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Bioenergetics > Lectures 11-15 > Flashcards

Lectures 11-15 Flashcards

1
Q

What is Acetyl CoA derived from what? (For FA synthesis)

A

From beta-oxidation/the glycolysis reaction in the mitochondria

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2
Q

How does glucagon work?

A

I’m works to raise the concentration of glucose and fatty acids in the bloodstream

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3
Q

How does insulin work?

A

It acts to lower the concentration of glucose and fatty acids in the bloodstream

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4
Q

How is lipogenesis regulated?

A

Acetyl CoA carboxylase

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5
Q

Describe allosteric regulation during lipogenesis

A

Acetyl CoA carboxylase is activated by citrate

Tells the cell that Acetyl CoA and ATP are available for lipogenesis

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6
Q

Describe hormone regulation during lipogenesis

A

Insulin promotes activation of Acetyl CoA carboxylase and therefore lipogenesis

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7
Q

Slide 12

A

Lecture 11

Fatty acids synthesis simple

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8
Q

What happens when there is an excess of glucose? (Fatty acid synthesis)

A

Fatty acids are synthesised in the cytosol of the cell from Acetyl CoA

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9
Q

How do we get Acetyl CoA? (Fatty acid synthesis)

A

From the ‘link reaction’ which links glycolysis and the TCA cycle

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10
Q

Acetyl CoA is synthesised to form what? (Fatty acid synthesis)

A

Malonyl CoA

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11
Q

When is fatty acid synthesis inhibited? (Fatty acid synthesis)

A

When there are plenty of fatty acids in the cell

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12
Q

When is fatty acid synthesis activated?

A

By excess glucose
And/Or
A decrease in fatty acid availability

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13
Q

The Malonyl CoA is used for what? (Fatty acid synthesis)

A

To create a new fatty acid

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14
Q

What is triglyceride synthesis?

A

Joining 3 fatty acids together with a glycerol

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15
Q

When is triglyceride synthesis more likely to occur? And less likely to occur?

A

More - after each meal

After - during exercise

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16
Q

How is a triglyceride formed?

A

Three fatty acids are attached to a glycerol backbone

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17
Q

Triglyceride synthesis is promoted by what?

A

Insulin

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18
Q

Triglyceride synthesis is inhibited by what?

A

Glucagon

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19
Q

What are the 3 main ketone bodies we have to know?

A

Acetoacetic acid

3-hydroxybutyric acid

Acetone

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20
Q

Are ketone bodies produced in large quantities?

A

No, they are produced in small quantities

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21
Q

What can ketone bodies be a fuel source for? And when would they be used?

A

For brain - when glucose availability is low

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22
Q

When do ketone bodies increase?

A

During hunger
Reduced carbohydrate availability
Starvation
Prolonged exercise

(Basically when there is a large amount of FA use)

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23
Q

During circumstances when there is a large amount of FA use, why does ketone body production increase?

A

When large amounts of FA are used, the liver cannot oxidise then quick enough, so the increased Acetyl CoA available is converted to ketone bodies
These are then released in the blood for energy

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24
Q

How are ketone bodies transported?

A

The blood

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25
Q

What organs use ketone bodies?

A

Brain
Heart
Kidney
Skeletal muscle

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26
Q

Why does the brain/heart/kidneys/skeletal muscle use ketone bodies?

A

To produce ATP via the TCA cycle in these cells

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27
Q

What has to happen to ketone bodies before they can be used to produce ATP via the TCA cycle in certain tissues?

A

Has to be re-concerted back to Acetyl CoA

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28
Q

What you really need to know slide

A

Lecture 11, slide 22

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29
Q

What are hormones?

A

Chemical messengers that regulate and co-ordinate metabolic activity within the body

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30
Q

What is an endocrine hormone?

A

A hormone produced in one tissue (gland) and travel through circulation to reach a target cell which has a receptor for that hormone

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31
Q

What is a paracrine hormone?

A

A hormone produced in one cell and only travels a short distance to reach a neighbouring target cell which has a receptor for that hormone

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32
Q

What is an autocrine hormone?

