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Gastrointestinal Biology > GB 16. Liver Biosynthetic Functions > Flashcards

GB 16. Liver Biosynthetic Functions Flashcards

1
Q

What are the 3 main functions of the liver? (just list them)

A

[1] Metabolism

[2] Synthesis

[3] Excretion + Detoxification

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2
Q

What is involved with the Metabolism function of the liver?

A
  • glycogen synthesis (glycogenesis)
  • glycogen breakdown (glycogenolysis)
  • gluconeogenesis
  • fatty acid metabolism

metabolizes:
[1] Carbohydrates
[2] Fats
[3] Protein

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3
Q

What is involved with the Synthesis function of the liver?

A
  • plasma proteins (including albumin)
  • coagulation factors
  • haem
  • lipoproteins
  • bile acids (primary)
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4
Q

What is involved with the Excretion + Detoxification function of the liver?

A
  • bilirubin
  • amino acids + NH3 (urea cycle)
  • cholesterol and steroid hormones
  • drugs
  • toxins
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5
Q

What are the 3 “zones” in the liver?

A

Zone 1: Periportal Zone

  • O2 rich
  • has the portal tract, hepatic artery, bile duct + portal vein

Zone 2:
- space between Periportal and Perivenous zones

Zone 3: Perivenous Zone
- has the central hepatic vein

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6
Q

In which direction does the blood flow in the zones of the liver?

A
  • it flows from the Periportal Zone to the Perivenous Zone

- from Zone 1 to Zone 3

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7
Q

What is ammonia detoxification? Why is it important?

A
  • ammonia (NH3) is toxic to the CNS
  • it is converted to urea in the liver (through the urea cycle)
  • NH3 is also used to convert glutamate to glutamine in the liver
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8
Q

What is the overall mechanism of carbohydrate metabolism in the liver? What are the important pathways?

A

GOAL: maintain blood glucose

[1] Glycogenesis
- excess glucose after meal is taken up by liver and stored as glycogen

[2] Glycogenolysis

  • glycogen broken down + glucose then exported into blood to go to tissues
  • when low blood glucose levels arise

[3] Gluconeogenesis
- glucose synthesized from amino acids + non-hexose carbohydrates when glycogen reserves depleted

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9
Q

Explain the process of fat metabolism in the liver.

A
  • hydrolysis of triglycerides releases 2 products:
    (A) Glycerol
  • metabolized by glycolytic pathway

(B) Fatty Acids

  • beta oxidized to acetoacetate (AcAc)
  • AcAc then used as an energy source in remote tissues
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10
Q

Explain how proteins are metabolized in the liver (hint: there are 2 processes involved)

A

[1] deamination + transamination of amino acids
- conversion of non-nitrogenous part to glucose/lipid
(glucogenic or ketogenic amino acids)

[2] removal of ammonia from body by synthesis of urea

  • ammonia is produced from leftover amino acids
  • it is toxic to the CNS
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11
Q

What are some of the proteins (and protein components) that are synthesized in the liver?

A

[1] non-essential amino acids (e.g. glutamine)
[2] plasma proteins (e.g. albumin - contributes to oncotic pressure)
[3] clotting factors
[4] acute phase proteins

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12
Q

What are some of the fats that are synthesized in the liver?

A

[1] Triglycerides
- liver converts excess carbs + proteins into fatty acids and triglycerides (exported + stored in adipose tissue)

[2] Cholesterol + Phospholipids

  • some packaged with lipoproteins and made available to rest of body
  • remainder excreted in bile as cholesterol or as bile acids

[3] Lipoproteins

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13
Q

What are some other molecules/things that are synthesized in the liver?

A 
[1] Ketones
- beta-hydroxybutarate and acetoacetate 
- ^^ 2 types of ketones 
[2] Haem
[3] Bile Acids
[4] Urea
[5] Nucleotide Precursors
- e.g. purines + pyrimidines
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14
Q

List all the molecules/things that can be synthesized in the liver.

A 
[1] Proteins/Protein Components
[2] Carbohydrates
[3] Fats
[4] Ketones
[5] Haem
[6] Bile Acids
[7] Urea
[8] Nucleotide Precursors
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15
Q

What are the 2 categories of proteins that are synthesized by the liver?

A

[1] Liver-Tissue Proteins

  • structural proteins
  • enzymes

[2] Exported Proteins

  • plasma proteins
  • albumin
  • alpha and beta globulins
  • fibrinogen
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16
Q

Where is the plasma protein, Albumin, synthesized?

A

ONLY in hepatic cells

  • approx. 15 g/d in healthy adult
  • althought rate varies with physiologic stress
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17
Q

What is the function of albumin?

A
  • transports many substances (e.g. bilirubin, fatty acids, metals, ions, hormoes, exogenous drugs…)
  • provides 75-80% of the ONCOTIC PRESSURE
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18
Q

What is Oncotic Pressure?

A

the pressure driving fluid into the vessel due to the presence of plasma proteins INSIDE the vessel
- it forces the vessels closed

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19
Q

What is the opposite of oncotic pressure?

A

Hydrostatic Pressure/Blood Pressure

  • it keeps the vessel open
  • blood pressure pushing the walls outwards
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20
Q

In oedema, where is there a higher concentration of albumin? Inside or outside the blood vessels?

A

Outside the blood vessels

- drawing water into the tissues

21
Q

What are alpha- and beta- globulins?

