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GI System Final I > Liver Biochemistry > Flashcards

Liver Biochemistry Flashcards

1
Q

What supplies most blood flow to liver?

A

portal vein

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2
Q

Bile canniculus

A

duct like structure that runs parallel to sinusoids

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3
Q

What are the 5 liver cell types

A

hepatocytes, endothelial cells, kupffer cells, hepatic stellate cells, pit cells

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4
Q

Kupffer cells

A

macrophages of liver

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5
Q

Hepatic stellate cells

A

specific to liver

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6
Q

Pit cells

A

NK cells that protect the liver against virus and tumor cells

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7
Q

Major function of the liver

A

central receiving, distribution, and recycling center

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8
Q

Major role of receiving, distribution and recycling center

A

monitoring, synthesizing, recycling, distributing, and modifying metabolites

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9
Q

How does liver convert harmful products

A

Converts into safe product and is excreted

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10
Q

2 vessels that provide blood to liver

A

portal vein and hepatic artery

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11
Q

Structure of liver cells

A

lack basement membrane, fenestrations in endothelial cells, low portal blood pressure

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12
Q

Functional reason for structure of liver

A

greater access and increased contact between liver and blood

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13
Q

What forms isopentenyl pyrophosphate?

A

3 acetyl CoAs

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14
Q

3 potential products from isopentenyl pyrophosphate

A
  1. Steroids (cholesterol, bile, steroid hormones)
  2. Lipid soluble vitamins (A, D, E, K)
  3. Other (ubiquinone, heme tails)
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15
Q

Sources of acetyl CoA

A

oxidative decarboxylation, beta oxidation of fatty acids, breakdown of amino acids

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16
Q

What part of the cell is Acetyl CoA generated in

A

mitochondria

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17
Q

How does Acetyl CoA get into cytolasm

A

citrate shuttle

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18
Q

Example of some steroids derived from IPP

A

cholesterol, estradiol, cholic acid

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19
Q

Structure of cholesterol

A

allicyclic compound made of 4 fused rings

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20
Q

Cholesterol is the precursor of what active compounds

A

bile acids and salts, vitamin D, steroid hormones

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21
Q

What is the daily production of cholesterol

A

1g

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22
Q

T/F biosynthesis is proportional to dietary intake of cholesterol

A

F- biosynthesis is inversely proportional to dietary intake. The less you intake the more you make

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23
Q

What enzyme is used to make HMG CoA from acetoacetyl CoA?

A

HMG CoA synthase

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24
Q

What is the rate limiting enzyme in cholesterol synthesis

A

HMG CoA reductase

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25
Q

What are the rate limiting intermediates for cholesterol synthesis

A

HMG CoA to mevalonate

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26
Q

What does positive feedback for rate limiting step

A

insulin and thyroxine

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27
Q

What does negative feedback for rate limiting step

A

sterols and statins

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28
Q

Statins and ubiquinone formation?

A

Statins inhibit ubiquinone formation and will mess up TCA cycle and muscle formation so need to make sure patients are supplemented

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29
Q

Fate of cholesterol in all tissues

A

cholesterol incorporated into cellular membranes

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30
Q

Fate of cholesterol in liver

A

synthesize bile acids

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31
Q

Fate of cholesterol in adrenal glands, ovaries and testes

A

synthesize steroid hormones

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32
Q

Fate of cholesterol in skin

A

synthesize vitamin D

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33
Q

Main/Major fate of cholesterol

A

packaged into VLDL and released into circulation

34
Q

Lipid rafts

A

microdomains enriched in cholesterol, sphingolipids, and gangliosides

35
Q

What happens at lipids rafts

A

center for signal transduction processes and abnormal processing of proteins

36
Q

Which way is the catalytic domain facing in choesterol

A

cytosol site where ubiquitination occurs

37
Q

Which domain is facing the luminal side?

