Blomquist: Cholesterol Flashcards Preview

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Flashcards in Blomquist: Cholesterol Deck (36)
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1

Role of cholesterol

membranes
precursor to bile salts/acids
precursor to hormones
precursor to vitamin D

2

This makes up greater than 80% of gall stones

cholesterol

3

How many carbons does cholesterol have? How many rings does cholesterol have? At what position is the hydroxyl group? At what positions are there methyl groups? At what position is there a double bond? How long is the carbon side chain?

27; four; 3; 18, 19; C5-C6; 8 carbons

4

Where is most of the cholesterol found in the human body?

In membranes

5

What is the concentration of cholesterol in the blood?

150-240mg/dL

6

In what form is most of the cholesterol carried in the blood?

As a cholesterol ester; lipoprotein

7

Is cholesterol polar or non-polar?

non-polar

8

Acetyl-CoA is required for cholesterol synthesis. What are two source of Acetyl-CoA?

carbohydrates or fatty acids

9

What is the regulated enzyme in cholesterol biosynthesis?

HMG-CoA reductase

10

HMG-CoA reductase takes Acetyl-CoA to what intermediate?

mevalonate

11

What two things combine to make HMG-CoA via HMG-CoA synthase?

acetoacetyl-CoA + acetyl-CoA

12

In the cytosol, what does HMG-CoA go to?
In the mito matrix, what does HMG-CoA go to?

cholesterol; ketone bodies

13

What does the HMG-CoA reductase reaction require?

2NADPH being reduced to 2NADP+

14

What is the complete equation for the formation of mevalonate from HMG-CoA?

HMG-CoA + 2NADPH + 2H+ --> mevalonate + 2NADP+ + CoA

15

In what ways is HMG-CoA regulated?

feedback inhibition
phosphorylation/dephosphorylation
control of gene expression
rate of enzyme degradation

16

Discuss the feedback inhibition of the cholesterol pathway.

If there is lots of cholesterol already in the body, this will inhibit HMG-CoA reductase

17

Phosphorylation is another method of control of HMG-CoA reductase. When HMG-CoA reductase is phosphorylated, is it active or inactive?

inactive

18

HMG-CoA reductase is also controlled at the gene level. The sterol receptor element binding protein can bind to the (blank) and increase (blank) of target genes, which increases the synthesis of (blank).

nucleus; transcription; HMG-CoA reductase

19

Because of its structural similarities to HMG-CoA, this can be used as a competitive inhibitor of HMG-CoA reductase

Lipitor; Lovastatin

20

What is a potential problem when using statins?

The cholesterol pathway produces intermediates that are essential to formation of prenylated proteins, vitamin D, bile salts, and steroids. So, when you block HMG-CoA reductase, you block the pathways for these other products as well.

21

Through what carbon intermediates does mevalonate pass through to make cholesterol (C27)?

C5, C10, C15, C30

22

19 oxidation steps take lanosterol to cholesterol. What do these steps require?

Cytochrome P450s

23

Where are bile salts made from cholesterol?

in the liver

24

Where are bile salts stored?

gall bladder

25

Where are bile salts transported after leaving the liver?

small intestine

26

Cholesterol is present in bile acids in small amounts and can form these

gall stones

27

If the gall bladder is removed, bile acids go directly to the (blank)

small intestine

28

What is the purpose of converting cholesterol to bile acids/salts?

to emulsify fats

29

What gets conjugated to bile acids/salts to make then better solubilizing agents?

Glycine, Taurine

30

How do conjugated bile acids/salts aid in the processes of the duodenum? (think pKa)

These conjugates have Pkas of 1-4, and the duodenum is 3-5