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Applied Biochemistry > Cholesterol Biosynthesis and Transport Genetics Part 1 > Flashcards

Cholesterol Biosynthesis and Transport Genetics Part 1 Flashcards

1
Q

cholesterol is a precursor for (3)

A

vitamin D
steroids
bile salts

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2
Q

cholesterol is necessary for — —

A

membrane stability

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3
Q

cholesterol is a major structural component of — —

A

myelin sheaths

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4
Q

myelin sheaths are synthesized by glial (what types of glial cells) cells and which surround axons in vertebrates

A

PNS: schwann cells
CNS: oligodendrocytes

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5
Q

what are nodes of ranvier?

A

non myelinated regions with a high concentration of Na+ channels which initiate depolarization of the membrane

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6
Q

all steroids contain the same four — —

A

hydrocarbon rings

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7
Q

the major portion of the molecule is — but the hydroxyl group is —

A

hydrophobic, hydrophilic

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8
Q

what two ways can cholesterol be absorbed?

A

dietary sources

synthesized de novo

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9
Q

what are the two main organs which synthesize cholesterol?

A 
liver (70-80%)
small intestine (10%)
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10
Q

cholesterol is also produced in the (2)

A

adrenal glands and gonads

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11
Q

why is cholesterol a critical component of cell membranes (~30%)?

A

it regulates membrane fluidity and has important functions in intracellular transport, cell signaling, and nerve conduction

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12
Q

cholesterol is the precursor for the biosynthesis of (3)

A

steroid hormones, bile acids, and vitamin D

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13
Q

an adults on a low cholesterol diet typically synthesizes about — mg of cholesterol on a daily basis

A

800 (de novo, liver)

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14
Q

LDL
most desirable
very high

A

under 100

over 190

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15
Q

HDL
undesirable
good, risk lowered

A

under 40

over 60

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16
Q

stage 1 of de novo biosynthesis of cholesterol

A

the synthesis of isopentenyl pyrophosphate

this stage becgins with the condensation of acetyl-coA and acetoacetyl-coA in the cytoplasm to form 3-hydroxyl-3-methylglutaryl coA (HMG-coA), which is then reduced to mevalonate by the enzyme HGM-coA reductase. mevalonate is then converted into isopentyl pyrophosphate

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17
Q

stage 2 of de novo biosynthesis of cholesterol

A

the condensation of 6 molecules of isopentyl pyrophosphate to form squalene

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18
Q

stage 3 of de novo biosynthesis of cholesterol

A

the cyclization of squalene to form the steroid 4-ring structure, which rearranges to form lanosterol. lanosterol is then converted into cholesterol

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19
Q

first committed step of cholesterol biosynthesis

A

HMG-coA is reduced by HMG-coA reductase to form mevalonate

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20
Q

in the cytosol, HGM-coA is converted into mevalonate whereas in the mitochondria, it is converted to — and —, which are further processed into — —

A

acetyl coA and acetoacetate

ketone bodies

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21
Q

what produces all of the acetyl coA?

A

fatty acid beta-oxidation

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22
Q

the source of carbon atoms in cholesterol are synthesized from

A

acetate

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23
Q

the rate of synthesis of reductase mRNA is controlled by the

A

sterol regulatory binding proteins (SREBP)

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24
Q

SREBP is a

A

transcription factor

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25
Q

this process is regulated by levels of cholesterol available by the — and — proteins that bind cholesterol

A

INGIG

SCAP

26
Q

INSIG and SCAP act as — to tell us if we need to keep SREBP available

A

sensors

27
Q

the rate of translation of reductase mRNA is inhibited by metabolites derived from — as well as — —

A

mevalonate

dietary cholesterol

28
Q

degradation of the reductase is tightly controlled by —

A

lanosterol

29
Q

phosphorylation of the enzyme decreases the activity of the

A

reductase

30
Q

this enzyme, along with acetyl-coA carboxylase which catalyzes a similar committed step in fatty acid biosynthesis, is switched off by an — — — —

A

AMP-activated protein kinase

31
Q

fatty acid and cholesterol biosynthesis cease when — is low in the cell

A

ATP

32
Q

why does FA and cholesterol biosynthesis cease when ATP is low in the cell?

