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Bioc 406 > Cholesterol Biosynthesis > Flashcards

Cholesterol Biosynthesis Flashcards

1
Q

True or False: Cholesterol is an essential component of eukaryotic cell membranes.

A

True

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2
Q

What is cholesterol a precursor to? (name 3 things)

A
  1. Bile salts (ex: cholate)
  2. Steroid hormones
  3. Vitamin D
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3
Q

How is cholesterol converted to cholesteryl ester?

A

Cholesterol is esterified and cholesteryl ester is made to be incorporated into lipid droplets

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4
Q

What are sources of hepatic cholesterol?

A
  1. Dietary cholesterol (delivered to liver by chylomicrons)
  2. Cholesterol from extrahepatic tissues (function of HDL)
  3. De novo synthesis (new cholesterol is formed)
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5
Q

What is the initial molecule that cholesterol is synthesized from?

A

Acetyl-CoA

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6
Q

How many molecules of Acetyl-CoA are needed to produce HMG-CoA?

A

3 molecules of Acetyl-CoA

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7
Q

Where does the synthesis of HMG-CoA take place?

A

In the cytosolic side of the ER membrane

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8
Q

Where is the primary site of cholesterol biosynthesis?

A

The liver

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9
Q

What are the secondary sites where cholesterol can be produced? (4 places)

A
  • intestinal epithelia
  • adrenal cortex
  • ovaries
  • testes
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10
Q

What is the committed step in cholesterol biosynthesis?

A

HMG-CoA Reductase

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11
Q

What does HMG-CoA reductase convert HMG-CoA into?

A

Mevalonate

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12
Q

What is Mevalonate converted into?

A

PyroPhospho-Mevalonate

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13
Q

What is PyroPhospho-Melavonate converted into?

A

Isopentyl pyrophosphate

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14
Q

__ molecules of isopentyl pyrophosphate are needed to produce __ molecule of Farnesyl pyrophosphate. And __ molecules of Farnesyl pyrophosphate are needed to make __ molecule of Squalene.

A

3, 1, 2, 1

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15
Q

Name 2 enzymes required in the conversion of squalene to a 4-ring sterol.

A
  1. Squalene Mono-Oxygenase

2. Cyclase

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16
Q

How many additional steps are completed after using squalene mono-oxygenase and cyclase?

A

19 more steps are required to convert lanosterol into cholesterol

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17
Q

True or False: Cholesterol synthesis is energetically expensive!

A

TRUE! It requires 18 molecules of ATP and Acetyl-CoA and 16 molecules of NADPH

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18
Q

True or False: Because synthesis of cholesterol is so expensive, it needs to be tightly regulated

A

True.

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19
Q

What are the fates of hepatic cholesterol? (4 things)

A
  1. A small amount of cholesterol can be incorporated into hepatic membranes
  2. Synthesis of cholesteryl esters by using ACAT
  3. Synthesis of bile salts to aid in digestion
  4. DIRECT secretion of cholesterol into bile
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20
Q

True or False: Bile is the only route to remove cholesterol from the body.

A

True

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21
Q

_______ occur when bile becomes supersaturated with cholesterol.

A

Gallstones

22
Q

True or False: Cholesterol intermediates, specifically Farnesyl (15) and GeranylGeranyl (20) can be used to post-translationally modify proteins.

A

True

23
Q

True or False: Vitamin D is not derived from an intermediate in cholesterol synthesis.

A

False

24
Q

_____ is the man-made active form of Vitamin D3

A

Calcitriol

25
Q

Vitamin D is involved in homeostasis of ______ and ______. It specifically regulates the synthesis of intestinal _____ binding, a protein essential for uptake of _____.

A

phosphorus, calcium

  • calcium
  • calcium
26
Q

A deficiency in Vitamin D leads to a skeletal disorder known as _____. This leads to weak/soft bones.

A

Rickets

27
Q

Name the steroid hormone involved in regulating ion balance, specifically reabsorption of Na+, Cl-, and HCO3- in the kidney

A

Aldosterone

28
Q

Name the steroid hormone that is crucial during pregnancy

A

Progesterone

29
Q

Name the hormone that affects protein, fat, and carb metabolism. Low doses can also be used to suppress immune response, inflammation, and allergic responses.

