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GI Final Exam > Liver Biochemistry > Flashcards

Liver Biochemistry Flashcards

1
Q

What supplies most of the blood to the liver?

A

protal vein

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2
Q

What do hepatic stellate cells do?

A

store lipids and vitamin A

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3
Q

What are some functions of the liver?

A
  • recycling center
  • lipid biosynth and management
  • make Albumin and IgG
  • N metabolism , Urea cycle
  • waste management: seonobiotic reactions
  • bilirubin metabolism
  • fuel management
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4
Q

What characteristics of the liver allow for greater access and increased contact b.w theliver and blood?

A
  • no basement membrane between endothelial cells and hepatocytes
  • gaps b/w endothelial cells
  • fenestrations in endothelial cells
  • low portal blood pressure
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5
Q

What are hepatocytes like?

A

well developed pasma membrane and ER, lots of mitochondria, lots of lysosomes

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6
Q

What is the building block of all isoprenoids and what is used to make it?

A

IPP

-3 acetyl coA’s go into it

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7
Q

What are some sources of Acetyl CoA?

A

generated in mitochondria from:

  • oxidative decarboxylation of pyruvate
  • B ox of fatty acids
  • breakdown of aa’s
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8
Q

how is Acetyl CoA transported into the cytoplasm?

A

via citrate shuttle

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9
Q

What is the backbone of most steroid?

A

the tetracyclic sterane ring

-made up of six IPP’s

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10
Q

What is one important characteristic about the structure of cholesterol?

A

the OH group at C3

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11
Q

What does cholesterol make?

A

Bile acids and salts
Vit D
Steroid hormones

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12
Q

How many ATP go into making one Cholesterol?

A

18

that’s a lot of energy

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13
Q

What are the 2 phases of Cholesterol synthesis?

A
  • Generation of IPP from Acetyl CoA

- Generation of cholesterol from IPP

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14
Q

What does HMG CoA synthase do?

A

Acetoacetyl CoA —> HMG CoA

*uses an Acetyl CoA here

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15
Q

What do HMG CoA reductase do?

A

HMG CoA—–> Mevalonate

*uses 2 NADPH’s… and a CoA pops off in this step

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16
Q

What is the rate limiting step?

A

The one involving HMG CoA reductase

- HMG CoA—–> Mevalonate

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17
Q

What enhances the rate limiting step of cholesterol synthesis?

A

Insulin and thyroxine

18
Q

What inhibits the rate limiting step?

A

Glucagon, sterols, high AMP, Vit E, and Statins

19
Q

What are some compounds derived from intermediates in cholesterol synthesis?

A

Quinol from ubiquinone

Heme A

20
Q

List the intermediates in order in cholesterol synthesis.

A

Acetyl CoA, Acetoacetyl CoA, HMG CoA, Mevalonate, IPP, Squalene, Lanosterol, cholesterol

21
Q

What happens to cholesterol after it is made?

A

gets packaged into VLDL and released into circulation

22
Q

How is Cholesterol cynthesis mainly regulated?

A

HMG CoA reductase

  • the rate limiting enzyme
  • can happen by direct inhibition, covalent mod, transcriptional control, translational control, or post-translational control- protein turnover
23
Q

How does direct inhibition go?

A
  • HMG CoA reductase inihibited by Free FA’s , buile acids, and oxysterols
  • also inibited by statins
24
Q

What are statins,

A

competitive inihibitors of HMG CoA reductase

  • compete w. HMG coA for binding to active site
  • statin lacks the Methyl group*
  • these are cholesterol lowering drugs
  • bind more tightly to the active site
25
Q

How does covalent modification go?

A

HMG CoA reductase is active when DEPHOSPHORYLATED

-inactive when P’ed

26
Q

What marks a low energy condition?

A

High AMP levels (result of low ATP)

-this stimulates AMPK which P’s and inactivates HMG CoA reductase

27
Q

How does glucago inhibit HMG CoA reductase?

A

by preventing deP

-insulin just does the exact opposite

28
Q

How does transcriptional control work?

A

HMG CoA reductase has a sterol regulatory element (SRE) in its promoter

  • that binds SREBP proteins
  • SCAP cleaves inactive SREBP to make it active
  • if we already have cholesterol or oxysterols, SREBP-SCAP is kept in the ER due to binding to INSIG
  • That slows transcription (makes sense)
29
Q

What happens with the transcriptional control when we have low sterol conditions?

A
  • SREBP-SCAP gets released from ER to Golgi
  • SREBP gets cut… now it’s mature
  • it dimerizes and goes to nucleus
  • binds to SRE and promotes transcription of HMG CoA reductase and others (like LDL receptor :D)
30
Q

How does translational and post-translational control work?

A
  • translation reduced by gamma-tocotrienol and oxylanosterols
  • in presence of cholesterol, HMG CoA interacts with INSIG
  • then, it gets ub’ed and degraded
  • things with “ol” at the end of them enhance this
31
Q

Describe cholesterol homeostasis.

A

liver packages it into VLDL, released into blood, metabolized into LDL by peripheral tissues

  • Liver is major source of HDL’s, help to clear lipoptns from blood
  • synthesizes bile acids and elminiates cholesterol into bile
32
Q

What is the main side effect with a statin?

A

myotoxic

-decreased formation of ubiquinone and prenylated proteins

33
Q

What is the significance of Cytochrome P450 (CYP)

A

these enzymes convert squalene into cholesterol

-also detoxify xenobiotic and pharmacological agents (statins!)

34
Q

What happens if we inhibit CYP?

A

statin levels will rise (and vice versa)

-leads to toxic side effects

35
Q

Can any enzyme degrade the sterane ring of cholesterol?

A

No

36
Q

When making bile acids, what is the first thing that cholesterol is converted to?

A

7-alpha-hyroxycholesterol

37
Q

What 2 things do we end with in bile synthesis?

A

Chenocholic acid and cholic acid

38
Q

What happens after we make cholic and chenocolic acid?

A

we either add taurine to make taruocholic acid or glycine to make glycocholic acid (just add cheno in there if other one)

39
Q

What do bile salts get inserted into after they’re made?

A

mixed micelles

40
Q

What are gallstones?

A

crystals made up of bile supersaturated with cholesterol

41
Q

What is cholelithiasis?

A

insufficient secretion of bile salts or phopholipids or excess cholesterol secretion

42
Q

What is used to dissolve small-medium sized stones?

A

oral administration of ursodeoxycholic acid

-it reduces cholesterol secretion into bile

GI Final Exam (10 decks)

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