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Sem 4, case 5 (hepatitis) > The normal liver - metabolism (lecture series) > Flashcards

The normal liver - metabolism (lecture series) Flashcards

1
Q

What are the main functions of the liver ?

A
  • controls metabolism of fats, proteins, carbs
  • produces bile
  • produces cholesterol + bilirubin
  • produces proteins (albumin + clotting factors)
  • filters blood
  • destroys old RBCs
  • stores glycogen, vitamins, minerals
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2
Q

Where does the liver receive blood from ?

A
  • spleen
  • stomach
  • pancreas
  • duodenum
  • mesentery

pretty much whole GI tract except rectum

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3
Q

Which vessel transports blood from the GI tract into the liver ?

A

the portal vein

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4
Q

Which hormones does the liver primarily respond to ?

A
  • glucagon
  • insulin
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5
Q

What are the key metabolic roles of the liver when the body is in a fasting state ?

A
  • glycogenolysis
  • gluconeogenesis
  • ketogenesis
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6
Q

What is glycogenolysis ?

A

Breaking down stored glycogen to release glucose when body is in a fasting state

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7
Q

Which hormone promotes glycogenolysis?

A

glucagon

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8
Q

What is gluconeogenesis ?

A

Producing new glucose from scratch in the fasting state, using scraps of other nutrients

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9
Q

Which hormone promotes gluconeogenesis ?

A

glucagon

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10
Q

What is ketogenesis ?

A

producing emergency fuel (ketone bodies) using Acetyl-CoA in the fasting state

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11
Q

What triggers ketogenesis ?

A

prolonged fasting causes breakdown of fatty acids from adipose tissue

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12
Q

Which hormone suppresses ketogenesis ?

A

insulin

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13
Q

What can ketogenesis be a sign of? why?

A

Type 1 diabetes

because ketogenesis is usually suppressed by insulin, so an increase in the process would suggest a decrease in insulin

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14
Q

What are the key metabolic roles of the liver when the body is in a fed/absorptive state ?

A
  • glycogenesis
  • fatty acid biosynthesis
  • removing surplus ammonia (AA metabolism)
  • producing gluconeogenesis precursors (AA metabolism)
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15
Q

What is glycogenesis ?

A

storing absorbed surplus dietary glucose as glycogen

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16
Q

What drives glycogenesis ?

A

high blood glucose

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17
Q

What hormone suppresses glycogenesis ?

A

glucagon

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18
Q

What is fatty acid biosynthesis ?

A

Use surplus carbon substrate to produce fatty acids for delivery to adipose tissue

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19
Q

What promotes fatty acid biosynthesis ?

A
  • insulin
  • high cellular ATP levels
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20
Q

Which hormone suppresses fatty acid biosynthesis ?

A

glucagon

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21
Q

How does amino acid metabolism dispose of surplus ammonia ?

A
  • surplus ammonia arrives in liver carried by glutamate, glutamine or alanine amino acids
  • transaminase hydrolyses the excess amino acids to release nitrogen
  • N is disposed as urea eventually
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22
Q

How does amino acid metabolism produce gluconeogenesis precursors ?

A
  • transaminase release N from amino acids

= N-free amino acids are the precursors for gluconeogenesis

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23
Q

What are the 2 methods of hepatic glucose production in a fasting state ?

A
  • gluconeogenesis
  • glycogenolysis
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24
Q

Which hormone usually suppresses hepatic glucose production ?

A

insulin

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25
Q

What is the main reason for hyperglycaemia in type 2 diabetes ?

A

failure to regulate hepatic glucose production

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26
Q

Which cells can perform glycolysis ?

A

almost all cells in the body

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27
Q

What process is the main player in carbohydrate metabolism ?

A

glycolysis

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28
Q

What is glycolysis ?

A

breaking down carbohydrates/glucose

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29
Q

What substance is produced by the end of glycolysis, if in aerobic conditions ?

A

pyruvate

30
Q

What substance is produced by the end of glycolysis, if in anaerobic conditions ?

A

lactate

31
Q

How does glucose enter cells ?

A

using glucose transporters via co-transport

transporters are tissue specific

32
Q

Which glucose transporter is used to let glucose in/out the liver ?

A

GLUT-2

33
Q

What stage of carbohydrate metabolism traps glucose within the cell ?

A

phosphorylation

34
Q

Which enzyme catalyses carbohydrate phosphorylation?

A

hexokinase

35
Q

What conditions are required for glucokinase to be effective at trapping glucose in the liver ?

A

glucose levels must be high - e.g after a meal

36
Q

What is the liver variant of hexokinase called ?

A

Hexokinase-IV or glucokinase

37
Q

What are the first 2 steps of glycolysis ?

A

glucose —> fructose-6-Phosphate (F-6-P)
F-6-P —> fructose-6-bisphosphate (F-6-BP)

38
Q

Which step of glycolysis is the most critically regulated step ?

A

F-6-P ——> F-6-BP

uses ATP

39
Q

What is the net result of glycolysis in aerobic conditions ?

