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CPR > Lipids and Lipoproteins - Cholesterol > Flashcards

Lipids and Lipoproteins - Cholesterol Flashcards

1
Q

Where is Acetyl CoA generated?

A

Mitochondria

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2
Q

How many Acetyl CoA are necessary to form 1 IPP (Isopentenyl Pyrophosphate)?

A

3

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3
Q

What are Isopentenyl Pyrophosphates the building blocks for?

A

Isoprenoids

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4
Q

What are 3 types of Isoprenoids?

A
  1. Steroids - ex. Cholesterol
  2. Fat soluble vitamins (ADEK)
  3. ubiquinone
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5
Q

How many carbons make up IPP?

A

5

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6
Q

How many carbons are in 1 Acetyl CoA?

A

2

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7
Q

How many units of IPP are needed to make a sterane (4-ring) ring?

A

6

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8
Q

Cholesterol is made of what type of ring?

A

Sterane (4-ring)

– From 6 units of IPP

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9
Q

What are the major physical features of cholesterol molecules?

A

Sterane ring with 27 carbons

Hydroxyl group on the 3rd carbon

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10
Q

Are cells able to degrade cholesterol?

A

NO - must be used or excreted by the liver

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11
Q

Biosynthesis of cholesterol is ______ proportional to the dietary intake of cholesterol

A

INVERSELY = the more cholesterol you eat the less you will make in your body

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12
Q

What is the overall reaction to make Cholesterol?

A

18 Acetyl CoA + 18 ATP + 16 NADPH = Cholesterol

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13
Q

What is the order of which products are made in phase 1 of cholesterol synthesis?

A 
Acetyl CoA
Acetoacetyl CoA
HMG CoA
Mevalonate
Isopentenyl Pyrophosphate (IPP)
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14
Q

What enzyme takes Acetoacetyl CoA to HMG CoA?

A

HMG CoA Synthase

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15
Q

HMG CoA

A

Hydroxymethylglutaryl CoA

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16
Q

What enzyme takes HMG CoA to Mevalonate?

A

HMG CoA Reductase

17
Q

What is the rate-limiting step of cholesterol synthesis?

A

HMG CoA (using HMG CoA Reductase and NADPH) goes to Mevalonate in phase 1

18
Q

What is the order of which products are made in phase 2 of cholesterol synthesis?

A

6 Isopentenyl Pyrophosphates (IPPs)
Squalene
Lanosterol
Cholesterol

19
Q

Once cholesterol is formed, what are its 2 options?

A
  1. Form Cholesterol Esters

2. Packaged into VLDL and sent into blood

20
Q

What do Statin drugs do?

A

LOWER cholesterol

21
Q

Where do Statin drugs work?

A

They INHIBIT HMG CoA Reductase enzyme (rate-limiting step)

22
Q

Good side effect of Statin drugs?

A

Help to clear cholesterol via LDL receptor mediated endocytosis

23
Q

Bad side effect of Statin drugs?

A

Deplete muscle levels of ubiquinone

– due to acting on pathway before IPP is generated!!

24
Q

Where is cholesterol synthesis regulated?

A

HMG CoA Reductase enzyme

25
Q

What can directly inhibit HMG CoA Reductase enzyme and thus, cholesterol formation?

A
  • Bile acids
  • Statins
  • Free fatty acids
26
Q

If HMG CoA Reductase enzyme is phosphorylated it is _____

A

INactive

27
Q

If HMG CoA Reductase enzyme is DEphosphorylated it is _____

A

ACTIVE

28
Q

What states or molecules want HMG CoA Reductase to be phosphorylated?

A

(INACTIVE)

Low energy states and Glucagon

29
Q

What states or molecules want HMG CoA Reductase to be dephosphorylated?

A

(ACTIVE)

Insulin

30
Q

Another way to regulate cholesterol synthesis is through transcriptional control. What protein is involved?

A

SREBP

31
Q

SREBP binds SCAP to form a complex in the ER. What will stimulate that complex to be moved to the Golgi?

A

LOW cholesterol levels

32
Q

Once the SREBP-SCAP complex is in the Golgi, what is formed and through what mechanism?

A

Mature SREBP through cleavage

33
Q

What does mature SREBP bind?

A

SRE in the nucleus

34
Q

Overall effect of mature SREBP binding to SRE in the nucleus?

A

INCREASED transcription of HMG CoA Reductase

35
Q

SREBP

A

Sterol Regulatory Element Binding Protein

36
Q

SCAP

A

SREBP - Cleavage Activating Protein

37
Q

SRE

A

Sterol Regulatory Element

38
Q

If there is increased transcription of HMG CoA Reductase, what does that cause?

A
  • Increase in cholesterol formation

- Upregulation of LDL receptor

39
Q

What will cause the SREBP-SCAP complex to be retained in the ER?

A

HIGH cholesterol levels – do not need to make more

CPR (48 decks)

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