Metabolic Functions Of The Liver Flashcards

1
Q

Where is glucose stored and what is it stored as?

A

Liver

Glycogen

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2
Q

What is the conversion of glucose to glycogen stimulated by?

A

Insulin

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3
Q

Why would glycogen need to be degraded to glucose?

A

Exercise (skeletal muscle stores)

Fasting (liver stores)

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4
Q

Summarise glycogenolysis

A

Glycogen -> glucose

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5
Q

Describe the process of glycogenolysis

A
  1. One residue of glycogen is removed and converted → glucose-1-P by glycogen phosphorylase
  2. Glucose-1-P → Glucose-6-p by phosphoglucomutase
  3. Glucose-6-P → Glucose by glucose-6-phosphatase
  4. This glucose enters the bloodstream
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6
Q

Summarise glyconeogenesis

A

Amino acids / lactate / pyruvate / glycerol → glucose

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7
Q

What is gluconeogensis stimulated and inhibited by?

A

Stimulated - cortisol & glucagon

Inhibited - insulin

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8
Q

Summarise lipogenesis

A

Acetyl-CoA → Fatty acids

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9
Q

Where does lipogenesis take place?

A

cytoplasm of hepatocytes

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10
Q

What does lipogenesis require?

A

ATP

NADPH

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11
Q

What is lipogensis stimulated and inhibited by?

A

Stimulated - glucagon

Inhibited - adrenaline

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12
Q

Describe the process of lipogenesis

A
  1. Acetyl-CoA → Malonyl-CoA by acetyl carboxylase*
  2. Fatty acid synthase adds malonyl-CoA to a growing fatty acid
  3. Fatty acid linked to carrier protein
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13
Q

Describe the regulation of lipogenesis

A

Activated by citrate

Inhibited by AMP

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14
Q

Summarise lipolysis

A

Fatty acid → Acetyl-CoA

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15
Q

When does lipolysis occur?

A

Fasting / stress

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16
Q

By what process does lipolysis occur?

A

β-oxidation

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17
Q

What happens to the Acetyl-CoA after lipolysis?

A

Enters TCA cycle
or
Used to produce ketone bodies

18
Q

What is lipolysis stimulated and inhibited by?

A

Stimulated - glucagon & adrenaline

Inhibited - insulin

19
Q

Describe the process of lipolysis

A
  1. Long chains of fatty acids broken down → series of 2-carbon acetate units
  2. Acetate units combined with co-enzyme A → Acetyl-CoA
  3. Acetyl-CoA can be combined with oxaloacetate → citrate for the beginning of TCA cycle
20
Q

Summarise protein synthesis

A

Amino acids → Protein

21
Q

What is protein synthesis stimulated by?

A

Insulin and GH

22
Q

Which proteins are synthesised in the liver?

A

Albumin
Blood clotting factors
Angiotensinogen

23
Q

Which blood clotting factors produced in the liver are Vitamin K dependent?

A

2, 7, 9, 10

24
Q

Summarise transamination

A

Amino group of amino acids transferred to ketoacids

25
Q

Describe the process of transamination

A

Either:

  • Amino group added to alpha-ketoglutarate → glutamate by aminotransferase

or

  • Amino group added to oxaloacetate → aspartate by aspartate aminotransferase
26
Q

Summarise deamination

A

Amino group removed → ketoacid + ammonia

27
Q

Describe the process of deamination

A
  1. Amino group removed from amino acid → ketoacid + ammonia by glutaminase
  2. Ammonia → ammonium ion
    1. Must be removed due to toxicity by:
      • glutamine
      or
      • urea cycle
28
Q

Why is ammonia toxic to cells:

A
  • Reduces TCA cycle activity
  • Affects neurotransmitter synthesis
  • Creates an alkaline pH
29
Q

Describe the process of detoxification of ammonia

A
  1. Ammonia is used to synthesise glutamine when combined with glutamate
  2. Glutamine is used to synthesise nitrogen compounds
  3. Ammonia transported to kidney:
    • Directly excreted
    or
    • Transported to liver to make urea
30
Q

what is the enzyme involved in lipolysis?

A

triglyceride lipase

31
Q

what happens to the products of lipolysis?

A
  • fatty acids -> mitochondria for beta-oxidation

- glycerol -> hepatocytes -> glycerol-3-phosphate -> glycolysis

32
Q

describe the process of ketogenesis

A

2-Acetyl-CoA
Acetoacetyl CoA (+ Acetyl-CoA) - thiolase
HMG-CoA - HMG-CoA synthase
Acetoacetate (+ Acetyl-CoA) - HMG-CoA lyase
beta-hydroxybutyrate + Acetone

33
Q

how does Acyl-CoA enter the mitochondria for beta-oxidation?

A

<12 carbons: diffusion

>12 carbons: carnitine shuffle

34
Q

what is the purpose of ketogenesis?

A

uses excess acetyl-CoA

exceeding capacity of Krebs’ cycle

35
Q

what is ketogenesis activated by?

A
  • low G-3-P
  • low ATP demands
  • high glucagon
36
Q

what is ketogenesis inhibited by?

A

high insulin

37
Q

why do heart and skeletal muscle preferentially utilise ketone bodies for energy?

A

preserve glucose for the brain

38
Q

what is ketosis?

A

build-up of ketone bodies in the blood

39
Q

what can cause ketosis?

A
  • diabetic ketoacidosis
  • alcoholic ketoacidosis
  • starvation
40
Q

describe the pathophysiology of diabetic ketoacidosis

A
  1. lack of insulin -> glucose not taken up by cells -> cannot be used for glucogenesis/glycolysis
  2. beta-oxidation stimulated for energy
  3. high acetyl-coA -> ketones -> ketosis -> acidosis
41
Q

what are symptoms of ketoacidosis?

A
  • hyperventilation

- vomiting

42
Q

how does ketoacidosis affect the blood?

A
  • excessive ketones lower pH of blood

- impairs ability of haemoglobin to bind oxygen