A

A hormone produced in a cell which is also the target cell for that hormone

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33
Q

What triggers insulin and glucagon?

A

Pancreas

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34
Q

What glands produce Adrenalin?

A

Adrenal glands

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35
Q

Are insulin and glucagon triggered by the hypothalamus?

A

No

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36
Q

What is the hormonal cascade?

A

Hormones released by one gland often stimulate the release of a hormone from another gland

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37
Q

How many different types of endocrine hormone are there?

A

Three

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38
Q

What are the different types of endocrine hormones?

A

Steroid
Peptide/protein
Amino acid derived (catecholamines)

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39
Q

What do the different types of endocrine hormones differ in?

A

Solubility characteristics

Mechanism of action

Speed of action

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40
Q

Describe the steroid type of endocrine hormone - are they lipid soluble?

A

Yes

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41
Q

Describe the steroid type of endocrine hormone - what is their structure?

A

A basic steroid structure

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42
Q

Describe the steroid type of endocrine hormone - how are they transported?

A

In the blood bound to specific transport proteins

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43
Q

Describe the steroid type of endocrine hormone - how do they enter the target cell?

A

The transport protein binds to a receptor on the cell surface, the hormone then enters the target cell

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44
Q

Describe the steroid type of endocrine hormone - how does the hormone act?

A

Binds to specific receptors (either in cytosol or nucleus)
If it binds to the cytosol the whole complex moves into nucleus
The hormone-receptor complex binds to specific regions of DNA

45
Q

Describe the steroid type of endocrine hormone - what happens once the hormone-receptor complex is bound to a specific region of DNA?

A

Influences transcription (up or down)
Alters proportions of specific proteins in a cell
Slow response hormone

46
Q

Describe the peptide/protein and amino acid derived (catecholamines) types of endocrine hormone - what size are they?

A

Small molecules - proteins/peptides/amino acid derivatives

47
Q

Describe the peptide/protein and amino acid derived (catecholamines) types of endocrine hormone - how are they transported?

A

In free form in blood

48
Q

Describe the peptide/protein and amino acid derived (catecholamines) types of endocrine hormone - how do they act?

A

They bind to specific cell surface receptors on the outside of the cell
They do not enter the cell
This binding initiated response in the target cell via second messenger

49
Q

Describe the peptide/protein and amino acid derived (catecholamines) types of endocrine hormone - what is the main function?

A

To influence activity of proteins already present in cells

50
Q

Describe the peptide/protein and amino acid derived (catecholamines) types of endocrine hormone - how long does the change in the cell take once hormone is bound etc?

A

There is a rapid response to the hormone

51
Q

Describe the peptide/protein and amino acid derived (catecholamines) receptors - what are they?

A

Transmembrane proteins with distinct domains
A ligand binding domain to interact with the hormone of the cell surface
Transmembrane domains crossing the membrane

52
Q

Describe the peptide/protein and amino acid derived (catecholamines) receptors - what happens after the binding of a hormone?

A

Induced a conformational change which results in either activation of intrinsic enzyme activity
Or
Interaction with other proteins in the membrane to affect enzyme activity

53
Q

What type of peptide and catecholamine receptor activates intrinsic enzyme activity?

A

Receptor tyrosine kinase

54
Q

What type of peptide and catecholamine receptor activates interaction with other proteins in the membrane to affect enzyme activity?

A

G Protein-linked receptor

55
Q

Describe the peptide/protein and amino acid derived (catecholamines) receptors - what is the effect of enzyme activation?

A

Induces a second messenger to be formed within the cell

56
Q

Describe the peptide/protein and amino acid derived (catecholamines) receptors - what do the second messengers activate?

A

A phosphorylation cascade initiated by protein kinases (PKs) which phosphorylate Ser or Thr residues on existing cell proteins

57
Q

Describe the peptide/protein and amino acid derived (catecholamines) receptors - what does phosphorylation of specific proteins do?

A

Converts them from inactive to active or vica versa, depending on the protein

58
Q

What is the process of signal transduction?

A

Signal -> Receptor -> Transduction -> Effect

59
Q

Describe G-protein linked receptors - how many subunits are there?

