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Biochemistry Post Midterm > Cholesterol Metabolism > Flashcards

Cholesterol Metabolism Flashcards

1
Q

What is the most abundant sterol in the body?

A

cholesterol

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2
Q

What is the function of cholesterol?

A
  1. component of all cell membranes
  2. precursor of bile acids
    3/ precursor of steroid hormones and Vitamin D
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3
Q

What does the synthesis of cholesterol require?

A

acetyl coA
NADPH
ATP

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4
Q

What is the rate limiting enzyme of cholesterol synthesis?

A

HMG CoA reductase

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5
Q

where does synthesis of cholesterol occur?

A

cytoplasm

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6
Q

where are the enzymes for synthesis of cholesterol located?

A

in cytosol and ER

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7
Q

what can too much plasma cholesterol lead to?

A

atherosclerosis

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8
Q

what can too much cholesterol secretion cause formation of?

A

gall stones

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9
Q

what are the 2 stages of synthesis of cholesterol ?

A

A. synthesis of mevalonic acid (mevalonate)

B. synthesis of cholesterol from mevalonate

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10
Q

What type of reaction is the synthesis of mevalonate?

A

irreversible

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11
Q

how does cholesterol regulate cholesterol biosynthesis?

A

cholesterol if a feedback inhibitor

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12
Q

what does AMP kinase do to HMG CoA Reductase?

A

phosphorylates and inhibits

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13
Q

what does glucagon do to HMG coA reductase?

A

phosphorylates (PKA dep.) and inactivates it - decreasing cholesterol synthesis

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14
Q

What competitevly inhibit HMG CoA reductase?

A

statins

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15
Q

how do statins contribute to long term regulation of cholesterol synthesis?

A

cause enzyme upregulation = reversible inhibitor of HMG CoA reductase

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16
Q

what does a high cholesterol diet cause?

A

down regulatin of HMG CoA reductase

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17
Q

What does low cholesterol levels stimulate the release of?

A

SREBP protein from the ER

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18
Q

what does SREBP bind to on the HMG CoA reductase gene?

A

sterol responsive element (SRE)

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19
Q

what does high intracellular concentrations of AMP stimulate?

A

AMP kinase which phosphorylates HMG -CoA and inactivates it!

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20
Q

How is HMG CoA activated?

A

insulin activates phosphorylation phosphatase which = dephosphorylation

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21
Q

degradation of HMG CoA reductase is controlled by what?

A

ubiquitin system in proteosomes

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22
Q

what does high concentration of cholesterol and/or mevalonate lead to?

A

rapid degradation (proteolysis) of the HMG CoA reductase enzyme

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23
Q

what does low intracellular cholesterol (with statin treatment cause)?

A

unreg of HMG CoA reductase
upreg of LDL receptor
inrease in uptake of LDL from serum
reduction in serum cholesterol

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24
Q

what is intracellular cholesterol a key regulator of?

A

HMG CoA reductase
LDL receptor endocytosis
ACAT

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25
What is Smith-Lemil-Opitz Syndrome (SLOS)?
autosomal recessive cholesterol synthesis disorder relatively common leads to microencephaly and other embryolic malformation surviving kids have low IQ
26
What enzyme is deficient in SLOS?
7-dehydrocholesterol reductase
27
what is 7-dehydrocholesterol reductase needed for?
the correct double bond formation in ring B
28
How is cholesterol eliminated since it cannot be degraded?
conversion of cholesterol into bile salts - excreted in feces
29
some cholesterol is modified by bacteria in the intestine to form?
cholestanol | coprostanol
30
why are cholestanol | coprostanol important
those + free cholesterol form the bulk of fecal sterols
31
what is bile made of?
organic and inorganic compounds - phosphatidylcholine (lecithin) - org - bile salts - org
32
What are the primary bile acids?
cholic acid | chenodeoxycholic acid
33
what is the rate limiting enzyme of the synthesis of bile acids?
7-alpha-hydroylase
34
how is 7-alpha-hydroylase inhibited?
by its own product, cholic acid (product inhibition)
35
What are bile acids conjugated with?
glycine = glycocholic acid and glycochenodeoxycholic acid taurine = taurocholic acid taurochenodeoxycholic acid
36
which are more effective at solubilizing lipids?
bile salts - much more than bile acids
37
What competitevly inhibit HMG CoA reductase?
statins
38
how do statins contribute to long term regulation of cholesterol synthesis?
cause enzyme upregulation = reversible inhibitor of HMG CoA reductase
39
what does a high cholesterol diet cause?
down regulatin of HMG CoA reductase
40
What does low cholesterol levels stimulate the release of?
SREBP protein from the ER
41
what does SREBP bind to on the HMG CoA reductase gene?
sterol responsive element (SRE)
42
what does high intracellular concentrations of AMP stimulate?
AMP kinase which phosphorylates HMG -CoA and inactivates it!
43
How is HMG CoA activated?
insulin activates phosphorylation phosphatase which = dephosphorylation
44
degradation of HMG CoA reductase is controlled by what?
ubiquitin system in proteosomes
45
what does high concentration of cholesterol and/or mevalonate lead to?
rapid degradation (proteolysis) of the HMG CoA reductase enzyme
46
what does low intracellular cholesterol (with statin treatment cause)?
unreg of HMG CoA reductase upreg of LDL receptor inrease in uptake of LDL from serum reduction in serum cholesterol
47
what is intracellular cholesterol a key regulator of?
HMG CoA reductase LDL receptor endocytosis ACAT
48
What is Smith-Lemil-Opitz Syndrome (SLOS)?
autosomal recessive cholesterol synthesis disorder relatively common leads to microencephaly and other embryolic malformation surviving kids have low IQ
49
What enzyme is deficient in SLOS?
7-dehydrocholesterol reductase
50
what is 7-dehydrocholesterol reductase needed for?
the correct double bond formation in ring B
51
How is cholesterol eliminated since it cannot be degraded?
conversion of cholesterol into bile salts - excreted in feces
52
some cholesterol is modified by bacteria in the intestine to form?
cholestanol | coprostanol
53
why are cholestanol | coprostanol important
those + free cholesterol form the bulk of fecal sterols
54
what is bile made of?
organic and inorganic compounds - phosphatidylcholine (lecithin) - org - bile salts - org
55
What are the primary bile acids?
cholic acid | chenodeoxycholic acid
56
what is the rate limiting enzyme of the synthesis of bile acids?
7-alpha-hydroylase
57
how is 7-alpha-hydroylase inhibited?
by its own product, cholic acid (product inhibition)
58
What are bile acids conjugated with?
glycine = glycocholic acid and glycochenodeoxycholic acid taurine = taurocholic acid taurochenodeoxycholic acid
59
which are more effective at solubilizing lipids?
bile salts - much more than bile acids
60
what can remove taurine or glycine from bile salts?
intestinal bacteria
61
how do intestinal bacteria convert primary bile salts to secondary bile salts?
by removing hydroxyl groups
62
what are the secondary bile salts?
deoxycholic acid from cholic acid | lithocholic acid from chenodeoxycholic acid
63
what will a deficiency in lecithin and or bile salts cause?
cholesterol in bile to precipiate in the gall bladder = gall stones

Biochemistry Post Midterm (24 decks)

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