A
  • 2 pyruvate
  • 2 ATP
  • 2 NADH
40
Q

What is the structure of glycogen like ?

A
  • highly branched
  • glucose polysaccharide
  • alpha-1,4 linked backbone
  • alpha-1,6 linked branches
41
Q

What are the 2 main glycogen store in the body ?

A
  • liver
  • skeletal muscle
42
Q

Are glucagon levels elevated or decreased in a fasting state ?

A

elevated

43
Q

Are insulin levels elevated or decreased in a fasting state ?

A

decreased

44
Q

What is glucagon’s effect on glycogenesis ?

A

glycogenesis = inhibited by glucagon

45
Q

What is glucagon’s effect on glycogenolysis ?

A

glycogenolysis = promoted by glucagon

46
Q

Describe how glucagon regulates formation/destruction of glycogen stores ?

A

increases cellular Protein Kinase A (PKA) which….

  1. directly inhibits glycogen synthase = stops glycogenesis
  2. indirectly activates glycogen phosphorylase (via phosphorylase kinase) = activates glycogenolysis
47
Q

What are the body’s primary and secondary methods of regulating blood glucose in periods of fasting/starvation ?

A

primary:
- glycogenolysis
- glycogenesis inhibiton

secondary:
- gluconeogenesis

48
Q

What are the substrates used to form new glucose in gluconeogenesis ?

A
  • Lactate re-oxidised into pyruvate via Cori Cycle
  • Glycerol released by lipid hydrolysis
  • amino acids metabolised to alpha-keto acids
49
Q

When does glucogneogenesis occur ?

A

when the body is well into starvation mode and glycogen stores have already been used

glycogenolysis can sustain an overnight fast but not much longer, so gluconeogenesis kicks in

50
Q

Which hormone is the main regulator of gluconeogenesis ?

A

glucagon

51
Q

How does glucagon increase gluconeogenesis ?

A

increases availability of PEP (molecule converted into pyruvate in glycolysis) by…
1. increasing expression of PEP carboxykinase
2. decreasing expression of pyruvate kinase

Increases glycolysis by activating F-6-P into F-6-BP (the early steps of glycolysis)

52
Q

What happens to levels of insulin and glucagon after a meal ?

A
  • insulin increases/spikes dramatically
  • glucagon decreases dramatically
53
Q

What processes does insulin up-regulate ?

A
  • glucose uptake
  • glycogenesis
  • protein synthesis
  • fat synthesis
54
Q

What processes does insulin down-regulate ?

A
  • ketogenesis
  • lipolysis
  • gluconeogenesis
  • glycogenolysis
55
Q

What processes does glucagon up-regulate ?

A
  • ketogenesis
  • lipolysis
  • gluconeogenesis
  • glycogenolysis
  • amino acid uptake
56
Q

What processes does glucagon down-regulate ?

A
  • glycogenesis
  • fat synthesis
57
Q

What factors affect the regulation of metabolism ?

A
  • availability of substrates
  • allosteric control (metabolites bind to allosteric site to modulate activity of enzyme)
  • regulatory phosphorylation (phosphorylation of glycogen synthase etc)
  • changes in transcription of enzymes that control each process
58
Q

Which enzyme catalyses the reaction of F-6-P —> F-6-BP in glycolysis ?

A

PFK-1

phosphofructokinase-1

59
Q

What is the rate limiting (slowest) step of glycolysis ?

A

F-6-P —> F-6-BP

60
Q

How is PFK1 activated ?

A
  • allosterically by activated AMP
  • by F-2,6-BP (fructose-2,6-bisphosphate)
61
Q

How is PFK1 repressed ?

A

by ATP + Citrate

62
Q

What is the interaction between PFK1 and PFK2 ?

A
  • PFK1 is activated by AMP and F-2,6-BP
  • F-2,6-BP is the product of an activated PFK2 molecule
63
Q

Which hormone
a) activates PFK 2?
b) deactivates PFK2?

A

activates = insulin
deactivated = glucagon

active in well-fed state

64
Q

Is PFK2 active in the fasting or well-fed state ?

A

well-fed state

65
Q

What is the link reaction ?

A

Pyruvate + CoA + NAD —> Acetyl CoA + NADH + CO2

66
Q

What are the products of the link reaction ?

A

Acetyl CoA + NADH + CO2

67
Q

What happens to pyruvate in the link reaction ?

A

it is oxidised into acetate

68
Q

What are the 4 main carbon compounds in the krebs cycle, in order from the 6c molecule ?

A

6c = citrate
5c = α-ketoglutarate
4c = succinate
4c = oxaloacetate

69
Q

Where does the krebs cycle take place ?

A

mitochondrial matrix

70
Q

Which molecule needs to be present in order for Acetyl CoA to enter the krebs cycle ?

A

Oxaloacetate (OAA)

71
Q

What is lipolysis ?

A

triglycerides —> fatty acids + glycerol

72
Q

what is lipogenesis ?

A

glycerol + fatty acids —> triglycerides

Sem 4, case 5 (hepatitis) (3 decks)

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