A

Three

60
Q

Describe G-protein linked receptors - what are the different subunits?

A

Alpha
Beta
Gamma

61
Q

Describe G-protein linked receptors - when the hormone binds to its receptor what does induce?

A

A change in shape in the intracellular part of the receptor molecule

62
Q

Describe G-protein linked receptors - what happens when the G protein interacts with the receptor?

A

It induces a change in the confirmation of the alpha subunit and replacement of GDP with GTP

63
Q

Describe G-protein linked receptors - what happens after conformational change of the alpha subunit?

A

The alpha subunit also interacts with its target enzyme

64
Q

Describe G-protein linked receptors - are G proteins stimulators or inhibitory?

A

Can be either stimulatory (Gs and Gq) or inhibitory (Gi) depending upon whether the alpha subunit is stimulatory or inhibitory

65
Q

Lectures 13&14 in folder

A

With recap, go through process she drew up on the board

Slide 19 (lecture 13 pp)

66
Q

G protein activation stuff

A

Slide 19, 22&23

Lecture 13

67
Q

What are tyrosine specific kinases?

A

Transmembrane receptor proteins (insulin receptor)

68
Q

Describe tyrosine specific kinases - what happens when their “x” binds
Also what is “x”

A

“x” = ligand

It causes a conformational change

69
Q

Describe G-protein linked receptors - what happens after the conformational change

A

It becomes a tyrosine kinase

70
Q

What does tyrosine kinase initiate?

A

It initiates cascades

71
Q

What cascades does tyrosine kinase initiate?

A

PIP3 and protein kinase B (PK(small B))

72
Q

Insulin responsive substrate (IRS-1) has two functions in the PIP3 - PK(small B) cascade - what is the first function?

A

It binds to and activated the enzyme PI-3K which forms PIP3 from PIP2 in the membrane

73
Q

Insulin responsive substrate (IRS-1) has two functions in the PIP3 - PK(small B) cascade - what happens as a result of the first function?

A

PIP3 attracts protein kinase B (PK(small B), Akt) which when bound to PIP3 is activated by phosphorylation by the enzyme PDK1

Active PK(small B) is then able to phosphorylate specific proteins modifying their activity

74
Q

Insulin responsive substrate (IRS-1) has two functions in the PIP3 - PK(small B) cascade - what is the second function?

A

It phosphorylate other proteins which influence gene expression

75
Q

The specificity of proteins for individual ligand gives proteins many of their functions such as:

A

Catalysis
Recognition
Transport

76
Q

Describe the characteristics of proteins showing sigmoidal kinetics - how many subunits?

A

Two or more

77
Q

Describe the characteristics of proteins showing sigmoidal kinetics - what shape are the subunits?

A

They can exist in two different shapes

78
Q

Describe the characteristics of proteins showing sigmoidal kinetics - when a target ligand binds to the binding site on one of the sub-units what happens? What is this called?

A

It increases the affinity of the other sub-units for the ligand

Co-operative binding or cooperativity

79
Q

Describe the characteristics of proteins showing sigmoidal kinetics - what does co-operative binding or co-operativity give rise too?

A

The sigmoidal curve

80
Q

Describe the characteristics of proteins showing sigmoidal kinetics - what groups show sigmoidal kinetics?

A

Allosteric enzymes are only one of the groups of proteins that show sigmoidal kinetics

81
Q

What is an allosteric protein?

A

A protein with multiple ligand-binding sites, such that ligand binding at one site affects ligand binding at another (known as cooperative binding)

82
Q

Look at allosteric proteins

A

Slide 4, lecture 15

83
Q

Look at effects of positive effectors on sigmoidal curve

A

Slide 8, lecture 15

84
Q

Questions - Slide 9-15

A

Lecture 15

85
Q 
If a cell has high energy stores, it will have:
High/low - ATP
High/low - AMP/ADP
High/low - NAD+
High/low - NADH+H+
A

High ATP
Low ADP/AMP (because most has been converted to ATP)
Low NAD+ (because most is in the form of NADH+H+ waiting to be oxidised through mitochondrial electron transport chain)
High NADH+H+

86
Q

How do positive effectors act on allosteric proteins?

