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S.N Biochemistry 3 > cholesterol synthesis > Flashcards

cholesterol synthesis Flashcards

1
Q

where does cholesterol synthesis occurs?

A

ER

cytosol

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2
Q 
overall process of 1 cholesterol involves how many?
acetylcoA
ATP
NADPH
enzymes
A

18 acetylcoA
36 ATP
20 NADPH
12 enzymes

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3
Q

what are the inhibitors of HMG coA reductase?

A

bile acids
cholesterol
mevalonate
(statins!!)

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4
Q

what does phosphorylation do to HMG coA reductase?

A

inactivation

by AMPK- which sense high AMP levels, means less ATP

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5
Q

how does insulin effects cholesterol synthesis?

A

activates it because it promotes dephosphorylation of HMG coA reductase

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6
Q

what family of proteins controll the number of HMG coA reductase?

A

SREBP

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7
Q

what happens to the insig-SCAP-SREBP when sterol levels are high?

A

insig-SCAP-SREBP complex is retained in the ER membrane

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8
Q

what is LXR? what activates it?

A

nuclear transcription factor

activated by oxysterol ligands (reflecting high cholesterol levels)

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9
Q

what happens to LXR when it binds oxysterol ligand?

A

LXR form heterodimer with RXR

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10
Q

write down what will happen when LXR-RXR dimerize:

A

they will activate transcription of

  1. acetyl co A carboxylase
  2. FA synthase
  3. cyt. P-450, CYP7A1
  4. Apo that are involved in cholesterol transport
  5. ABC transporters
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11
Q

what will activate ACAT?

A

high intracellular conc of cholesterol

ACAT will increase esterification of cholesterol for storage

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12
Q

what will high cholesterol levels will do to the transcription of LDL receptors?

A

diminish transcription -> reducing production of the receptor -> reducing the uptake of cholesterol from the blood

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13
Q

write down levels of regulation of HMG coA reductase (4)

A
  1. protein degregation (through insig)
  2. reversible covalent modification (by AMPK)
  3. gene transcription (by SREBP-SCAP)
  4. inhibition of translation (by mevalonate)
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14
Q

what is the long term modification of HMG coA reductase?

A

inhibition of translation (by mevalonate)

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15
Q

what will lower cholesterol levels (when intracellular cholesterol is high) ?

A
  1. insig-SREBP-SCAP complex is deactivated (stay in ER)
  2. LDL receptor transcription is reduced
  3. miR-33a is inhibited by cholesterol
  4. LXR-RXR dimer is activated -> promote bile formation and cholesterol transport
  5. ACAT activation is increased
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16
Q

what is the job of ABCA1/ABCG1 ?

A

transport cholesterol out of the cell

17
Q

what is the job of NPC1L1 ?

A

uptake of free cholesterol into enterocytes of the intestine

18
Q

what is the job of ACAT ?

A

esterify cholesterol to CE in the ER membrane insidr the cell

19
Q

what is the job of LCAT ?

A

esterify cholesterol to CE in the HDL particle

20
Q

what is reversed cholesterol transport????

who is the main lipoprotein?

A
  • mechanism by which the body removes excess cholesterol from peripheral tissues and delivers them to the liver!!!
  • HDL!
21
Q

how does cholesterol from non hepatic cell being transferred to HDL?

A

by the ABCA1

22
Q

what Apo will bind LDL?

A

Apo B100

Apo E

23
Q

how do LDL taken up?

A

by endocytosis

24
Q

what does LDL conc in the blood depends on?

A

amount of LDL receptors

25
Q

how does statins work regarding LDL receptors?

A

they induce LDL receptors!

so more LDL uptake and less in the blood

26
Q

what will high levels of cholesterol do to IDOL?

A

will cause IDOL to bind to LDL receptor and initiate autoubiquitination -> degregation

27
Q

what is the ligand of FXR?

A

bile acids

28
Q

what nuclear receptor with what ligand will cause increase in bile acids?

A

LXR with Oxysterol

29
Q

which hydroxyl group appears in all bile acids?

A

3a

30
Q

what are the cofactors of bile acids synthesis?

A

NADPH
NAD
CoA
vit.C

S.N Biochemistry 3 (14 decks)

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