A

they are plasma proteins!

22
Q

What is the structure of alpha- and beta- globulins?

A

glycoproteins

23
Q

How are alpha- and beta- globulins cleared from the cell?

A

cleared by ASIALOGLYCOPROTEIN receptors on the surface of hepatocytes

24
Q

What are some of the functions of alpha- and beta- globulins?

A
  • transport proteins
  • protease inhibitors
  • clotting factors
25
Q

If there is decreased alpha- and beta- globulins in the plasma what may this be indicative of?

A
  • genetic disorders (alpha1-antitrypsin deficiency)

- malnutrition

26
Q

If there is increased alpha- and beta- globulins in the plasma what may this be indicative of?

A
  • acute phase reactants. post-inflammatory or traumatic conditions
  • retention of high MW proteins following compensatory increased synthesis (alpha2-macroglobulin)
27
Q

What are porphyrins?

A

a group of organic compounds which include haem

28
Q

What is the chemical structure of haem?

A

a ferrous ion (Fe) is chelated in the centre of a porphyrin ring (heterocyclic organic ring)

Ferrous Ion is OXYGENATED, not oxidised! (Fe2+)

29
Q

What are some of the functions of haemoproteins?

A
  • oxygen transport
  • catalysis
  • electron transfer
30
Q

What haemoprotein is synthesized in the bone marrow?

A

Haemoglobin

31
Q

What haemoprotein is synthesized in the muscle?

A

Myoglobin

32
Q

What haemoprotein is synthesized in the liver?

A

[1] Cytochrome P450 Proteins

[2] Catalase

33
Q

What is the rate-limiting step in the synthesis of haem in the liver?

A

ALA Synthase

  • first enzyme in haem synthesis
  • rate-limiting step
  • converts succinyl coA + Glycine TO ALA
34
Q

What is the enzyme ALA synthase, which is used in the synthesis of haem, inhibited by?

A

inhibited by FREE, NON-PROTEIN BOUND HAEM by negative feedback

35
Q

What is the half life of ALA synthase?

A

only 1 to 3 hours

36
Q

Describe how haem and globin synthesis is physiologically regulated.

A
  • haem inhibits activity of ALA-synthase
  • haem diminishes transport of ALA-synthase from cytoplasm to mitochondria after it is made
  • haem represses the production of ALA-synthase by regulating gene transcription
  • haem stimulates globin synthesis to make sure that free haem remains low
37
Q

What is important in balancing haemoglobin production?

A
  • inhibiting ALA-synthase

- stimulating globin synthesis

38
Q

What does ALA Dehydratase do? Where is it located?

A
  • part of the synthesis of haem
  • second enzyme involved
  • cytoplasmic enzyme
  • converts 2x ALAL molecules to Porphobilinogen (PBG)
39
Q

What structural component does ALA Dehydratase contain? What may this lead to?

A
  • it contains suphydryl groups
  • it is sensitive to inhibition by lead (Pb2+) and other heavy metals
  • – this results in high ALA synthase enzyme and symptoms of lead poisoning
40
Q

What are the 3 important enzymes associated with the synthesis of haem in the liver?

A

[1] ALA Synthase
[2] ALA Dehydratase
[3] Uroprophyrinogen Synthase I (Hyroxymethybilane Synthase/PBG Deaminase) + UP-Cosynthase

41
Q

What is the overall steps in the formation of haem?

A

[1] decarboxylation of acetate + propionate side groups to methyl + vinyl groups
[2] transfer into mitochondria
[3] chelation of iron

42
Q

What is Porphyrias?

A

a group of metabolic disorders caused by partial defects in one of the haem biosynthetic enzymes
- leads to an overall reduction in haem synthesis

43
Q

What happens in porphyrias?

A
  • low haem synthesis
  • accumulation of toxic intermediate products!!
  • less haem means increased production to try and increase haem (positive feedback - leads to more toxic intermediates)
  • can be photosensitive or non-photosensitive
44
Q

What happens if there is a complete deficiency in haem?

A
  • it would be fatal

- no oxygen

45
Q

What is Acute Intermittent Porphyria (AIP)? What are the clinical manifestions due to?

A
  • defect in uroporphyrinogen synthase I (hydroxymethylbilane synthase/PBG deaminase)
  • – 50% reduction in enzyme activity
  • – 90% with genetic trait never present :(
  • haem synthetic pathway terminated early
  • accumulation of ALA + PBG (clinical manifestations)
46
Q

What are the acute attacks of Acute Intermittent Porphyria (AIP) precipitated by?

A
  • induction of haem protein cytochrome P450 synthesis

- – slide 39

47
Q

What is the treatment of Acute Intermiitent Porphyria (AIP)?

A

HAEMATIN - derived from haem (haem hydroxide) or Haemin

- it represses ALA synthase

48
Q

What is the cause and features of Porphyria Cutanea Tarda (PCT)?

A

Cause:
- deficiency in uroporphyrinogen decarboxylase

Features:

  • itching
  • erythema
  • blistering
49
Q

What is the consequences of Porphyria Cutanea Tarda (PCT)?

A
  • acccumulation of porphyrins
  • accumulation of porphyrinogens (non-enzymatically converted to porphyrin)

note: photo-excited by sunlight, causing cellular damage

Gastrointestinal Biology (15 decks)

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