lecture 8: cholesterol synthesis Flashcards

1
Q

what is the common factor of cholesterol-containing foods?

A

animal sources - comes from liver

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2
Q

cholesterol fluidity

A

increases fluidity in colder temperatures
decreases fluidity in warmer temperatures

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3
Q

atherosclerosis

A

thickening of arteries from deposition of cholesterol and cholesterol lipoproteins in arteries

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4
Q

chylomicrons

A

transport dietary lipids throughout the body

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5
Q

how does the liver repackage cholesterol? how is it taken up?

A

repackage from chylomicrons into VLDL > IDL, LDL
most tissues take up LDL as cholesterol source

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6
Q

cholesterol synthesis site

A

liver and intestine are major sites
occurs in the cytosol, closely associated with ER

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7
Q

substrate for cholesterol synthesis

A

acetyl-CoA

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8
Q

conversion of acetyl-CoA to mevalonate

A

three 2C acetyl-CoA condensed to form 6C HMG-CoA

HMG-CoA reductase to mevalonate

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9
Q

cholesterol synthesis steps

A

conversion of acetyl-CoA to mevalonate
mevalonate to isoprenoids (5C)
isoprenoids to squalene, cholesterol, lanosterol

intermediates reduced by NADPH

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10
Q

primary target of cholesterol regulation

A

HMG-CoA reductase (controls production of melavonate)

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11
Q

HMG-CoA reductase

A

anchored to ER membrane
negative feedback from mevalonate and cholesterol
inhibited by statins (lipid lowering drugs)

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12
Q

sterol regulatory element-binding protein (SREBP) and regulation of transcription

A

sterol regulatory element (SRE) controls transcription, bound by SREBP to promoter region of genes

SREBPs induce transcription of genes involved in cholesterol metabolism and TAG/FA synthesis

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13
Q

when cholesterol levels in ER membrane is low…

A

SCAP (SREBP cleavage-activating protein) binds to component of COPII coat proteins > vesicles bud off ER and sent to golgi
SREBP cleaved, releasing active form

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14
Q

when cholesterol levels are high…

A

cholesterol binding to SCAP causes SCAP to bind to Insig > prevents SCAP from interacting with COPII (cannot be sent to golgi, active SREBP not released)

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15
Q

HMG-CoA reductase degredation

A

high cholesterol > HMG-CoA reductase binds to insig > ubiquitination and proteosomal degradation

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16
Q

HMG-CoA reductase phosphorylation

A

phosphorylates via AMPK
active when AMP levels are high (low energy charge) > makes HMG-CoA reductase less active

17
Q

how is cholesterol transported through the blood?

A

inside lipoprotein particles (HDL, IDL, LDL, VLDL, chylomicrons)

18
Q

similarities btw FA synthesis and cholesterol synthesis

A

acetyl-CoA is the building block

require a series of condensation, decarboxylation, and reduction reactions

intermediates reduced by NADPH