A

membrane domain

38
Q

Direct inhibition of HMG CoA reductase

A

free fatty acids, bile acids, and oxysterols

39
Q

T/F Statins are noncompetitive inhibitors of HMG CoA Reductase

A

F- statins are competitive inhibitors of HMG CoA Reductase

40
Q

Where does the stain bind to compete for HMG CoA reductase

A

the active site, and statins have similar structures

41
Q

Covalent modifications of HMG CoA Reductase

A

Active when dephosphorylated, inactive when phosphorylated

42
Q

Low energy - high AMP levels on AMP

A

phosphorylates it through AMP activated kinase and inactivates it

43
Q

Glucagon impact on HMGR

A

inhibits enzyme by preventing dephosphoylattion

44
Q

Insulin impact on HMGR

A

activates HMGR phosphatase and promotes dephosphoylation

45
Q

AMP kinase

A

puts phosphate on HMGR to inactivate it

46
Q

HMGR phosphatase

A

takes phosphate off HMGR to activate it

47
Q

Promoter for transcriptional Control of HMG

A

sterol regulatory element SRE

48
Q

sterol regulatory element binding protein (SREBP)

A

sequence that binds trascription factors

49
Q

What does SREBP interact with

A

SREBP cleave activating protein

50
Q

What does SREBP-SCAP complex bind to?

A

INSIG

51
Q

When does SREBP-SCAP complex bind to INSIG

A

in the presence of cholesterol

52
Q

Is transcription slow or fast when cholesterol is present and binding to the SREBP-SCAP complex

A

slow

53
Q

What promotes release of SREBP-SCAP complex from ER

A

low sterol

54
Q

What binds to SRE to promote transcription of HMG CoA reductase

A

mature form of SREBP

55
Q

What reduces translastion of HMG

A

vitamin E family (gamma-tocotrienol) and oxylanosterols

56
Q

What happens to HMG when there is more cholesterol?

A

degrade HMG CoA reductase

57
Q

Role of liver and cholesterol

A

cholesterol metabolism and homeostasis

58
Q

Where does cholesterol biosynthesis occur?

A

liver

59
Q

What does liver do to cholesterol

A

package it into VLDL, release it into blood, metabolize to LDL by peripherial tissues

60
Q

How is dietary cholesterol delivered to the liver

A

chylomicron remnants

61
Q

Inhibitors of HMG CoA Reductase

A

statins because they are competitive inhibitors

  • citrus juices
  • grapefruit juice
62
Q

Function of cytochrome P450

A

convert linear isoprenoid squalene into cholesterol

63
Q

What happens if you inhibit cytochrome P450

A

increase in statin levels leaving to toxic effects

64
Q

Function of agents that induce cytochrome P450

A

decrease levels of statin in plasma

65
Q

What is the precursor of bile acids and bile salts

A

hepatic cholesterol

66
Q

Characteristics of strong detergents

A

amphipathic with polar and nonpolar regions

67
Q

Where is bile made

A

hepatocytes

68
Q

Where is bile stored and concentrated

A

gallbladder

69
Q

What is bile made of

A

bile acids, cholesterol, phosphoipids, fatty acids, proteins, bile pigments, inorganic salts

70
Q

Lipid emulsification

A

aids in lipid digestion, forming micelles to increase surface area of lipids

71
Q

How is cholesterol is converted to bile salt

A

Cholesterol + Cytrochrome P450 –> 7a- hydroxycholesterol

72
Q

2 fates of 7a-hydroxycholesterol

A

chenocholic acid and cholic acid

73
Q

Difference between chenocholic acid and cholic acid

A

cholic acid the 2nd hydroxyl group is added at 12th position and bile acids can be conjugated

74
Q

Taurocholic acid

A

taurine is added to replace CoA, lower pKa makes them efficient in surfactant ability

75
Q

Glycocholic acid

A

glycine added to replace CoA

76
Q

Difference between cholesterol and bile salt

A

to make a bile salt, remove H from carboxylic acid of cholesterol

77
Q

Micelle

A

surrounded by bile salt and has hydrophobic and hydrophilic areas so we can digest certain things

78
Q

Gallstones

A

bile supersaturated with cholesterol

79
Q

Cholelithiasis

A

insufficient secretion of bile salts or phospholipds or excess cholesterol secretion

80
Q

Chronic disturbance in bile salt metabolism

A

steatorrhea and deficiency in fat soluble vitamins

GI System Final I (7 decks)

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