The cardiovascular system - Biochemistry

Question 1

What do we need cholesterol for?

Answer 1

Used to make steroid hormone and bile salts

Increase cell membrane fluidity

Question 2

There are 3 main types of lipids in our bodies. What are they?

Answer 2

1. Triglyceride
2. Phospholipid
3. Steroid

Question 3

a) Describe the structure of lipoproteins

b) Describe the function of lipoproteins

Answer 3

a)
Phospholipid shell with polar head groups

Hydrophobic lipid core - cholesterol, triacyglycerols

b) Lipid transport

Question 4

Describe the function of apolioprotien

Answer 4

Apolipoprotein is receptor targeting.

The Hydrophobic domain binds lipid and hydrophilic domain targets particles

Question 5

In terms of density, how is cholesterol transferred?

Answer 5

Cholesterol is transferred from low to high density lipoprotein particles

Question 6

a) Where are bile salts made and stored?

b) Describe the role of bile salts

Answer 6

a) Made my liver and stored in gall bladder

b) Act as a detergent to assist in the absorption of insoluble cholesterol by emulsifying large fat droplets into small ones

Question 7

Describe lipid transportation

Answer 7

Cholesterol (in complex with bile salts) is taken into intestinal epithelium, esterified, and packaged into lipoprotein particles (chylomicrons) for transport in the blood

Question 8

Describe the take up of chylomicrons in the intestine to bile salts

Answer 8

1. Chylomicrons taken up from intestine and used in muscle, adipose
2. Chylomicron remnants generated in liver
3. VLDL formed in liver and used in muscle, adipose
4. Chylomicron forms IDL
5. IDL converted to LDL and used in numerous tissues via LDL receptor
6. Pickup from tissue by HDL
7. HDL taken to liver for excretion as bile salts

Question 9

What is good and bad cholesterol known as?

Answer 9

Good cholesterol - HDL

Bad cholesterol - LDL

Question 10

Why is LDL ‘bad cholesterol’

Answer 10

Because I is a measure of cholesterol headed to tissues

Question 11

Why is HDL ‘good cholesterol’ ?

Answer 11

Because it is a measure of cholesterol headed to liver for excretion via bile salts

Question 12

a) Describe the role of the sterol regulatory element (SRE)?

b) What is the expression of SRE regulated by?

Answer 12

a) The SRE is a short DNA sequence that promotes the expression gene for hMG-CoA reductase (and other sterol-responsive genes, like LDLR gene)

b) Expression of the SRE gene is regulated by transcription factors called sterol regulatory element binding proteins (SREBPs or STREBP) (that binds to the SRE and promote gene expression)

Question 13

What is the location of the sterol regulatory element binding protein (SREBPs) controlled by?

Answer 13

Cholesterol

Question 14

Describe the role of the sterol regulatory element binding proteins (SREBPs)

Answer 14

SREBP binds to sterol regulatory element (SRE) and promotes its gene expression. SRE upstream HMG CoA reductase gene

Question 15

Describe the role of the sterol regulatory element binding protein (SREBP) when cholesterol is low

Answer 15

1. When cholesterol is low SREBP can move to nucleus, bind to SRE and stimulate the expression of SRE
2. SRE promotes the expression of HMG CoA reductase gene
3. Expression leads to intracellular cholesterol synthesis
4. High cholesterol keeps SREBP in the cytoplasm

Question 16

Describe the 2 ways that Statins lower cholesterol

Answer 16

1. Stains directly inhibit the enzyme HMG CoA reductase, which catalyses the rate limiting step in cholesterol synthesis in our cells (has little direct effect on blood cholesterol levels)
2. Statins indirectly promote cholesterol uptake into cells via the LDLR (main effect)

Question 17

a) Satins indirectly promote cholesterol uptake into cells via the LDLR. What mechanism is this by?

b) Describe how satins indirectly promote cholesterol uptake into cells via the LDLR

Answer 17

a) Negative feedback mechanism

b)
1. When statins inhibit HMG CoA reductase the level of cholesterol drops
2. SREBP then moves to nucleus to switch on genes (for HMG CoA reductase) and the LDL receptor
3. More LDL receptors are synthesised
4. LDL particles are taken into cell
5. Cholesterol levels in the blood fall