Lecture 24: Cholesterol Flashcards

1
Q

cholesterol (“bile solids”)

A

-ubiquitous
-30% of human cell membrane
-precursor of BILE ACIDS and STEROID hormones

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

Where can solid form cholesterol be found?

A

gallstones

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

Cholesterol is the precursor of

A

-bile acids
-steroid horomones

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

Atherosclerosis

A

-coronary artery disease and stroke
-caused by cholesterol

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

Souurces of cholesterol

A

-diet: 200-300mg/day
-synthesis: 1g/day

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

major producer of cholesterol

A

-liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Chemical properties of cholesterol

A

-amphipathic
-LOW solubility in water
-high concentration in plasma and bile

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Cholesterol transport

A

-by lipoproteins as a free form (30%) or cholesterol ester (70%)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Cholesterol in bile is solubilized by

A

-bile acids
-phospholipids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Synthesis of Cholesterol

A

-from ACETYL CoA in the CYTOSOL
-involves HMG-CoA synthase
-NO HMG-coA lyase activity

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

Fates of HMG-CoA:

A

-mevalonate (reductase) (cystols)
-acetoacetate + acetyl-CoA (lyase)(mitochondria)

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

HMG-CoA reductase

A

-HMG-CoA to MEVALONATE
-IRREVERSIBLE RATE-limitng step
-uses NADPH reducing cofactor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

HMG-CoA supressed by

A

-cholesterol
-statins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Statins

A

-COMpetitive INhibtors of HMG-CoA reductase
-can lower plasma cholesterol up to 50%
-atorvastatin (lipitor)

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

Cholesterol ester

A

-stored form of cholesterol in the liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Fates of cholesterol

A

-cholesterol ester in the liver
-sent out for membranes and steroid synthesis
-converted to bile acids

16
Q

bile acids

A

-AMPHIPATHIC
-secreted into bile
-stored in gall bladder
-secreted to small intestine
-EMULSIFYING agents for dietary fat

17
Q

Bile acids facilitate ___ to emulsify dietary fat

A

-hydrolysis by pancreatic lypase
-absorption of fat-soluble vitamins

18
Q

bile acid sequestrants

A

-cholestryamine and colestipol
-promote excrection of bile acids

19
Q

Regulation point of cholesterol synthesis

A
20
Q

Plasma lipoproteins

A

-protein/lipid complexes that for aggregates in plasma
-transport lipids from tissue to tissue and participate in lipid metabolism
-distinguished by their density differences

21
Q

Apolipoproteins

A

-each class of lipoprotein has characteristic composition
-serve as ligands for cell receptors

22
Q

Classes of lipoproteins

A

-HDL
-LDL
-IDL (intermediate)
-VLDL
-chylomicrons

23
Q

Lipoprotein structure

A

-INSOLUBLE core
-AMPHIPATHIC shell

24
Q

Chylomicron role

A

-transport lipid from INTESTINE to LIVER
-or to becme glycerol and fatty acids (these go to peripheral tissues)

25
Q

VLDL role in lipid transport

A

-from liver to IDL
-or gycerol + fatty acids

26
Q

IDL role in lipid transport

A

-send to LDL and back to liver
-or glycerol and fatty acids

27
Q

LDL role in lipid transport

A

-send back to liver
-send to peripheral tissues

28
Q

HDL role in lipid transport

A

-reverse cholesterol transport back to and from liver

29
Q

Familial hypercholesterolemia

A

-inherited
-high LDL blood levels
-no feedback inhibtion of cholesterol synthesis
-premature arthreosclerosis and heart attacks
-mutation of LDL receptor or apo B100

30
Q

Mutations causing hypercholesterolemia

A

-LDL receptor or apoB100
-little/no LDL receptor production
-delivered to wrong place
-bad binding
-cannot be internalized