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Fundamentals of the Living Cell > Lipid Transport > Flashcards

Lipid Transport Flashcards

1
Q

What factors affect the concentration of lipid in the blood?

A
  • the nutritional status of the organism

- individual constitution

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2
Q

Why are lipids not able to be transported free in the circulation?

A

As they have a hydrophobic nature.

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3
Q

What is the differences between unesterified fatty acids and the following: triglycerides, phospholipids and cholesterol esters?

A

Unesterified esters are transported in association with albumin whereas the others form large covalent aggregates with proteins which are also known as lipoproteins.

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4
Q

Where are lipids transported from?

A
  • The gut to the liver.
  • The liver to non-hepatic tissue including adipocytes.
  • Non-hepatic tissue back to the liver.
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5
Q

What are the different functions for fatty acids?

A
  • polyunsaturated fatty acids can act as ligands for transcription factors involved in energy metabolism e.g. they can play a role in insulin regulation.
  • they regulate lipid oxidation in the liver and muscle
  • down regulate genes involved in lipogenesis in the liver and adipose tissue.
  • increase the expression of UCP-2 and 3 in mitochondria to increase thermogenesis.
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6
Q

What are the percentages of different fats in blood?

A
  • triglycerols = 45%
  • cholesterol esters = 15%
  • phospholipids = 35%
  • free fatty acids = 5%
  • NOTE: the percentages above can vary due to the nutritional state and they are all insoluble in water.
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7
Q

What is the composition that lipids can be transported as other than lipoproteins?

A

They can be transported as free fatty acids which are formed from triglycerides and are stored in adipose tissue. However they are also actually bound to a proteins such as albumin as Na+ salt as if they would act as a detergent causing damage to the cell membrane if it were transported as a fatty acid alone.

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8
Q

What is the amount of fatty acids needed to achieve saturation?

A

2mM

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9
Q

How do fatty acids move in and out of the cell?

A

Through simple diffusion

*Note: the concentrations of fatty acids within the cell are kept low.

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10
Q

How are lipoproteins carried into the blood as?

A

As plasma lipoproteins

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11
Q

What are the five major types of lipoproteins?

A
  • chylomicrons- a little different as they are synthesised from dietary fats in the gut lining.
  • very low density lipoproteins (VLDL)
  • low density lipoproteins (LDL)
  • intermediate density lipoprotein (IDL)
  • high density lipoproteins (HDL)
  • Note: each type has a different function
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12
Q

What is the structure of a lipoprotein?

A

LOOK AT NOTES FOR DIAGRAM

  • each lipoprotein contains one very large protein called apolipoprotein.
  • contains phospholipids, cholesterol and triglycerides.
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13
Q

What is the composition of chylomicron?

A 
Protein= 1-2%
Cholesterol= 3-7%
Phospholipid= 3-8%
Triglyceride= 90-95%
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14
Q

What is the composition of a VLDL?

A 
Protein= 10%
Cholesterol= 19%
Phospholipid= 15%
Triglyceride= 53%
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15
Q

What is the composition of a LDL?

A 
Protein= 18%
Cholesterol= 11%
Phospholipid= 22%
Triglyceride= 31%
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16
Q

What is the composition of a IDL?

A 
Protein= 25%
Cholesterol= 50%
Phospholipid= 21
Triglyceride= 4%
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17
Q

What is the composition of a HDL?

A 
Protein= 49%
Cholesterol= 22%
Phospholipid= 28%
Triglyceride= 2%
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18
Q

What is the apolipoprotein associated with a chylomicrons?

A

B48, Apo C2, C3 and E

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19
Q

What is the apolipoprotein associated with a VLDL?

A

B100, Apo C1, C2, C3 and E

*Note: VDLD acquires the Apo C1,C2,C3 and E from HDLs when it circulates in the blood- it starts off only with B100

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20
Q

What is the apolipoprotein associated with a LDL?

A

B100 and Apo E

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21
Q

What is the apolipoprotein associated with a IDL?

A

B100

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22
Q

What is the apolipoprotein associated with a HDL?

A

Apo A1, A2, C1, C3, D and E

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23
Q

Are the different types of lipoproteins able to interact with each other?

A

Yes they are able to interact and can exchange apolipoproteins.

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24
Q

What are the functions of the apolipoprotein?

A

-Structural- they are the backbone of lipoproteins
-To solubilize lipids- they allow the lipids to become soluble in aqueous environments
-Act as enzymes or enzyme cofactors
*Apo C2 activates lipoprotein lipases
*Apo A1 for lecithin: activates cholesterol
acyltransferase
-Targeting lipoproteins to different tissues
*Apo B100 and Apo E bind to the LDL receptor
*Apo E binds to the HDL receptor

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25
Q

How are chylomicrons formed?

A

They are formed in the cells that line the gut. In the lumen of the gut, under the influences of lipases, triglycerides are broken down into free fatty acids and monoacylglycerols.
These are then taken into the cell and become reformed into triglycerides which will bind the the apolipoproteins to form the chylomicrons.

