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Quiz 2 > Q2-CB16/Cholesterol > Flashcards

Q2-CB16/Cholesterol Flashcards

1
Q

What are the 3 important lipid components of the biological membrane?

A

phospholipids, spingolipids, and cholesterol

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2
Q

which of the lipid components of the biological membrane is the least solube?

A

cholesterol

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3
Q

cholesterol is more ______ than other membrane lipids

A

rigid

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4
Q

cholesterol inserts itself between __________

A

fatty acid chains

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5
Q

cholesterol inserts itself between fatty acid chains to prevent their ___________

A

crystallization

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6
Q

cholesterol is synthesised from acetyl CoA in ______ stages

A

three

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7
Q

What is the structure of cholesterol?

A

condensed 4 ring structure

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8
Q

How many atoms does cholesterol have?

A

27 carbon atoms

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9
Q

What are the 3 stages of cholesterol synthesis?

A
  1. synthesis of isopentenyl pyrophosphate
  2. condensation of 6 mols of isopentenyl pyrophosphate to form squalene
  3. squalene cyclizes and the tetracyclic product is turned into cholesterol
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10
Q

What reaction does HMG CoA reductase help in?

A

it turns acetoacetyl CoA + acetyl CoA into mevalonate

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11
Q

How is mevalonate converted to isopentenyl pyrophosphate?

A

it is converted in 3 consecutive reactions that require ATP

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12
Q

squalene is made from ______ mols of isopentenyl pyrophosphate

A

6

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13
Q

What is the reaction sequence from isopentenyl pyrophosphate to squalene?

A
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14
Q

Explain how squalene cyclizes for form cholesterol.

A

squalene is first oxidized to squalene 2,3-epoxide.

squalene 2,3-epoxide cyclizes to form lanosterol.

a few 1,2-methyl groups and hydrides (H-) on the lanosterol shift along the molecule to turn into 4 rings which finally turns the lanosterol into cholesterol

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15
Q

What are normal cholesterol levels in adult humans?

A

140g cholesterol, 3.7 - 5.2 mmol/L

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16
Q

where are the major sites of cholesterol synthesis?

A

liver, intestine, reproductive tissues, adrenal gland

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17
Q

What regulates cholesterol biosynthesis?

A

negative feedback mechanism controlled mostly by changes in the amt and activity of HMG CoA reductase (3-hydroxy-3-methylglutaryl CoA reductase)

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18
Q

What is HMG CoA reductase inhibited by?

A

statins

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19
Q

What are the 4 ways to control HMG CoA reductase?

A

rate of synthesis of reductase mRNA, rate of translation of reductase mRNA, degradation of the reductase, and phosphorylation

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20
Q

explain how the rate of synthesis of reductase mRNA controls HMG CoA reductase

A

the process of making reductase mRNA is controlled by the sterol regulatory element binding proteins (SREBP). When cholesterol levels are low this transcription factor starts transcription of HMG CoA reductase.

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21
Q

What is the rate of translation of reductase mRNA inhibited by?

A

it is inhibited by nonsterol metabolites derived from mevalonate and dietary cholesterol

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22
Q

Why would reductase mRNA become degraded?

A

in response to increasing levels of cholesterol, the enzyme can undergo proteolysis

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23
Q

What does phosphorylation do to the activity of reductase?

A

it decreases the activity of reductase in response to low levels of ATP

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24
Q

cholesterol and triacylglycerols are transported in the form of ___________

A

lipoprotein particles

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25
Q

What are VLDLs?

A

cholesterol in excess of the liver’s own needs are exported to the blood in the form of Very Low Density Lipoproteins (VLDLs)

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26
Q

What are the precursors of LDLs?

A

VLDLs

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27
Q

What is the role of LDLs?

A
  • they carry cholesterol esters, primarily linoleate
  • they carry this cholesterol to peripheral tissues
  • they regulate de novo cholestrol synthesis at these sites
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28
Q

Explain the role of HDLs? (high density lipoproteins)

A

HDL picks up extra cholesterol that has been released into the plasma after a cell has died

the acyltransferase in HDL esterifies the cholesterol

once the cholesterol has been esterified, it is shuttled back to LDLs or returned to the liver

29
Q

What do statins do?

A

inhibition of de novo synthesis of cholesterol in the liver, HMG CoA inhibitors

30
Q

What do cholestyramine/colestipol do?

A

they sequester bile acids in the intestine, reduces the absorption of exogenous cholesterol and inc. the metabolism of endogenous cholesterol into bile acids

31
Q

What do fibrates do?