A

Cortisol

30
Q

Name the hormones involved in secondary sexual characteristics (1 for each gender)

A

Testosterone and Estradiol

31
Q

How are steroid hormones regulated?

A

Gene expression

32
Q

How many domains do steroid receptors have?

A

3 (activation domain, zinc finger domain, steroid binding domain)

33
Q

What is the general structure of LDL?

A
  • It has a core with TAGs and ~1500 molecules of cholesteryl esters
  • Shell consists of 500 molecules of cholesterol and ~800 phospholipids, including 1 ApoB-100
34
Q

What do LDL receptors on cell surfaces specifically recognize?

A

ApoB-100

35
Q

How are LDLs taken up by cells?

A
  • receptors w/ LDL concentrate in clathrin-coated pits
  • the LDL is internalized to form a clathrin-coated vesicle
  • the clathrin coat is disassembled and forms an endosome
  • the receptors release and can be recycled
  • the endosome fuses wih a secondary lysosome which releases cholesterol
36
Q

What is the function of ACAT?

A
  • esterifies cholesterol to produce cholesteryl ester

- promotes packaging cholesterol into lipoproteins (chylomicrons, VLDL) for transport OUT of the cell

37
Q

Does insulin activate HMG-CoA reductase?

A

Yes

38
Q

Does AMPK activate HMG CoA reductase?

A

No

39
Q

Does glucagon activate HMG-CoA reductase?

A

No

40
Q

What do high levels of intracellular cholesterol lead to? (4 things)

A
  1. Activates ACAT for cholesterol synthesis
  2. Decrease HMGR synthesis
  3. Decrease synthesis of LDL receptors
  4. Increase HMGR degradation
41
Q

When HMGR is activated, it is ________. When HMGR is not activated, it is ________.

A

dephosphorylated

phosphorylated

42
Q

What molecules activates HMGR? What molecules deactivates HMGR?

A
  • insulin activates HMGR because blood glucose levels are high, thus we want to synthesize and store cholesterol
  • glucagon and AMPK because glucagon indicates low glucose and AMPK indicates low cellular energy, so we do not want to synthesize cholesterol which is an expensive process
43
Q

True or False: HMGR is an integral membrane protein that is found in the lumen of the ER

A

False. It is found in the cytosolic side of the ER membrane

44
Q

What happens w/ long term regulation when cholesterol levels are high?

A

cholesterol binds to the sterol sensing domain (SCAP) and this stabilizes the interactions between SCAP and INSIG. SREBP (transcription factor) will thus stay in the membrane…this SCAP/SREBP/INSIG/cholesterol complex stays in the membrane and prevents expression of genes that increase LDL receptor synthesis and HMGR

45
Q

What happens when low cholesterol is present?

A
  1. INSIG dissociates from the complex.
  2. SREBP/SCAP migrate from the ER membrane into the Golgi membrane
  3. S1P protease cleaves SREBP
  4. S2P releases bHLH transcription factor domain into the Golgi
  5. bHLH dimerizes and is transported into the nucleus to turn on genes that synthesize LDL receptors and HMGR
46
Q

What does bHLH specifically bind to?

A

SRE (DNA sequences that can be found in the promotor region of HMGR and LDL receptors)

47
Q

_____ also has a sterol-sensing domain, because we don’t need it when cholesterol levels are high.

A

HMGR

48
Q

Describe the HMGR/INSIG complex

A
  1. When there is high cholesterol, cholesterol binds to the sterol-sensing domain of HMGR, which then allows INSIG to bind
  2. INSIG brings enzymes that promote ubiquitylation
  3. This leads to destruction of HMGR by the proteasome/ubiquitin system
49
Q

Name ways to treat high cholesterol levels (3 things

A
  1. Bile Acid Binding Resins
  2. Statins
  3. Inhibitors of Cholesterol Absorption
50
Q

What do statins target?

A

Statins inhibit HMGR to reduce circulating LDL

51
Q

What is special about statins that allows them to bind HMGR much stronger than HMG-CoA?

A
  • Statins have HMG like groups that bind to the active site of HMGR
  • Statins have hydrophobic rings which allows HMGR to bind more tightly

Bioc 406 (15 decks)

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