26
Q

What happens after chylomicrons are formed?

A

They are secreted into the lymphatic system (it doesn’t directly go into the portal vein and go to the liver as it will just become metabolised), and it makes the lipids available to the extraphetic tissue. Once the molecules are in the lymphatic system, it is carried to the superior vena cava via the thoracic duct, straight into the heart s that it is able to directly go into circulation.

27
Q

How a is a mature chylomicron formed?

A

When they are first formed, majority of the chylomicron is made up of a lot of triglyceride and the protein present within, is Apo B48. This will form a nascent chylomicron which will circulate and interact with HDLs, exchanging apolipoproteins- Apo C2 and Apo E will be gained and so a mature chylomicron is formed.

28
Q

What a the key features of chylomicrons?

A
  • they reflect on your meal composition
  • they contain fat-soluble vitamins (A&E (strong antioxidants) which are important to maintain the chemical nature of the lipid and stopping it from oxidation.
  • the vitamins are needed to stop the oxidation of lipids especially the ones associated with heart disease.
29
Q

What is the half-life of a chylomicron?

A

They have an hour half-life but triglycerides has a 5 minute half-life

30
Q

What happens as chylomicrons are circulated around?

A

They are acted upon by lipoprotein lipases which are expressed on endothelium cells that line the blood vessels. The lipoproteins lipases vary from tissue to tissue- the tissues that have the greatest lipoprotein lipases will be those which use lipids the most e.g. mammary, muscle and adipose tissue. They will also have different isoforms. The lipases will break down the triglycerides into monoacylglycerols fatty acids and those fatty acids will then diffuse into the endothelial cells.

31
Q

What happens as chylomicrons are slowly depleted?

A

Their density will increase in proportion to the decrease of triglyceride levels, forming chylomicrons remnants. Theses remnants will end up in the liver and will bind to specific receptors on the liver, and the entire lipoprotein will be taken up, broken down and recirculated.

32
Q

Why are different isoforms expressed by different tissues?

A

As the activity of the lipoprotein lipase varies depending on the tissues.

33
Q

What is the Km value like for lipoprotein lipases in adipocytes and what does it mean?

A

The Km value for lipoprotein lipases is much higher than the Km for muscles, so the high KM means the lipoprotein lipases will be saturated in higher concentrations of circulating lipoproteins than it will be in the muscle- the muscle is fully saturated in lower levels and this means that muscles are able to uses circulating lipoproteins at lower concentrations.

34
Q

How are lipoproteins lipases in adipocytes stimulated?

A

By insulin.

35
Q

What is hyperlipidaemia and what are the types?

A

It is when the concentration of lipids such as cholesterol or triglycerides in the blood are much higher than normal.
Type 1= caused by the deficiency in lipoproteins lipase or Apo C2- characterised by high plasma triglyceride
Type 2= characterised by high LDL levels- most are caused by a genetic defect in the synthesis, processing or function of the LDL.
Type 4= Most common form results in raised VLDL concentrations due to obesity or alcohol abuse.

36
Q

Where are VLDLs synthesised?

A

In the liver ER and modified in the golgi

37
Q

What are VLDLs responsible for?

A

Transporting endogenously synthesised lipids

38
Q

How are VLDLs metabolised?

A

They are metabolised by lipoprotein lipids are they circulate- their triglycerides have a half-life of 15-60 minutes.
The remnants are removed in the liver by Apo E

39
Q

What factors can increase the formation of VLDLs?

A
  • dietary carbohydrates
  • circulating free fatty acids
  • alcohol
  • raised insulin and decreased glucagon
40
Q

What are the two fates of VLDLs?

A
  • when majority of the triglycerides have been lost, the VLDL will return to the liver for it to be broken down
  • the other fate is that they form intermediate density lipoproteins.
41
Q

How are mature VLDLs formed?

A

The VLDLs are released in the nascent form where they mainly have Apo B100. They interact with a HDL in order to gain Apo C2 and Apo E and then becomes a mature VLDL.

42
Q

How are LDLs formed?

A

They are formed from VLDLs which turn into IDLs which turn into LDLs through the actions of the lipase.

43
Q

What are the features of LDLs?

A
  • rich in cholesterol- they carry the cholesterol to the periphery and regulate de novo synthesis
  • used for hormone production
  • metabolised slowly- takes three days
  • contain 1 ApoB100 which can bind to a specific receptor on hepatocytes
44
Q

How are LDLs removed?

A

60% of LDLs are removed by the liver and 40% are removed by non-hepatic tissue particularly the ones used for steroid biosynthesis.

45
Q

What are HDLs?

A

They are circulating reservoirs of apolipoproteins (Apo C2 and E) and donates them to VLDLs and Chylomicrons as well as obtaining from the,.
They also remove cholesterol from the plasma.

46
Q

What enzymes do HDLs use remove cholesterol from the plasma?

