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GI Final > Liver Biochemistry > Flashcards

Liver Biochemistry Flashcards

(52 cards)

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1
Q

What are pit cells of the liver?

A

They are natural killer cells that protects the liver against virus and tumor cells.

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2
Q

What are the functions of the liver?

A
  1. receiving, distribution and recycling center of the body
  2. lipid biosynthesis and management (TG, phospholipids, steroids)
  3. Protein biosyntehsis - albumin, IgG
  4. Nitrogen metabolism - Urea cycle
  5. Waste management - Xenobiotic reaction (compounds with no nutritional value)
  6. Bilirubin metabolism
  7. Fuel management
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3
Q

The liver has no basement membrane between endothelial cells and hepatocytes, has gaps and fenestrations between endothelial cells, and low portal blood pressure. What is the purpose of these structural features?

A

They allow greater access and increased contact between liver and blood.

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4
Q

Describe the features of the organelles found in a hepatocytes.

A
  1. Well developed plasma membrane with endocytic and exocytic system.
  2. Well developped ER (smooth and rough)
  3. hepatocytes are metabolically active
  4. Numerous mitochondria
  5. Numerous lysosomes
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5
Q

What is the building block for the synthesis of isoprenoids, including steroids and lipid soluble vitamins?

A

Isopentenyl pyrophosphate (IPP) which are made up of three acetyl CoA.

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6
Q

name some sources of Acetyl CoA?

A
  1. Oxidative decarboxylation of pyruvate
  2. beta oxidation of fatty acids
  3. breakdown of amino acids
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7
Q

How do Acetyl CoA go from the mt to the cytoplasm?

A

Via citrate shuttle.

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8
Q

What is the backbone structure of most steroids?

A

A sterane ring

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9
Q

It requires six units of IPP to form a tetracyclic _ which is the backbone of most steroids.

A

Isopentyenyl pyrophosphate (IPP)

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10
Q

You are given a sterane ring and you’re asked to add side chains and groups to make an cholesterol. What side chains and groups would you add and where to turn the sterane ring into a cholesterol?

A

Sterene rings comes with 17C. you would add the following:

  1. two methyl groups at C10 and C14
  2. One OH- group at C3
  3. One double bond between C5 and C6
  4. A side chain of 8C at C17.
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11
Q

Cholesterol is a component of plasma membrane. What other compounds are cholesterol a precursor of?

A
  1. Bile acids and bile salts
  2. Vitamin D
  3. Steroid hormones (progesterone, aldosterone, cortisol, testosoterone, and estradiol)
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12
Q

A weight lifter takes in 500 mg of cholesterol daily. Is he above or below the daily recommended intake?

A

Above. Daily recommended intake is less than 300 mg.

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13
Q

If you’re on a cholesterol free diet, would your body be able to produce the bile salts, vitamin D, and other steroid hormones that the body needs to make?

A

Yes. The body produces about 1g of cholesterol daily.

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14
Q

In order to make a cholesterol molecule, how many Acetyl CoA, ATP, NADPH, H+ and O2 are needed?

A 
18 AcetylCoA
18 ATP
16 NADPH
16 H+
4 O2
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15
Q

Write out the chemical formula of cholesterol synthesis.

A

18 AcetylCoA + 18 ATP + 16 NADPH + 16 H+ + 4O2 –>

1 Cholesterol + 16 NADP+ + 18ADP + 18 Pi

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16
Q

Cholesterol Synthesis is done in two phases. What is each phase responsible for?

A

Phaes I is responsible for mkaing thte backbone for the strene ring isopentyenyl pyrophosphate (IPP)
Phase II is involved in all the cyclization and making the tetracyclic strene ring and adding all the hydrocarbon chains.

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17
Q

Cholesterol synthesis starts off with 2 Acetyl CoA coming together to make Acetoacetyl CoA and then a third acetyl Coa comes in to make what intermediate?

A

hydroxymethylgluterol CoA (HMG COA)

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18
Q

List the intermediates starting at acetyl CoA in making cholesterol.

A

Acetyl CoA –> Acetoacetyl CoA –> HMG CoA –> mevalonate –> IPP –> Squalene –> Lanosterol –> Cholesterol.

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19
Q

What is the rate limiting step in cholesterol biosynthesis and is the enzyme that is involved?

A

Rate limiting step is going from HMG COA to Mevalonate. The enzyme is HMG reductase.

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20
Q

What are some positive mediators that will push HMG CoA to proceed to Mevalonate?

A
  1. Insulin

2. Thyroxine

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21
Q

What are some inhibitors of HMG CoA reductase?

Study These Flashcards
A
  1. Glucagon
  2. sterols,
  3. High conc of AMP
  4. Vit E, Statin
22
Q

in the choleterol synthesis pathway, which intermediate is the first cyclic molecule?

23
Q

Azoles, micronazole, KCN, tamoxifen, morpholine, triparenol are all inhibits of which intermediate step in cholesterol biosynthesis?

Study These Flashcards
A

Going from lanosterol to Cholesterol.

24
Q

Patients who are on long-term statin use experience myotoxic effects where the muscles starts to degenerate. What is the cause of the myotoxic effects?

Study These Flashcards
A

ubiquonone and hemeA are side products of cholesterol biosynthesis. Patients who are on statin to reduce their cholesterol level, will not be making cholesterol and thus will also not be able to make ubiquinone and Heme A (cytochromes) which will interfere with the TCA cycle involved in generating ATP.

