Biochemistry week 3 Flashcards

(32 cards)

1
Q

What is the function of cholesterol

A
  • Structural component for all cell membranes
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2
Q

What is cholestorl a percursor for?

A
  • Bile acids
    -Steroid hormones
    -Vitamin D
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3
Q

Early cholesterol synthesis provides substrates important for what

A
  • Cell proliferation
    -Electron transport–Combating oxidative stress
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4
Q

What regulates cholesterol homeostasis

A
  • The liver
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5
Q

What does plasma cholestrol depend on

A
  • Endogenous ( body made) synthesis
    -Dietary intake
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6
Q

Explain the structure of cholesterol

A
  • Very hydrophobic
    -Contains 4 fused hyrocarbon rings called steriod nucles
    -
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7
Q

What does Ring A on cholesterol have

A
  • Hydroxyl group at carbon 3
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8
Q

What does Ring B on cholesterol have

A

-Has double boned between C5 and C6

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9
Q

Where can cholesterol be synthesized

A
  • Liver
    -Adrenal cortex
    -Intestine
    -Reproductive organs
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10
Q

In cholestorl synthesis where do all the carbon atoms come from

A

acetyl coA`

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11
Q

What provides the reducing power in cholesterol synthesis

A
  • NADPH
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12
Q

Where are the enzymes involved in cholesterol synthesis located in

A
  • Cytosol
    -SER
    -Perioxisome
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13
Q

To make 1 mol of cholestrol how much acetylcoA, ATP ans NADPH is used

A
  • 18 moles of acetyl CoA

-36 moles of ATP

-16 moles of NADPH

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14
Q

Name what regulates cholesterol synthesis

A

-Sterol-dependent regulation of gene expression
-Sterol independent phosphorylation/dephosphorylation
-Drug inhibition
-Hormonal regulation

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15
Q

Name the proteins involed in Sterol-dependent regulation of gene expression

A

SREBP2
-SCAP

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16
Q

Explain what happens in sterol-dependent regulation when cholesterol levels are LOW

A
  • SREBP2, moves from ER to the golgi
    -Proteolysis activates SREBP
    -Then the active SREBP2 enters the nucles and promotes gene transcription for cholesterol synthesis
17
Q

Explain what happens in sterol-dependent regulation when cholesterol levels are HIGH

A
  • Cholesterol binds to SCAP, causing a conformational change
    -SCAP binds to insig-1, keeping the SCAP complex in the ER
    -SREBP remains inactive so gene transcription is repressed
18
Q

In sterol independent regulation(phosphorylation/dephosphorylation):
- When is HMG CoA reductase inactive and active

A
  • Inactive when phosphorylated
    -Active when dephosphorylated
19
Q

What is HMG CoA reductase controlled by + FUNCTION

In sterol independent regulation(phosphorylation/dephosphorylation)

A
  • AMPK, which phosphorylates and inhibts the enzyme
    -Phosphoprotein phosphatase which dephosphorylates and activates the enzyme
20
Q

In sterol independent regulation(phosphorylation, dephosphorylation) WHAT DOES LOW ATP DO

A
  • Activates AMPK , which reduces cholesterol
21
Q

Name a drug used in drug inhibition which is used to regulate cholesterol synthesis

22
Q

Explain how statins work in drug inhibition

A
  • They act as competitive inhibitors of HMG CoA reductase
    -They mimic HMG CoA
23
Q

How is cholesterol broken down

A
  • It is converted to bile acids , secreted into bile and then into the feces
24
Q

During bile acid synthesis name the rate limiting enzyme

A

7a-hydroxylase

25
Explain the structural changes to cholesterol that occurs during bile acid synthesis
- Insertion of OH groups into cholesterol -Reduction of double bonds in the B ring -Shortening of side chains by 3 carbons
26
Explain how biles salts are formed
- Bile acids are conjugated with glycine or taurine, forming bile salts
27
Exlain the function of intestinal flora on bile salts
- They can remove glycine and taurine from bile salts, regenerating bile acids
28
What is gall stone disease caused by
- CAUSED BY choesterol precipitates when it exceeds the solubilizing capacity of bile
29
What are other contributing factors to gallstone disease
- Excess cholesterol -Malabsorption of bile acids -Severe liver dysfunction
30
What is familial hypercholesterolemia
High levels of cholesterol in the blood
31
What is the cause of familial hypercholesteroemia
- Defective LDL receptors
32
What is the inhertitance pattern of familial hypercholesterolemia
- Autosomal dominant