A

They contain the enzyme lecithin cholesterol acyltransferase (LCAT) which esterifies cholesterol and then retains it within the HDL in order to prevent it from diffusing it out of the HDL. They are made:

  • in the liver and intestine
  • by budding from VLDL and chylomicrons
  • form around free Apo A1.
47
Q

How doe HDLs remove cholesterol?

A

The cholesterol is present in plasma membranes. The endothelial cells express the transporter Apo A1 which transfers the cholesterol from the inner surface of the membrane to the extracellular surface where it can then interact with Apo A1 on the HDL and then int can be transported to the cells that need it or to the liver.

48
Q

How are the cholesterols attached to HDLs taken up by the liver?

A

It binds through Apo E to LDL receptors on the liver.

49
Q

What is the HDL/LDL ratio?

A

It is a ratio used to assess the susceptibility to heart disease.

50
Q

What is the normal HDL/LDL ratio?

A

3.5

51
Q

How are lipoproteins removed from circulation?

A

Through receptor mediated endocytosis:
ApoB100 and Apo E bind to receptors on the surface of hepatocytes. There are LDL receptors which will bind both Apos- these are very specific saturable receptors. There is also scavenger receptors which are not regulate- they bind lipoproteins but only at high concentrations. They are expressed on endothelial cells and macrophages.

52
Q

How does an LDL interact with receptors expressed by the liver?

A

The LDL will bind to LDL receptors on hepatocytes.
These receptors are concentrated in coated pits. These pits have clathrin which are important in the uptake of the LDL.
The membrane pinches off to form an endosome.
These endosomes will start the process of breaking down the receptor which is recycle and the remaining endosome with LDL will fuse with lysosomes which contain hydrolytic enzymes.
These enzymes break down the component of LDL.
The cholesterol esters wll be converted to cholesterol which will then diffuse out into the cytoplasm where they are immediately re-esterified as free cholesterol which is not desirable in the cell.
The fat component (i.e. triglycerides) will be broken down to give fatty acids which are further metabolised. The amino acids will be broken down too.

53
Q

How is the process of LDL interacting with receptors expressed by the liver regulated?

A

By intracellular concentration of cholesterol. When this goes up, the expression of a new receptor and existing receptor at cell surface goes down. The cell regulates how much LDL it takes up depending how much cholesterol is present.

54
Q

What regulates cholesterol uptake and synthesis?

A

Cholesterol regulates its own uptake and synthesis.
Increased cholesterol: inhibits HMG-CoA reductase activity, HMG-CoA reductase reduces LDL receptor expression, HMG-CoA is a target for therapy as it. The more HMG reductase activity we have the more cholesterol we have so the less the cell needs from outside.

55
Q

What effect does an increase in HMG CoA reductase have on the level of expression of LDL receptors?

A

This is perhaps a little more tricky and worthy of a question. The synthesis of the LDL receptor and its expression at the cell surface is negatively regulated by the intracellular concentration of cholesterol. When the intracellular concentration of cholesterol decrease the synthesis of cholesterol from acetyl-CoA and the LDL receptor increase. HMGCoA reductase is the rate limiting step in the synthesis of cholesterol.

56
Q

What effect do statins have on the relationship between the increase of HMG CoA reductase on the level of expression of LDL receptors?

A

Statins inhibit HMGCoA reductase and therefore decrease cholesterol synthesis within cells this will result in an increase in the synthesis and expression of the LDL receptor at the cell surface and so increase LDL-cholesterol uptake and therefore lowering circulating cholesterol.

57
Q

What happens if there is a loss of LDL receptor function?

A

This is a genetic disorder and is called familial hypercholesterolemia.
Homozygous individuals:
1. High serum cholesterol (800 mg/ml, normal is 200mg/ml) This activates scavengers receptors
2. Develop blocked arteries (atherosclerosis)
3. Die young from heart attacks
4. De novo synthesis is not regulated by LDL
Single amino acid substitution that prevents localisation of the LDL receptor to the coated pits.

58
Q

What are the two types of LDL receptors?

A

High affinity LDL receptor and Low affinity scavenger receptor
Present on:
* Endothelial cells
* Macrophages
* VSMC
Low affinity active when plasma LDL high or when chemically modified ie oxidised. Not regulated by cholesterol

59
Q

How are lipoproteins regulated?

A
  • Hormonal regulation: insulin, cortisol, thyroid hormones
  • Nutritional status: decreased synthesis during fasting, increased by dietary fats – unsaturated fats best
  • LDL expression: oestrogen
60
Q

What are the abnormalities that are caused by lipid transport?

A
  • Diabetes Mellitus: increased FFA mobilisation, decreased Chylomicron and VLDL utilisation.
  • Gene defects: apolipoproteins, enzymes or receptors.
  • Leading to: hypercholesterolemia, atherosclerosis.
  • Obesity: hypertension, NIDDM, hyperlipidaemia and hyperglycaemia.

Fundamentals of the Living Cell (34 decks)

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