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GI System Final I > Liver Biochemistry > Flashcards

Liver Biochemistry Flashcards

(80 cards)

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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
What are the rate limiting intermediates for cholesterol synthesis
HMG CoA to mevalonate
26
What does positive feedback for rate limiting step
insulin and thyroxine
27
What does negative feedback for rate limiting step
sterols and statins
28
Statins and ubiquinone formation?
Statins inhibit ubiquinone formation and will mess up TCA cycle and muscle formation so need to make sure patients are supplemented
29
Fate of cholesterol in all tissues
cholesterol incorporated into cellular membranes
30
Fate of cholesterol in liver
synthesize bile acids
31
Fate of cholesterol in adrenal glands, ovaries and testes
synthesize steroid hormones
32
Fate of cholesterol in skin
synthesize vitamin D
33
Main/Major fate of cholesterol
packaged into VLDL and released into circulation
34
Lipid rafts
microdomains enriched in cholesterol, sphingolipids, and gangliosides
35
What happens at lipids rafts
center for signal transduction processes and abnormal processing of proteins
36
Which way is the catalytic domain facing in choesterol
cytosol site where ubiquitination occurs
37
Which domain is facing the luminal side?
membrane domain
38
Direct inhibition of HMG CoA reductase
free fatty acids, bile acids, and oxysterols
39
T/F Statins are noncompetitive inhibitors of HMG CoA Reductase
F- statins are competitive inhibitors of HMG CoA Reductase
40
Where does the stain bind to compete for HMG CoA reductase
the active site, and statins have similar structures
41
Covalent modifications of HMG CoA Reductase
Active when dephosphorylated, inactive when phosphorylated
42
Low energy - high AMP levels on AMP
phosphorylates it through AMP activated kinase and inactivates it
43
Glucagon impact on HMGR
inhibits enzyme by preventing dephosphoylattion
44
Insulin impact on HMGR
activates HMGR phosphatase and promotes dephosphoylation
45
AMP kinase
puts phosphate on HMGR to inactivate it
46
HMGR phosphatase
takes phosphate off HMGR to activate it
47
Promoter for transcriptional Control of HMG
sterol regulatory element SRE
48
sterol regulatory element binding protein (SREBP)
sequence that binds trascription factors
49
What does SREBP interact with
SREBP cleave activating protein
50
What does SREBP-SCAP complex bind to?
INSIG
51
When does SREBP-SCAP complex bind to INSIG
in the presence of cholesterol
52
Is transcription slow or fast when cholesterol is present and binding to the SREBP-SCAP complex
slow
53
What promotes release of SREBP-SCAP complex from ER
low sterol
54
What binds to SRE to promote transcription of HMG CoA reductase
mature form of SREBP
55
What reduces translastion of HMG
vitamin E family (gamma-tocotrienol) and oxylanosterols
56
What happens to HMG when there is more cholesterol?
degrade HMG CoA reductase
57
Role of liver and cholesterol
cholesterol metabolism and homeostasis
58
Where does cholesterol biosynthesis occur?
liver
59
What does liver do to cholesterol
package it into VLDL, release it into blood, metabolize to LDL by peripherial tissues
60
How is dietary cholesterol delivered to the liver
chylomicron remnants
61
Inhibitors of HMG CoA Reductase
statins because they are competitive inhibitors - citrus juices - grapefruit juice
62
Function of cytochrome P450
convert linear isoprenoid squalene into cholesterol
63
What happens if you inhibit cytochrome P450
increase in statin levels leaving to toxic effects
64
Function of agents that induce cytochrome P450
decrease levels of statin in plasma
65
What is the precursor of bile acids and bile salts
hepatic cholesterol
66
Characteristics of strong detergents
amphipathic with polar and nonpolar regions
67
Where is bile made
hepatocytes
68
Where is bile stored and concentrated
gallbladder
69
What is bile made of
bile acids, cholesterol, phosphoipids, fatty acids, proteins, bile pigments, inorganic salts
70
Lipid emulsification
aids in lipid digestion, forming micelles to increase surface area of lipids
71
How is cholesterol is converted to bile salt
Cholesterol + Cytrochrome P450 --> 7a- hydroxycholesterol
72
2 fates of 7a-hydroxycholesterol
chenocholic acid and cholic acid
73
Difference between chenocholic acid and cholic acid
cholic acid the 2nd hydroxyl group is added at 12th position and bile acids can be conjugated
74
Taurocholic acid
taurine is added to replace CoA, lower pKa makes them efficient in surfactant ability
75
Glycocholic acid
glycine added to replace CoA
76
Difference between cholesterol and bile salt
to make a bile salt, remove H from carboxylic acid of cholesterol
77
Micelle
surrounded by bile salt and has hydrophobic and hydrophilic areas so we can digest certain things
78
Gallstones
bile supersaturated with cholesterol
79
Cholelithiasis
insufficient secretion of bile salts or phospholipds or excess cholesterol secretion
80
Chronic disturbance in bile salt metabolism
steatorrhea and deficiency in fat soluble vitamins

GI System Final I (7 decks)

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