs
  • These TGs along with other lipids like cholesterol/esters will form a nascent chylomicron (which contain apo B48)
  • Nascent chylomicron is secreted to lymph system via reverse pinocytosis
  • Drain into thoracic duct, then start to circulate in body
    • Enter lymphatics, and not portal vein - allows chylomicrons to be distributed to non-hepatic tissue before it gets to liver
  • Once nascent chylomicron released into circulation, interacts with HDLs, pick up apo proteins
    • Picks up ApoE and Apo CII
    • Forms mature chylomicron
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Explain the enzymatic degradation of chylomicron

A
  • Interaction w lipoprotein lipase
  • This enzyme is expressed on tissue that metabolise lipids e.g. muscles, adipocytes, mammary glands
  • Km of LPL isoform in adipocytes is greater than in muscles which means fatty acids have a preference to take up in adipocytes
    • LPL binds and is activated by Apo CII which is stimulated by insulin
  • Once degradation is completed the Apo CII is returned to the HDL
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Describe VLDL

A
  • Synthesised by liver when dietary intake of carbs exceed immediate needs
  • TGs formed are packaged with FFA, phospholipids and cholesterol esters and Apo B100 to form nascent VLDL
  • Formation stimulated by insulin and inhibited by glucagon
  • Nascent VLDLs receive ApoE and ApoCII from HDL
  • Remnant removed by liver by ApoE (TG 15-60 mins)
    • 60% remnants removed by liver, 40% by adrenal and gonadal tissue + cholesterol used for hormone production. Both use the ApoB100 to bind to the LDL receptor
    • If there’s too much LDL, receptors become saturated, and so excess can be removed via a low affinity scavenger receptor
    • Synthesised in liver ER and golgi, released with B100, then acquire Apo E and C from HDL
    • Metabolised by LPL as they circulate (TG 1/2 life of 15-60 mins)
  • Formation enhanced by:
    • Dietary carbs
    • Circulating FFA
    • Alcohol
    • Raised insulin and decreased glucagon
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

How are VLDLs degraded?

A
  • VLDL from endothelial cell contains Apo CII and ApoB100
  • Apo CII activates LPL
  • the tryglyceride is broken down into FA and glycerol
    • enters cell
    • if that cell is adipocytes then glycerol and FA is converted into triglyeride stores
    • if the cell is muscle cell then FA are converted to CO2 and H2O
  • due to the loss of the glyceride it has now formed a IDL
    • lower TG content
  • 60% of IDLs go back to liver
  • some go and interact w HDLs which will take back the Apo CII and Apo E for future donations to other lipoproteins
  • the resultant lipoprotien is the LDL
  • this only contains Apo B100
  • some LDLs react w the LDL receptor on non-heptaic tissue cells and the FA, CH, Glyercol and amino acids w be broken down and used for metabolism
  • 60-70% of LDL will return to liver
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What’s the normal composition of HDL:LDL?

A

3.5

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

What’s the composition % by weight of VLDL:LDL:HDL in terms of protein, cholesterol, PPI and TG?

A

Protein:

  • 10:25:49

Cholesterol:

  • 19:50:22

PPI:

  • 15:21:28

TG:

  • 53:4:2
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the function of apolipoproteins?

A
  • Act as receptors, enzymes or enzyme co-factors
  • Help solubilise lipids + provide structure to lipoprotein
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Describe the 5 types of lipoproteins

A
  • Carried in blood as plasma lipoproteins
  • 5 types:
    • Chylomicrons
      • Apoproteins - B48, Apo CII and E
    • Very Low density lipoproteins (VLDL)
      • Apoproteins - B100, Apo CI, CII, CIII and E
      • VLDL made in liver is release with ONLY B100. As it circulates it acquires Apo C and E from HDL
    • Intermediate density lipoprotein (IDL)
      • Apoproteins - B100, Apo E
    • Low density lipoproteins (LDL)
      • Apoprotein - B100
    • High density lipoproteins (HDL)
      • Apoproteins - Apo AI, AII, CII, CIII, D and E
  • Each particle has diff function
  • Apolipoproteins = Apoproteins
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

How are lipoproteins removed from circulation?