A

the change the relative levels of diff. lipoproteins

32
Q

What do PCSK9 inhibitors do?

A

PCSK9 is ubiquitously expressed across tissues.

Blocking PCSK9 enhances the number of LDL receptors on target tissue and also lowers circulating LDLs.

33
Q

What are some derivates of cholesterol?

A
34
Q

humans can/cannot metabolism cholesterol to CO2 + H2O

A

cannot

35
Q

Since we cant metabolise cholesterol, how do we eliminate it from the body?

A

by secreting cholesterol into the bile and converting it into bile acids and bile salts. this is then excreted in the feces

36
Q

What is bile?

A

watery mixture of organic and inorganic compounds including bile salts and lecithin

37
Q

After bile is made by the liver where does it go?

A

it is either excreted via the common bile duct or stored in the gall bladder

38
Q

What is the chemical structure of bile acids?

A

24 Carbons, 2-3OH, and a COOH group

39
Q

What is the PKa of the COOH group on a bile acid?

A

around 6, therefore it is not fully ionized at physiologic pH

40
Q

Bile acids are _____ molecules

A

amphipathic

41
Q

Why is the fact that bile acids are amphipathic molecules a good thing?

A

since they have a hydrophilic or hydrophobic face, they can act as emulsifying agents in the intestine (bile acids help to break down dietary triglycerides)

42
Q

cholesterol is turned into 7-alpha-hydroxycholesterol via ___________

A

7-alpha-hydroxylase

43
Q

how are bile salts produced?

A

they are produced in the liver by conjugating bile acids with either glycine or taurine

44
Q

bile salts are _____ at physiologic pH

A

fully ionised, negative charge

45
Q

bile salts are more effective ________

A

detergents

46
Q

bile salts are exposed to ____________ of the intestine

A

bacterial flora

47
Q

what can happen after bile salts are exposed to bacterial flora of the intestine?

A

the regeneration of bile acids by removal of glysine or taurine

OR

production of secondary bile salts by removed of an OH group

48
Q

What is cholesterol gall-stone disease caused by?

A

not enough bile salts being secreted to handle the amt of cholesterol being secreted.

49
Q

What are some causes of cholesterol gall-stone disease?

A
50
Q

What is the result of cholesterol gall-stone disease?

A

cholesterol precipitatees in the gall bladder

51
Q

What is the operation that removes gall bladder stones called?

A

cholecystectomy

52
Q

Cholesterol is the precursor of the 5 major classes of steroid hormones. what are they?

A

progestagens, glucocorticoids, mineralocorticoids, androgens, estrogens

53
Q

What is progesterone?

A
  • a progestagen
  • prepares uterine lining for ovum implantation
  • essential for the maintenance of pregnancy
54
Q

What are androgens?

A
  • ex. testosterone
  • responsible for development of male secondary sex characteristics
55
Q

What are estrogens?

A
  • responsible for development of female secondary sex characteristics
  • participates in ovarian cycle (like progesterone)
56
Q

What are Glucocorticoids?

A
  • promotes gluconeogenesis and breakdown of glycogen
  • enhance breakdown of fats and proteins
  • inhibits inflammatory response
57
Q

What are mineralocorticoids?

A
  • ex. aldosterone
  • acts on distal tubules of kidney to inc. reabsorption of sodium and excretion of potassium and hydrogen
58
Q

What is the precursor of vitamin D?

A

cholesterol

59
Q

Explain the role of 7-dehydrocholesterol in vitamin d3 production.

A

7-dehydrocholesterol is photolysed by UV light from the sun to pre-vitamin D3, which spontaneously isomerizes to Vitamin D3

60
Q

What is another name for vitamin d3?

A

cholecalciferol

61
Q

Hydroxylation rxns in the liver and kidneys turns vitamin D3 to ________

A

calcitriol

62
Q

What does vitamin d bind onto on proteins?

A

intracellular receptors (similar to steroid receptors)

63
Q

Vitamin D selectively stimulates ___________

A

gene transcription

64
Q

Vitamin D regulates plasma levels of _____ and _______

A

calcium and phosphorus

65
Q

What is rickets?

A

Vitamin D deficiency in kids, characterized by inadequate calcification of cartilage and bone

66
Q

When does a vitamin D deficiency occur?

A

deficiency occurs when 7-hydrocholesterol in the skin is not photolysed to pre-vitamin D3 and dietary intake of vitamin D is low

67
Q

What is osteomalacia?

A

a vitamin D deficiency in adults that leads to the softening and weakening of bones

68
Q

recommended daily intake of vitamin D?

A

400 international units

Quiz 2 (18 decks)

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