A

cholesterol and FA are not needed when ATP is low. these are ATP requiring steps, so they wont occur when ATP is low

33
Q

synthesis of cholesterol and fatty acids is regulated by transcription factors — and —

A

SREBP 1 and SREBP 2

34
Q

SREBP target genes are used in (4)

A

cholesterol metabolism
fatty acid metabolism
triglyceride synthesis
plasma lipoprotein metabolism

35
Q

SREBP target genes in cholesterol metabolism (7)

A 
LDL receptor 
HGM coA synthase
HGM coA reductase 
farnesyl diphosphate synthase
squalene synthase 
SREBP-2
lanosterol-14-alpha-demethylase (cyp51)
36
Q

SREBP target genes in fatty acid metabolism (8)

A 
acetyl coA carboxylase
fatty acid synthase
stearoyl coA desaturase-1 and 2
acyl-coA binding protein (diazepam)
SREBP-1
ATP citrate lyase
PPAR gamma
acetyl coA synthetase
37
Q

SREBP target genes in triglyceride synthesis (1)

A

glycerol-3-phosphate acyltranferase

38
Q

SREBP target genes in plasma lipoprotein metabolism (2)

A 
lipoprotein lipase
HDL receptor (SRBI)
39
Q

statins act by competitively inhibiting

A

HMG-coA reductase

40
Q

by inhibiting HMG-coA reductase, the amount of — produced is reduced

A

mevalonate

41
Q

reduced mevalonate ultimately leads to reduced — synthesis

A

cholesterol

42
Q

when the liver can no longer produce cholesterol, levels in the blood will fall since most of the circulating cholesterol comes from

A

internal synthesis, rather than diet

43
Q

cholesterol synthesis occurs mostly at — so statins with a short like are usually taken at — to maximize their benefit

A

night

44
Q

statins inhibit the reabsorption of

A

ostetoclasts

45
Q

statins inhibit the reabsorption of osteoclasts since they also inhibit the formation of prenylated proteins which is required for

A

osteoglastogenesis

46
Q

what do statins ressemble?

A

the 3-hydroxy-3-methylglutaryl moiety recognized by HMG-coA reductase

47
Q

statins act as a competitive inhibitor by preventing

A

HMG-coA reductase from producing HMG-coA

48
Q

bisphosphonates are used for treating bone diseases such as — and —

A

osteoporosis

osteogenesis imperfecta

49
Q

bisphosphonates inhibit

A

osteoclast resorption of bone

50
Q

pyrophosphate is an inhibitor of

A

mineralization

51
Q

what was the first bisphosphonate developed?

A

alendronate

52
Q

zoledronate is a bisphosphonate used to treat

A

osteocronosis of the jaw

53
Q

what is protein prenylation?

A

post-translational modification of proteins that adds a farnesyl or geranylgeranyl to the c-terminal cysteines of target proteins

54
Q

the prenylation adds a — — to the target protein, which can serve to

A

hydrophobic molecule

anchor the protein to the membrane surface

55
Q

what is the role of prenylation in osteoclast function?

A

prevents osteoclasts from resorption of bone

56
Q

prenylation in osteoclast function

A

small GTPase localize to specific membrane compartments and assist in cytoskeleton rearrangement needs to form the sealing zone. this localization is dependent upon post-translational prenylation of these GTPases

57
Q

bile salts are made in the — and stored in the — between meals

A

liver

gallbladder

58
Q

after we eat and there are fats present in our digestive tracts, out hormones send. signal to our gallbladders to

A

release bile

59
Q

bile salts aid in digestion by breaking down

A

fats

60
Q

bile salts help absorb

A

fat-soluble vitamins

61
Q

bile salts eliminate

A

waste products

Applied Biochemistry (52 decks)

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