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GI Exam 2 > Liver Biochemistry > Flashcards

Liver Biochemistry Flashcards

1
Q
  • Structure of the liver
A
  • Largest solid organ in the body
  • 1500 g
  • 2 lobes divided into multiple lobes and sinusoids
  • Blood supply: 75% from portal vein, 25% from hepatic artery
  • Biliary components of bile duct and gallbladder
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2
Q
  • Liver cell types and their functions
A
  • Hepatocytes:
    • ​Metabolic functions of liver
    • Capable of regeneration
    • Ribosomes, ER, enzymes
  • Endothelial Cells:
    • ​Exchange of material from liver to blood and vice versa
    • Fenestrations in plasma membrane allows for exchange
  • Kupffer cells
    • ​Macrophages of liver
    • Protect from microbes, remove damaged RBCs, secrete cytokines
    • Lots of lysosomes
  • Hepatic stellate cells
    • ​Storage site for Vitamin A and other lipids
  • Pit Cells
    • ​NK cells
    • Protect livert against viruses and tumor cells
  • Cholangiocytes
    • ​Line bile duct
    • Control bile flow rate and pH
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3
Q
  • Functions of the liver in lipid and carbohydrate metabolism
A
  • Carbohydrate metabolism
    • Glycolysis
    • Glycogenolysis and Glycogenesis
    • Gluconeogenesis (exclusive to liver)
  • Lipid metabolism
    • Biosynthesis of TAGs, phospholipids, steroids (Steroids, cholesterol, bile acids and bile salts), lipoproteins
    • Degradation of TAG and plasma lipoproteins
    • Regulation of FFA metabolism
    • Breakdown of FFA via beta oxidation
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4
Q
  • Waste management functions of liver
A
  • Inactivation
  • Detoxification
  • BIotransformation of metabolites and xenobiotics
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5
Q
  • Structural adaptations of the liver
A
  • Unique circulation:
    • Receives blood from enteric circulation and from periphery
    • Low portal blood pressure (3-5 mm Hg)
  • Structural features:
    • Fenestrations in endothelial membrane allow for greater access and increased contact between liver and blood
    • Lack of basement membrane and absence of tight junctions between hepatocytes and endothelial cells
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6
Q
  • Three acetyl coA molecules combine to generate one _ (5 carbon compound)
  • This molecule serves as a building block for synthesis of isoprenoids
  • Isoprenoids include:
    • ​Steroids
    • Lipid Soluble Vitamins (A,D,E,K)
    • Prenyl groups that attach to plasma membrane
A
  • Isopentenyl phosphate (IPP)
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7
Q
  • Sources of acetyl coA
A
  • Generated in mitochondria from:
    • Oxidative decarboxylation of pyruvate
    • Beta oxidation of fatty acids
    • Breakdown of amino acids
  • Transported into cytoplasm via citrate shuttle
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8
Q
  • Six units of IPP combine to form _ which serves as the backbone for most steroids
A

Tetracyclic stearene ring

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9
Q
  • Structural features of cholesterol
A
  • Allicyclic compound-made of stearene ring
  • Has OH on C3
  • Cyclic part consists of stearene ring
  • Alliphilic part consists of hydrocarbon chain
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10
Q
  • Functions of cholesterol
  • How much is made per day
  • What is unique about the biosynthesis of cholesterol
A
  • Component of plasma membranes
  • Precursor for:
    • Bile acids and bile salts
    • Vitamin D
    • Steroid hormones
  • Daily production: 0.7-1.0 g (most in liver)
  • Biosynthesis is inversely proportional to dietary intake
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11
Q
  • What is phase I of cholesterol synthesis?
  • What is phase II of cholesterol synthesis ?
  • What is the rate limiting step in cholesterol synthesis and which phase does it occur in?
A
  • Converting Acetyl CoA into IPP
  • Making IPP into cholesterol
  • Conversion of HMG CoA to Mevalonate via HMG CoA reductase
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12
Q
  • Antifungal drugs/Azoles target which part of cholesterol synthesis?
A
  • Last step of cholesterol synthesis converting lanosterol to cholesterol
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13
Q
  • Key features of HMG CoA reductase
A
  • 8 pass TM ER protein with catalytic domain
  • Target of statin drugs that inhibit cholesterol synthesis
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14
Q
  • Statins
A
  • Competitive inhibitors of HMG CoA reductase
  • Ki is ten times stronger than Km for HMG CoA Reductase
  • Also increases SREBP maturation and transcription of LDL receptor and enhanced clearance of cholesterol via LDL receptor mediated endocytosis
  • Mytotoxic side effects-statin-mediated myopathy caused by depletion of muscle levels of ubiquinone (coQ10) and resultant impairment of mitochondrial function
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15
Q
  • Fate of cholesterol
A
  • Packaged into VLDL and transported into the blood
  • Goes to various areas:
  • In liver:
    • Used to synthesize bile acids
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16
Q
  • Regulation of cholesterol synthesis
A
  • via regulation of HMG CoA Reductase
    • Direct inhibition
      • Free fatty acids, bile acids and oxysterols and statins
    • Covalent modification
      • ​Inactive in phosphorylated form acitve in dephosphorylated form
    • Transcriptional control
      • ​Binding of transcriptional factors to promotor on HMG CoA reductase gene increases its mRNA levels
    • Translational control
      • ​Protein synthesis level
      • Reduced by gamma-tocrotrienol (Vitamin E family) and oxylanosterols
    • Post-Translational Control
      • ​Protein turnover/degradation
      • Enhanced by sterols, oxysterols and gamma tocotrienol
17
Q
  • Mechanism of transcriptional control
A
  • Inactive form of SREBP interacts with SREBP Cleavage protein (SCAP)
  • In presence of cholesterol, SREBP-SCAP complex is retained in the ER d/t binding of INSIG
  • Transcription of HMG CoA reductase is low in this case

Low sterol:

  • Promotes release of SREBP-SCAP from ER to Golgi
  • SREBP undergoes proteolysis to release mature form that dimerizes and translocates to the nucleus
  • Mature SREBP binds SRE and promotes transcription of HMG CoA reductase and other enzymes in the cholesterol synthesis pathway
18
Q
  • Late stage inhibitors of cholesterol synthesis
A
  • Antimycotics-inhibit formation of ergosterol (needed to maintin the plasma membrane of fungal cells)

At high concentrations, inhibit enzyme that converts lanosterol to cholesterol

GI Exam 2 (14 decks)

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