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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
Q

What is Smith-Lemil-Opitz Syndrome (SLOS)?

A

autosomal recessive cholesterol synthesis disorder
relatively common
leads to microencephaly and other embryolic malformation
surviving kids have low IQ

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26
Q

What enzyme is deficient in SLOS?

A

7-dehydrocholesterol reductase

27
Q

what is 7-dehydrocholesterol reductase needed for?

A

the correct double bond formation in ring B

28
Q

How is cholesterol eliminated since it cannot be degraded?

A

conversion of cholesterol into bile salts - excreted in feces

29
Q

some cholesterol is modified by bacteria in the intestine to form?

A

cholestanol

coprostanol

30
Q

why are cholestanol

coprostanol important

A

those + free cholesterol form the bulk of fecal sterols

31
Q

what is bile made of?

A

organic and inorganic compounds

  • phosphatidylcholine (lecithin) - org
  • bile salts - org
32
Q

What are the primary bile acids?

A

cholic acid

chenodeoxycholic acid

33
Q

what is the rate limiting enzyme of the synthesis of bile acids?

A

7-alpha-hydroylase

34
Q

how is 7-alpha-hydroylase inhibited?

A

by its own product, cholic acid (product inhibition)

35
Q

What are bile acids conjugated with?

A

glycine = glycocholic acid and glycochenodeoxycholic acid

taurine = taurocholic acid
taurochenodeoxycholic acid

36
Q

which are more effective at solubilizing lipids?

A

bile salts - much more than bile acids

37
Q

What competitevly inhibit HMG CoA reductase?

A

statins

38
Q

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

A

cause enzyme upregulation = reversible inhibitor of HMG CoA reductase

39
Q

what does a high cholesterol diet cause?

A

down regulatin of HMG CoA reductase

40
Q

What does low cholesterol levels stimulate the release of?

A

SREBP protein from the ER

41
Q

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

A

sterol responsive element (SRE)

42
Q

what does high intracellular concentrations of AMP stimulate?

A

AMP kinase which phosphorylates HMG -CoA and inactivates it!

43
Q

How is HMG CoA activated?

A

insulin activates phosphorylation phosphatase which = dephosphorylation

44
Q

degradation of HMG CoA reductase is controlled by what?

A

ubiquitin system in proteosomes

45
Q

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

A

rapid degradation (proteolysis) of the HMG CoA reductase enzyme

46
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

47
Q

what is intracellular cholesterol a key regulator of?

A

HMG CoA reductase
LDL receptor endocytosis
ACAT

48
Q

What is Smith-Lemil-Opitz Syndrome (SLOS)?

A

autosomal recessive cholesterol synthesis disorder
relatively common
leads to microencephaly and other embryolic malformation
surviving kids have low IQ

49
Q

What enzyme is deficient in SLOS?

A

7-dehydrocholesterol reductase

50
Q

what is 7-dehydrocholesterol reductase needed for?

A

the correct double bond formation in ring B

51
Q

How is cholesterol eliminated since it cannot be degraded?

A

conversion of cholesterol into bile salts - excreted in feces

52
Q

some cholesterol is modified by bacteria in the intestine to form?

A

cholestanol

coprostanol

53
Q

why are cholestanol

coprostanol important

A

those + free cholesterol form the bulk of fecal sterols

54
Q

what is bile made of?

A

organic and inorganic compounds

  • phosphatidylcholine (lecithin) - org
  • bile salts - org
55
Q

What are the primary bile acids?

A

cholic acid

chenodeoxycholic acid

56
Q

what is the rate limiting enzyme of the synthesis of bile acids?

A

7-alpha-hydroylase

57
Q

how is 7-alpha-hydroylase inhibited?

A

by its own product, cholic acid (product inhibition)

58
Q

What are bile acids conjugated with?

A

glycine = glycocholic acid and glycochenodeoxycholic acid

taurine = taurocholic acid
taurochenodeoxycholic acid

59
Q

which are more effective at solubilizing lipids?

A

bile salts - much more than bile acids

60
Q

what can remove taurine or glycine from bile salts?

A

intestinal bacteria

61
Q

how do intestinal bacteria convert primary bile salts to secondary bile salts?

A

by removing hydroxyl groups

62
Q

what are the secondary bile salts?

A

deoxycholic acid from cholic acid

lithocholic acid from chenodeoxycholic acid

63
Q

what will a deficiency in lecithin and or bile salts cause?

A

cholesterol in bile to precipiate in the gall bladder = gall stones

Biochemistry Post Midterm (24 decks)

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