25
After cholesterol is synthesized where does the cholesterol go next?
it is packaged into VLDL and released into the circulation and goes to different parts of the body namely: 1. All tissues = cholesterol incorporated into cellular membrens 2. Liver: cholesterol used to synthesize bile acids 3. Adrenal glands, ovaries, testes: synthesize steroid hormones Skin: synthesize vitamin D
26
what are lipid rafts and what physiological purpose does it serve?
It's cholesterol, sphingolipids, and gangliosides enriched microdomains see on the plasma membrane. It's detergent insolubale and have low buoyant density. it's the local centers for signal transduction processes.
27
Lipid rafts may have clinical significance in patients with AD and PD, how?
Lipid rafts serves as sites for abnormal processing of proteins in neurodengeneratve disorders like AD and PD. It was found that beta amyloids are generated on the surface of lipid rafts.
28
What is the main target of the cholesterol biosynthesis pathway for regulating cholesterol synthesis?
HMG CoA reductase.
29
HMG CoA reductase can be regulated via multiple mechanism, what are they?
1. direct inhibition 2. covalent modification 3. transcriptional control 4. translational control 5. post-translational control - protein turnover
30
In direct inhibition of HMG CoA reductase in regulating cholesterol biosynthesis, what compound is clinically used?
statin, which is an analog of the enzyme and is a competitive inhibitor.
31
besides statin what other compounds can directly inhibit HMG CoA reductase?
Free fatty acids, bile acids, and oxysterols.
32
Is HMG CoA reductase active or indactive when it is dephosphorylated?
It is active when dephosphorylated and inactive when phosphorylated
33
During low energy, AMP levels are high which simulates AMP-activated kinase (AMPK). What does AMPK do to HMG CoA reductase?
it phosphorylates it and thus inactivates it
34
What effects does glucagon and insulin have HMG CoA reductase?
Glucogon inhibits AMPK and thus prevents dephosphorylation of HMG CoA, and thus HMG CoA reductase is inactivated and cholesterol synthesis is inhibited. Insulin has the opposite effect. Insulin activates AMPK and thus promotes dephosphorylation of HMG CoA and thus is active and cholesterol synthesis is able to proceed.
35
Explain how HMGR gene transcription is regulated?
Steroid regulatory element binding protein (SREBP) are usually present on ER membrane and is boudn to SCREBP-cleaage activating protein (SCAP). During high levels of cholesterol, SREBP is retained in ER membrane via binging to SCAP to INSIG. and thus transcription is halt. During low cholesterol, SREBP-SCAP is NOT bound to INSIG (INSIG is what keeps the complex bound to the ER membrane) and thus SCREBP-SCAP complex is able to go into the cytoplasm and there it undergoes proteolysis and a DNA binding elelment is released and it translocates to the nucleus and binds to the SRE promoter region and upregulates HMGR. this also upregulates production of LDL receptors so that newly made cholesterol can be taken up by cells.
36
During translationa and Post-translational control of HMGR, what happens when there's cholesterol present?
In presence of cholesterol and/or oxysterols, HMG CoA interacts with INSIG which promotes polyubiquitination of HMG CoA reductase which leads to removal from ER and degradation by the 26S proteasome. Degradation is enhanced by sterols, methylated sterols, oxysterols, tocotrienol, mevalonate derivatives and bisphosphate SR-12813. All of these is like feedback inhibition.
37
In what organ of the body does cholesterol biosynthesis take place?
liver
38
Packaged in what form does dietary cholesterol come to the liver? Packaged in what form does newly synthesized cholesterol leave the liver?
Comes into the liver in chylomicrons remnants. | Leaves the liver in LDL.
39
What enzyme converts the linear isoprenoid squalene into lanosterol and then to cholesterol?
Cytochrome P450
40
How does CYP detoxify xenobiotics and pharmacological agents and help clear it from the body?
It works by making the compound more polar nd by adding OH group and then conjugating it which makes it into a safer metabolites suitable for excretion.
41
What is the consequence when drug agents interfere with cytochorme p450?
Agents that inhibit CYP will cause increase in statin levels leading to toxic side efects (myopathy and rhabdomyolysis) which are toxic for the kidney. You will see the effects of rhabdomyolysis in urine which will appear brownish in color.
42
What are some examples of CYP inhibitors?
itraconozole, clarithromysin, and cyclosporine, citrus juices, grapefruit juices
43
What are some examples of agents that induce CYP?
rafampicin, carbamazepine and St. Johns's wort which decrease levels of statin in plasma.
44
How does bile acids and bile salts aid in digesting fats?
It creates an lipid emulsifying mixture which aids in lipid digestion by forming micelles which increase surface area of lipids exposed to lipases.
45
What is the precursor for bile acids and bile salts?
Cholesterol
46
What chemical properties of bile acids and bile salts make it a good emulsifier?
they are strong detergents -- is amphipathic with polar and non polar regions.
47
What contents make up bile?
bile acids, cholesterol, phospholipids, fatty acids, proteins, bile pigments, and inoranic salts
48
In the bile synthesis, cholesterol is made into 7a-hyroxycholesterol via what enzyme?
7a-hydroxylase which requires CYP450
49
In the synthesis of bile, cholic acid is converted to cholyl CoA when then undergoes conjugation to produce products with lower pKa. How do these conjugates with lower pKa make bile better doing it's job?
lower pKa makes the molecule to act as a better surfactant and thus is able to increase surface area of lipids. More surface area means more areas that lipase can act on to break it down.
50
What is gallstones made up of?
made up of bile supersatruated with cholesterol.
51
What is cholelithiassis?
insufficient secretion of bile salts or phospholipids, OR excess cholesterol secretion.
52
What oral substance can be taken to dissolve small-medium sized gallstones and also to redue cholesterol seceretion into bile?
ursodeoxycholic acid.

GI Final (11 decks)

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