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

The normal liver - metabolism (lecture series) Flashcards

(72 cards)

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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
What is the main reason for hyperglycaemia in type 2 diabetes ?
failure to regulate hepatic glucose production
26
Which cells can perform glycolysis ?
almost all cells in the body
27
What process is the main player in carbohydrate metabolism ?
glycolysis
28
What is glycolysis ?
breaking down carbohydrates/glucose
29
What substance is produced by the end of glycolysis, if in aerobic conditions ?
pyruvate
30
What substance is produced by the end of glycolysis, if in anaerobic conditions ?
lactate
31
How does glucose enter cells ?
using glucose transporters via co-transport *transporters are tissue specific*
32
Which glucose transporter is used to let glucose in/out the liver ?
GLUT-2
33
What stage of carbohydrate metabolism traps glucose within the cell ?
phosphorylation
34
Which enzyme catalyses carbohydrate phosphorylation?
hexokinase
35
What conditions are required for glucokinase to be effective at trapping glucose in the liver ?
**glucose levels must be high** - e.g after a meal
36
What is the liver variant of hexokinase called ?
Hexokinase-IV or **glucokinase**
37
What are the first 2 steps of glycolysis ?
glucose —> fructose-6-Phosphate (F-6-P) F-6-P —> fructose-6-bisphosphate (F-6-BP)
38
Which step of glycolysis is the most critically regulated step ?
F-6-P ——> F-6-BP *uses ATP*
39
What is the net result of glycolysis in aerobic conditions ?
- 2 pyruvate - 2 ATP - 2 NADH
40
What is the structure of glycogen like ?
- highly branched - glucose polysaccharide - alpha-1,4 linked backbone - alpha-1,6 linked branches
41
What are the 2 main glycogen store in the body ?
- liver - skeletal muscle
42
Are glucagon levels elevated or decreased in a fasting state ?
elevated
43
Are insulin levels elevated or decreased in a fasting state ?
decreased
44
What is glucagon’s effect on glycogenesis ?
glyco**genesis** = **inhibited** by glucagon
45
What is glucagon’s effect on glycogenolysis ?
glycogeno**lysis** = **promoted** by glucagon
46
Describe how glucagon regulates formation/destruction of glycogen stores ?
**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
What are the body’s primary and secondary methods of regulating blood glucose in periods of fasting/starvation ?
primary: - glycogenolysis - glycogenesis inhibiton secondary: - gluconeogenesis
48
What are the substrates used to form new glucose in gluconeogenesis ?
- **Lactate** *re-oxidised into pyruvate via Cori Cycle* - **Glycerol** *released by lipid hydrolysis* - **amino acids** *metabolised to alpha-keto acids*
49
When does glucogneogenesis occur ?
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
Which hormone is the main regulator of gluconeogenesis ?
glucagon
51
How does glucagon increase gluconeogenesis ?
**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
What happens to levels of insulin and glucagon after a meal ?
- insulin **increases**/spikes dramatically - glucagon **decreases** dramatically
53
What processes does insulin up-regulate ?
- glucose uptake - glycogenesis - protein synthesis - fat synthesis
54
What processes does insulin down-regulate ?
- ketogenesis - lipolysis - gluconeogenesis - glycogenolysis
55
What processes does glucagon up-regulate ?
- ketogenesis - lipolysis - gluconeogenesis - glycogenolysis - amino acid uptake
56
What processes does glucagon down-regulate ?
- glycogenesis - fat synthesis
57
What factors affect the regulation of metabolism ?
- 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
Which enzyme catalyses the reaction of F-6-P —> F-6-BP in glycolysis ?
PFK-1 *phosphofructokinase-1*
59
What is the rate limiting (slowest) step of glycolysis ?
F-6-P —> F-6-BP
60
How is PFK1 activated ?
- allosterically by **activated AMP** - by **F-2,6-BP** (fructose-2,6-bisphosphate)
61
How is PFK1 repressed ?
by **ATP + Citrate**
62
What is the interaction between PFK1 and PFK2 ?
- PFK1 is activated by AMP and F-2,6-BP - F-2,6-BP is the product of an activated PFK2 molecule
63
Which hormone a) activates PFK 2? b) deactivates PFK2?
activates = insulin deactivated = glucagon *active in well-fed state*
64
Is PFK2 active in the fasting or well-fed state ?
well-fed state
65
What is the link reaction ?
Pyruvate + CoA + NAD —> Acetyl CoA + NADH + CO2
66
What are the products of the link reaction ?
Acetyl CoA + NADH + CO2
67
What happens to pyruvate in the link reaction ?
it is **oxidised into acetate**
68
What are the 4 main carbon compounds in the krebs cycle, in order from the 6c molecule ?
6c = citrate 5c = α-ketoglutarate 4c = succinate 4c = oxaloacetate
69
Where does the krebs cycle take place ?
mitochondrial matrix
70
Which molecule needs to be present in order for Acetyl CoA to enter the krebs cycle ?
Oxaloacetate (OAA)
71
What is lipolysis ?
triglycerides —> fatty acids + glycerol
72
what is lipogenesis ?
glycerol + fatty acids —> triglycerides

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

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