A

They enhance the activity of the protein

87
Q

How do negative effectors act on allosteric proteins?

A

They decrease the proteins activity

88
Q

What is the allosteric enzyme in the glycogenolysis pathway?

What is this allosteric enzymes positive effector

What is this allosteric enzymes negative effector?

A

Allosteric enzyme = glycogen phosphorylase

Positive effector = AMP

Negative effector = ATP

89
Q

What are the allosteric enzymes in glycolysis?

A

Hexokinase

PFK

Pyruvate kinase

90
Q

What is the positive and negative effector of PFK? (One of the allosteric enzymes present in glycolysis)

A

Positive = AMP

Negative = ATP

91
Q

What is the negative effector of pyruvate kinase? (One of the allosteric enzymes present in glycolysis)

A

ATP

92
Q

What are the allosteric enzymes present in the TCA cycle?

A

Pyruvate deHase
Citrate synthase
Isocitrate deHase

93
Q

What are the positive and negative effectors of Pyruvate deHase? (One of the allosteric enzymes present in the TCA cycle)

A

Positive = AMP, NAD+

Negative = NADH

94
Q

What is the negative effector of Citrate Synthase? (One of the allosteric enzymes present in the TCA cycle)

A

Negative = ATP

95
Q

What are the negative and positive effectors of Isocitrate deHase? (One of the allosteric enzymes present in the TCA cycle)

A

Positive = ADP

Negative = NADH

96
Q

What may happen once control enzymes have been turned off/on?

A

There may be a build up in concentration of their substrates/products
These substrates/products may act as allosteric effectors of the other enzymes

97
Q

What happens when the allosteric enzyme PFK is turned off? (Slide 17, lecture 15)

A

There is a build up of its substrate Glc-6-P
Glc-6-P acts as a -ve effector for glycogen phosphorylase and hexokinase
This reduces flow of glucose into glycolysis

98
Q

What happens when the allosteric enzyme citrate synthase is turned off? (Slide 18, lecture 15)

A

When citrate synthase is turned off there is a build up of its substrates Acetyl CoA
Acetyl CoA acts as a -ve effector for pyruvate dehydrogenase (product inhibition)
This reduces flow of metabolites from glucose into TCA cycle

99
Q

What happens if the flow of metabolites into the TCA cycle is not turned off quickly enough? What is the effect of this? (slide 18, lecture 15)

A

The concentration of citrate rises

Citrate acts as a -ve inhibitor of PFK

100
Q

What happens when PFK is turned on? (Slide 18, lecture 15)

A

When PFK is turned on there is a build up of Fru-1,6-bP

Fru-1,6-bP acts as a +ve effector for pyruvate kinase

101
Q

Go over lecture 15

A

Dr Helen Mason one

102
Q

Slides 20-22

A

Lecture 15

103
Q

If a cell has high energy stores it will:

A

Need to convert excessive ATP into glycogen or lipids because you have too much
This acts as a store for periods of starvation

104
Q

If a cell needs energy it will:

A

Release energy generating nutrients from stores

These will go through the energy generating pathways to yield ATP

105
Q

What is the negative effector of the allosteric enzyme glycogen synthetase? (Energy storage pathways) (which acts in what process)

A

ADP

Glycogen synthesis

106
Q

What are the allosteric enzymes involved in gluconeogenesis? (Energy storage pathways)

A

Fru-1,6-bPase

Pyruvate carboxylase

PEPCK

107
Q

Positive and negative effector of the allosteric enzyme involved in gluconeogenesis Fru-1,6-bPase? (Energy storage pathways)

A

Positive = ATP

Negative = AMP

108
Q

Negative effector of the allosteric enzyme involved in gluconeogenesis pyruvate carboxylase? (Energy storage pathways)

A

ADP

109
Q

Negative effector of the allosteric enzyme involved in gluconeogenesis PEPCK? (Energy storage pathways)

A

GDP

Bioenergetics (5 decks)

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