A

By receptor mediated endocytosis

LDL receptor- High affinity, lipoproteins VLDL and LDL, binds to ApoB100 and ApoE, regulated by cholesterol, distributed in liver

LDL-like receptor - High affinity, lipoproteins VLDL, HDL, chylomicron, binds to ApoE, regulated by cholesterol, distributed in liver, brain, placenta

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

Describe the function of apoproteins

A
  • Apo E binds to HDL receptor
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Describe the transport of dietary lipids

A
  • Low density due to high TG
  • B48 added in SER
  • Secreted by reverse pinocytosis into lymphatics
  • Apoproteins C2, 3 and E transferred from HDLs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Describe the transport of chylomicrons

A
  • Chylomicrons secreted into lympathics, carries them via thoracic duct to SVC
  • By this pathway dietary fats avoid direct delivery to liver, instead made available to exttrahepatic tissue
  • In contrast, digested proteins + carbs released into portal vein + delivered directly to liver
17
Q

Describe hyperlipidaemia

A

Type 1 - Deficiency in lipoprotein lipase or Apo C2 - characterised by high plasma triglyceride

Type 2 - Characterised by high LDL - most are caused by a genetic defect in the synthesis, processing or function of the LDL receptor

Type 4 - Most common form results in raised VLDL concentrations often due to obesity or alcohol abuse

18
Q

Describe HDL synthesis and function

A

Can be created 3 ways:

  • As nascent particles by liver + intestine
  • Budding of apolipoproteins from chylomicrons
  • From free ApoAI

Nascent HDL acquire cholesterol and phospholipids from endothelial cells

Reverse cholesterol transport, doesn’t need enzymes

HDL possess lecithin cholesterol acyltransferase (LCAT) which catalyses cholesterol esterification preventing it from returning to cell. Important in vascular cells and prevents foam cell formation

Cholesterol rich HDL can either deliver it to liver or exchange it with other particles including VLDL and VLDL remnants

19
Q

What regulates cholesterol uptake and synthesis?

A

Cholesterol regulates its own uptake and synthesis

Increased lvls inhibits HMG-CoA reductase activity

Decreased lvls increases LDL receptor synthesis and expression

  • The synthesis of the LDL receptor + its expression at the cell surface is negatively regulated by the intracellular concentration of cholesterol. When intracellular concn cholesterol decreases, synthesis of cholesterol from acetyl-coA and LDL receptor incrreases
  • HMG-CoA reductase is the rate limiting step in the synthesis of cholesterol

HMG-CoA is a target for therapy

20
Q

What effect do statins have on HMGCoA reductase?

A

Statins inhibit HMGCoA reductase, therefore cholesterol synthesis ecreases within cells, resulting in increase in synthesis and expression of LDL receptor at cell surface, so increase LDL-cholesterol uptake, therefore lowering circulating cholesterol

21
Q

What is familial hypercholesterolemia?

A

Homozygous individuals:

  • High serum cholesterol
  • Develop blocked arteries
  • Die young from heart attacks
  • De novo synthesis not regulated by LDL

Single amino acid substitution that prevents localisation of LDL receptor to coated pits

22
Q

Discuss some abnormalities of lipid transport

A
  • Diabetes Mellitus
    • Increased FFA mobilisation
    • Decreased chylomicron and VLDL utilisation
  • Obesity
    • Hypertension, NIDDM, hyperlipidaemia and hyperglycaemia
  • Gene defects
    • Apolipoporteins, enzymes or receptors

Leading to: Hypercholesterolaemia, atherosclerosis

23
Q

Describe LDL

A
  • Major carrier of cholesterol, carries it to periphery and regulate de novo synthesis
  • Metabolised slowly - 3 days
  • Contain 1 ApoB100 which can bind to specific receptor on hepatocytes
  • VLDL converted to IDL via lipase, IDL can either be removed by liver or converted into LDL (rich in cholesterol), LDL can then be removed by non-hepatic tissue (40%) or by liver (60%)
24
Q

Describe scavenger receptors

A
  • SRB1, low, HDL, unregulated - Endothelial cells, intestine, macrophages, smooth muscle cells, keratinocytes, apidocytes, placenta, adrenal, testis, ovary
  • SR-A!, SR-A2 - low, LDL, unregulated- Macrophages

Life support (Year 1) (29 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions