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ESA 2 > Metabolism > Flashcards

Metabolism Flashcards

1
Q

How is energy conserved primarily

A

In the form of ATP

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2
Q

Generally catabolic pathways are what and do what?

A

Oxidative, release free energy and produce intermediates

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3
Q

Generally anabolic pathways are what?and do what

A

Reductive, use intermediates and energy in synthesis

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4
Q

ADP+Pi, to become ATP what is generally needed and what are the byproducts

A

Oxygen added, CO2 H2O and heat biproducts

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5
Q

What are NAD+, FAD and NADP+ examples of?

A

Carriers of reducing power

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6
Q

What is the purpose of carriers of reducing power?

A

When a substrate is oxidised these are reduced, storing the energy of the bond

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7
Q

What concentration should carrier of reducing power be kept at in a cell

A

Needs to be a constant concentration

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8
Q

How are carriers of reducing power kept at a constant concentration?

A

Reoxidation reactions:
Cell respiration
Reactions where the substrate is reduced

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9
Q

What is a key example of carriers of reducing powers being kept at a constant concentration when oxygen isn’t available for cell respiration

A

Pyruvate +NADH+H+-> Lactic acid + NAD+

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10
Q

What are some examples of reduced carrier states

A

NADH + H+
NADPH + H+
FAD2H

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11
Q

NAD+, NADP+ and FAD are all examples of what? What do they need to be synthesised in the body?

A

Oxidised carriers
Nicotinamide from niacin
Flavin from vitamins

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12
Q

What needs a constant supply of glucose

A

Brain and RBC

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13
Q

How else can glucose be obtained other than diet

A

Gluconeogensis of amino acids, glycerol, dietary sugars

Glyconeolysis

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14
Q

What are dietary fat soluble vitamins

A

D E A K

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15
Q

What essential fatty acids are part if the cell membrane component

A

Linoleic and linolenic

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16
Q

How is glucose released from dietary polysacharides like starch and glycogen

A

Glycosidase enzymes

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17
Q

What are dietary polysacharides broken down into?

A

Glucose, maltose, dextrins

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18
Q

Where does the digestion of polysacharides begin?

A

In the most with salivary amylase

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19
Q

After partial digestion of dietary polysacharides in the mouth, what happens in the jejunum

A

Pancreatic amylase continues to break down to maltose, lactose, sucrose, dextrins, glucose

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20
Q

Where does the digestion of maltose, lactose, sucrose occur

A

Brush border of epithelial cells in jejunum and duodenum

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21
Q

What enzymes release glucose, fructose and galactose from the partially broken down polysacharides in the gut

A

Lactase, sucrase, isomaltase, glycoamylase.

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22
Q

Who’s lactase activity is high?

A

Babies/infants

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23
Q

Where are polypeptides initially broken down

A

Stomach, pepsin breaking peptide bonds

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24
Q

Once peptide bonds of polypeptides have been broken in the stomach, what continues the breakdown in the small intestine

A

Trypsin, chymotripsin, carboxypeptidase

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25
Q

What are the 9 essential amino acids+ mnemonic

A

If learned this huge list may prove truly valuable

Isoleucine, leucine, threonine, histidine, lysine, methionine, phenylalanine, tryptophan, valine

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26
Q

What 3 additional amino acids to the essential amino acids, can become essential in pregnancy and childhood?

A

And Then Children

Arginine, Tyrosine, Cysteine

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27
Q

Where is fat broken down initially, and by what?

A

Small intestine by pancreatic lipase

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28
Q

What is the purpose of bile salts in relation to fat

A

Emulsifies the fat, making it small enough for pancreatic lipase to break it down

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29
Q

What are fats broken down to so that they can be absorbed

A

Free fatty acids and monoglycerides

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30
Q

What happens to the monoglycerides and free fatty acids once entering gut epithelial cells?

A

In the ER they are resynthesised to TAGs. Coated in protein to form chylomicrons. Enter lymphatic capillaries (lacteals), then entering blood via thoracic duct

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31
Q

Where do the chylomicrons drain into from the gut

A

Left subclavian vein from the thoracic duct

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32
Q

What is the first reaction in glycolysis

A

Glucose +ATP -> glucose-6-phosphate +ADP

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33
Q

What enzymes are needed for the first step of glycolysis

A

Glucokinase in liver and pancreas

Hexokinase in other cells

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34
Q

What is the first step in glucose metabolism an example of

A

Phosphorylation

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35
Q

What is the purpose of the first step of glycolysis

A

Makes sugar anion (prevents leaving plasma membrane)
Increase sugar reactivity
Allows for substrate level phosphorylation

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36
Q

What is difference about glucokinase to hexokinase

A

Glucokinase only works at high glucose concentrations

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37
Q

What is dietary lactose broken down into

A

Glucose and galactose

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38
Q

What is the time line of conversions from galactose to glucose 6 phosphate

A

Galactose -> galactose 1-P -> glucose 1-P -> G6P

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39
Q

What is required in the first step of galactose metabolism

A

Galactokinase enzyme

ATP

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40
Q

What enzyme is required for the forward reaction from galactose 1P to glucose 1P
What enzyme is required for the reverse reaction and why is the reverse reaction important

A

Galactose 1-P uridyl transferase (forward)

UDP-galactose 4 epimerase, important in breast feeding

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41
Q

What does accumulation of galactose result in

A

Galactitol

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42
Q

How is galactitol produced

A

In galactose excess, Aldose reductase (req NADPH)

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43
Q

What happens if the production of Galactitol is favoured in galactose excess

A

Depletes NADPH-> cataracts

Increases ocular pressure-> glaucoma

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44
Q

What enzyme is commonly absent in galactossaemia

A

Galactose 1-p uridyl transferase

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45
Q

An absence of galactose 1-P uridyl transferase results in what

A

Accumulation of galactose 1-P and galactose (that’s converted to Galactitol)

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46
Q

Why is accumulation of galactose 1-P dangerous?

A

It sequesters Pi, damages liver kidney and brain

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47
Q

What is dietary sucrose converted into

A

Glucose, fructose

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48
Q

Where is fructose converted and what is it converted to, to enter glycolysis

A

Glyceraldehyde 3 phosphate in the liver

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49
Q

What is the first unique reaction to glycolyis

A

Conversion of fructose 6 phosphate to fructose 1-6 bis phosphate

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50
Q

What is the second step of glycolysis. Reversible or irreversible ?

A

G6P -> F6P reversible

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51
Q

What is the 3rd step of glycolysis?
What enzyme?
What’s special about this step?

A

F6P-> Fructose 1,6,bisphosphate
PFK
Committing step of glycolysis

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52
Q

Why is the conversion to F1,6BP with catalyst PFK the ‘commiting step’

A

It’s irreversible with a large negative value (energy)

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53
Q

What size carbon ring is F1,6,BP?

A

6 carbon

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54
Q

Step 4 and 5 of glycolysis represents what (in relation to structure)
Starting compound is F1,6,BP

A

Cleave from 6 carbon to 2 3 carbon molecules that are interconvertible
Dihydroxyacetone-P and Glyceraldehyde 3-P

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55
Q

What is important about the 3 carbon intermediate produces from step 4 in the glycolysis pathway what’re F1,6,BP has been cleaved to form dihydroxyacetone-P and glyceraldehyde 3-P

A

Dihydroxyacetone-P needed to make glycerol phosphate

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56
Q

In step 6 of glycolysis, what is glyceraldehyde converted into?
What does it reduce?
What’s important about its converted molecule?

A

1-3- bisphosphoglycerate
NAD->NADH
1-3 bisphosphoglycerate goes on to form 2,3 BPG for o2 affinity

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57
Q

Reaction 7 of glycolysis with 1-3 bisphosphoglycerate.
What’s the end product
What is produced
What is this an example of

A

3 phosphoglycerate
ATP
Substrate level phosphorylation

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58
Q

What is step 10 of glycolysis
What’s the end product
Why is it irreversible
What’s it an example of

A

Phospheonolpyruvate -> pyruvate
Large energy change
Substrate level phosphorylation
ATP produced

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59
Q

What are 4 key points about the first 10 steps of glycolysis

A

No co2 lost
2 atp required, 4 produced
Glucose oxidise to pyruvate
Some C3 intermediates made that are needed for other things

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60
Q

What’s the most important rate limiting step in glycloysis phase 1/2

A

Step 3 with PFK

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61
Q

How is glycolysis regulated

A

High energy signalling and hormonal control

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62
Q

How is PFK regulated

A

Allosterically but ATP/ADP
Insulin stimulates
Glucagon inhibits

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63
Q

In low oxygen circumstances what is pyruvate converted to? What’s required

A

Lactate

NADH

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64
Q

Under normal physiological conditions how much lactate is produced in a day?
Where from mainly?

A

50g

RBC, brain, Skin, Lungs, GI

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65
Q

If rate of lactate production is equal to utilisation, what is blood lactate

A

<1mmol/L

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66
Q

Where is blood lactate processed

A

Liver, kidney and heart

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67
Q

How is lactate processed in the heart?

A

Converted to pyruvate with LDH

Oxidation into energy

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68
Q

How is lactate processed in the liver and kidney

A

Converted to pyruvate with LDH

Then either enters TCA cycle or undergoes gluconeogensis

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69
Q

When is lactate ‘above the renal threshold’

A

5mmol and up

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70
Q

What are the 2 overarching causes of increased blood lactate

A

Increased production or decreased utilisation

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71
Q

What can increase the production of lactate

A

Exercise
Big meal
Shock
Congestive heart disease

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72
Q

What can decrease the utilisation of lactate

A

Liver disease
Thiamine defficency
Alcohol metabolism

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73
Q

How does the body have a constant supply of glucose between meals?

A

Glycogen stores

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74
Q

How is glycogen described

A

A highly branches polymer of glucose

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75
Q

What bonds does glycogen have at branch points?

A

Alpha 1,6

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76
Q

What bonds does glycogen have, not at the brach points

A

Alpha 1,4 glycosidic

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77
Q

Where is glycogen stored

A

Granules in liver and skeletal muscles

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78
Q

Where is the highest amount (g) of glycogen stored?

A

Skeletal muscles 300g

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79
Q

What limits the amount of glycogen that can be stored

A

It’s very polar

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80
Q

What are the 2 enzymes involved in addidng further glucose to glycogen

A

Glycogen synthase and branching enzyme

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81
Q

What’s the ratio of glycosidic bonds to branch points in glycogen

A

10:1

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82
Q

In glycogenesis what is G6P initially converted to and with what enzyme?
Reversible or not?

A

G1p with phosphoglucomutase

Reversible

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83
Q

In glycogenesis how is G1P altered to eventually join glycogen?

A

UTP+ H20 added creating UDP glucose +2Pi

UDP glucose added to glycogen, losing UDP in the process

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84
Q

What promotes the formation of glycogen and what inhibits it

?

A

Insulin promotes it

Adrenaline and glucagon inhibit it

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85
Q

When is glyconeolysis initiated?

A

In response to exercise in skeletal muscle

In response to fasting in the liver

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86
Q

What enzymes are active in glyconeolysis and what do they catalyse?

A

Glycogen phosphorylase acts on alpha 1,4 bonds

De-branching enzyme acts on alpha 1,6

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87
Q

What can muscle stores not make from glucose 1 p in glyconeolysis?

A

Glucose due to lack of glucose 6 phosphotase

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88
Q

Where is glucose 6 phosphotase and what is its purpose

A

In the liver and can convert G6P to glucose to be mobilised into the blood

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89
Q

What is glucagon action on glycogen synthase

A

Decrease

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90
Q

What is insulins action on glycogen synthase

A

Increase

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91
Q

What is glucagon action on glycogen phosphorylase

A

Increase

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92
Q

What is insulins action on glycogen phosphorylase

A

Decrease

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93
Q

Where is the pentose phosphate pathway very important

A

Liver
RBC
Adipose
Dividing tissues

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94
Q

Why is the pentose phosphate pathway important

A

Produces NADPH for anabolic processes

Produces C5 sugar ribose for nucleotides

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95
Q

Why is the pentose phosphate pathway essential in RBC

A

Maintains free -SH groups on cysteine residues

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96
Q

Why is the pentose phosphate pathway essential in adipose tissue

A

Provides NADPH for lipid synthesis

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97
Q

Where does the c5 sugar ribose come from for nucleotides

A

Pentose phosphate pathway

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98
Q

How much ATP is generated in the pentose phosphate pathway

A

Nil

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99
Q

What is the start product in the pentose phosphate pathway

A

G6P

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100
Q

What is phase 1 of the pentose phosphate pathway
Start
Enzyme
Product

A

G6P + 2NADP+
Glucose 6 phosphate dehydrogenase G6PD
C5 + 2NADPH + 2H+ + 2CO2

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101
Q

Where is G6PDH located chromosomally

A

X

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102
Q

Why do you get Heinz bodies with a G6PDH defficency?

A

NADPH (from pentose phosphate pathway)needed to recycle glutathione
Gluatathione protects against free radicals
RBC can only get NADPH from PPP therfore chromatin becomes damaged and haemolysis occurs

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103
Q

What happens to the c5 sugars from the PPP that arent used up?

A

Converted to 2-fructose-6 phosphate and glyceraldehyde-3-phosphate and rejoin glycolysis

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104
Q

How is pyruvate inverted to Acetly Coa?
What is produced?
What enzyme ?

A

Pyruvate dehydrogenase
Co2 produced
NAD+ converted to NADH

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105
Q

What is important about the conversion of pyruvate to Acetly coa

A

Acetly coa can not be used in gluconeogenesis, conversion is large energy step

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106
Q

If Acetly coa wasn’t under some kind of control, what would happen?

A

Glucose dependent tissues would use up all of the glycogen stores

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107
Q

What other pathway is important so that acetyl coa levels are kept high?

A

Beta oxidation of fatty acids

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108
Q

What inhibits the activity of PDH

A

Acetly Coa

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109
Q

What activates PDH activity

A

Insulin

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110
Q

What are the 3 classes of lipids in the body?

A

Fatty acid derivatives
Hydroxyl-methyl-glutoric-acid derivatives
Vitamins DEAK

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111
Q

What are some examples of fatty acid derivatives?

A

Fatty acids
Triacyglycerol
Phospholipids
Eicasonoids

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112
Q

What are some examples of hydroxy-methyl-glutamic acid derivatives

A

Ketone bodies
Cholesterol
Cholesterol esters
Bile salts

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113
Q

The breakdown of triacyglycerol is called what? And the build up of it is called what?

A

Lipolysis

Esterfication

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114
Q

Triacyglycerol have what properties

A

Anhydrous

Hydrophobic

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115
Q

What promotes esterfication and what promotes lipolysis hormonally

A

Insulin promotes esterfication

Glucagon, cortisol, adrenaline, growth hormone and thyroxine promote lipolysis

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116
Q

What enzyme is responsible for the breakdown of triacyglycerols

A

Hormone sensitive lipase

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117
Q

Once TAG has been broken down, how and where do the components travel

A

Glycerol in the blood to the liver

Fatty acids bound to albumin to tissues

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118
Q

When glycerol reaches the liver what enzyme acts on it?
What does it make?
Where can this new component now go ?

A

Glycerol kinase
Glycerol phosphate
Glycerol phosphate can now be used either for TAG synthesis or to enter glycolyis by conversion to dihydroxyacetone phosphate

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119
Q

Where can fatty acids not be utilised? Why is this?

A

RBC- no mitochondria

Brain- cant cross BBB

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120
Q

When fatty acids reach a desired tissue what reaction takes place?
What enzyme
Where in the cell

A

CoA added to make fatty accyl CoA
Fatty Acyl CoA synthase
Outside the mitochondira

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121
Q

What is the purpose of linking fatty acids to CoA?

A

Form high energy of hydrolysis bond

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122
Q

How does fatty accyl CoA enter the mitochondria for beta oxidation

A

Transport using carinitine?

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123
Q

What inhibits the transport of fatty acyl CoA into the mitochondria?
Why does it do this?

A

Malonyl CoA- an intermediate in fatty acid synthesis

Stops newly synthesised fatty acids entering mitochondria

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124
Q

What happens in beta oxidation within the mitochodnria?

A

A sequence of oxidative reactions to remove C2 at a time, the c2 compound goes on to for Acetly CoA

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125
Q

What is essential for beta oxidation to occur?

A

Oxygen as the reducing agents need to be reoxidised by ETC

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126
Q

What are ketone bodies?

A

Important fuel molecules used by all tissues, including the CNS

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127
Q

What are the 3 ketone bodies produced in the body?

A

Acetoacetate, acetone, beta hydroxybutyrate

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128
Q

How are high plasma concentrations of ketone bodies possible?

A

They are water soluble

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129
Q

What levels of ketone bodies is normal in a restin state?

A

Less than 1 mol

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130
Q

What level of ketone bodies can be seen in starvation

A

2-10mol

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131
Q

If ketone level is above 10 what is likely they case?

A

Untreated type 1 DM

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132
Q

Which ketone bodies are strong organic acids?

A

Acetoacetate

Beta hydroxybutyrate

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133
Q

What does the ketone body acetone account for?

A

Nail varnish breath, its volatile

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134
Q

What 2 things do you need for ketone synthesis?

A

Available fatty acids

Fall in plasma insulin level

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135
Q

What are ketone bodies synthesised from

A

Acetly CoA

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136
Q

What enzyme catalyses the precursor for ketone body formation from Acetly coa?

A

Synthase

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137
Q

What enzyme converts HMG COA to mevalonate?
What does this go on to form?
What drugs target this enzyme?

A

HMG CoA reductase
Mevalonate goes on to form cholesterol
The enzyme is a target for statins

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138
Q

What enzyme is needed to convert HMG CoA into ketone bodies?

A

Lyase

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139
Q

What does lyase convert HMG CoA into?

A

Acetoacetate

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140
Q

What does acetoacetate go on to form?

A

Acetone via spontanous non enzymatic decarboxylation

Beta hydroxybutyrate

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141
Q

Ketone body formation is controlled by what?

A

Insulin/glucagon ratio

Glucagon activates ketone formation, insulin inhibits

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142
Q

What effect does insulin have on lyase and HMG reductase

A

Inhibits lyase, activates reductase

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143
Q

What is ketonuria?

A

Ketone level reaching above renal threshold and ending up detectable in urine

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144
Q

When are ketone bodies primarily utilised?

A

In starvation

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145
Q

How much of alcohol is metbolised and how much is excreted?

A

90% metabolised

10% excreted

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146
Q

What 2 enzymes are key in the metabolis of alcohol?

A

Alcohol dehydrogenase

Aldehyde dehydrogenase

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147
Q

What is alcohol converted to initially?
What enzyme
What is the issue with the intermediate?

A

Acetaldehyde
Alcohol dehydrogenase
Acetaldehyde is toxic to cells

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148
Q

How is the fact that the intermediate of alcohol metabolism- acetaldehyde being toxic to the cells compensated for by the body?

A

Aldehyde dehydrogenase has a very low Km for acetaldehyde

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149
Q

What is the end product of alcohol metabolism, where does it go on to?

A

Acetate-> acetyl coa to TCA

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150
Q

What happens if acetaldehyde accumulates?

A

Liver damage
Hyperbillirubaemia
Hyperammonaeamia
Decreased synthesis of clotting proteins and albumin

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151
Q

How is liver damage detected e.g from alcohol damage?

A

Leaky plasma membranes- transaminases and gamma glutanmyl transpeptidase leak out

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152
Q

If there is reduced ability to produce urea due to liver damage, what will occur

A

Hyperammonaemia

Raised glutamine

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153
Q

Why do you get fatty liver with alcohol intake?

A

Liver damage means inability to produce adequate lipoproteins, they accumulate in the liver.

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154
Q

Other than accumulation of acetaldehyde what other issue is there with processing excess alcohol?

A

Uses up the NAD+ as NADH levels rise. Decreased ability to oxidise anything

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155
Q

If the NADH levels are very high due to alcohol metabolism, what are some resultant issues?

A

Inability to oxidise fatty acids
Can’t convert lactate to pyruvate
Can’t metabolise glycerol

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156
Q

If the NADH levels are high due to alcohol metabolism, and the lactate cant be converted to pyruvate, what is the knock on effect

A

Lactic acidosis
Decreases kidneys ability to excrete Uric acid
Uric acid builds up contributing to gout

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157
Q

If there is decreased levels of NAD+ due to alcohol metabolism, and therfore an inability to use glycerol and lactate. What is the outcome?

A

Decreased gluconeogensis

Danger of hypoglycaemia

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158
Q

What are the 4 big consequences of the increased NADH in alcohol metabolism?

A

Lactic acidosis
Urate crystal formation
Hypoglycaemia
Fatty liver

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159
Q

What 4 specific defficencies of nutrients does excess alcohol intake cause?
What can they lead to?

A

Thiamine and pyrixodine- neurological sx
Folic acid- anaemia
Thiamine- korsacoffs

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160
Q

What can chronic alcohol intake do to the pancreas

A

Cause chronic pancreatitis

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161
Q

What is disulfirams purpose?

A

Inhibits aldehyde dehydrogenase resulting in acetaldehyde build up and feeling of extreme nausea

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162
Q

What are fatty acids synthesised from? What does it require?

A

Acetly coa

Requires ATP and NADPH

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163
Q

What is acetyl CoA converted into?
What enzyme catalyses it?
What’s needed?
What change has it made?

A

Malonyl CoA
Acetyl CoA carboxylase
ATP
C2-> C3

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164
Q

When Malonyl CoA is enters the fatty acid synthase complex what is released?

A

CO2

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165
Q

Where does lipogensis occur?

A

Liver cell cytoplasm

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166
Q

Where is the NADPH coming from for lipogenesis?

What needs it?

A

PPP, TCA

Fatty acid synthase complex

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167
Q

What is the fatty acid synthase complex?

Why is it less important than the Acetly CoA carboxylase?

A

Group of enzymes that work together to form fatty acids

It isn’t a control step like Acetly coa carboxylase

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168
Q

How is acetyl coa carboxylase activity controlled?

A

Citrate and insulin activate it

AMP, Glucagon and adrenaline inhibit it

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169
Q

Once the fatty acid is made, where does the glycerol come from?

A

The glycolysis pathway

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170
Q

What is the TAG synthesised from lipogenesis transported out the liver as/in

A

VLDL

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171
Q

What is the function of chylomicrons?

A

Transport dietary TAG to tissues like adipose

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172
Q

What is the function of VLDL

A

Transport TAG synthesised in liver to adipose for storage

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173
Q

What is the function of IDL

A

Short lived precursor of LDL, transporting cholesterol from liver

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174
Q

What is the function of LDL

A

Cholesterol transport from liver to tissues

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175
Q

What is the function of HDl

A

Transport excess tissue cholesterol to the liver for disposal as bile salts or to other tissues that need it

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176
Q

What is ‘good cholesterol’

A

HDL

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177
Q

What stimulates uptake of amino acids into tissues?

A

Insulin and growth hormone

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178
Q

What promotes breakdown or nitrogen based compounds (proteolysis)

A

Cortisol

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179
Q

What is the majority of body protein in the form of?

A

90% DNA and RNA

10% purines, pyramidines, neurotransmitters, creatine etc

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180
Q

How much of the amino acid pool is resynthesised back to body proteins?

A

75%

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181
Q

Hoe are nitrogen containining compounds lost from the body?

A

In faeces and urine as urea, creatine, ammonia, Uric acid

As hair and skin

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182
Q

Where are non essential amino acids made from?

A

Intermediates of glycolysis for carbon base chain

Transammination or ammonia for the amino group

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183
Q

What cycles supply the carbon based chains for non Essential amino acids?

A

Glycolysis C3
PPP C4, C5
Krebs C4, C5

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184
Q

What happens to excess dietary amino acids??

A

Converted to intermediates of carbohydrate or lipid metabolism

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185
Q

What are 2 important signalling molecule that come from amino acids?

A

Nitric oxide from L arginine

Hydrogen sulphide from L cytstein

186
Q

Where is the main site of amino breakdown?

A

The liver

187
Q

Although each amino has is own metabolic pathway, what 3 common features do all the pathways share

A

The Carbon atoms are converted into intermediates for carbohydrate or lipid metabolism
The NH2 group is removed (trans or deam)
The N atoms are usually converted to urea

188
Q

When converting an amino acid to a carbohydrate intermediate, what are the 2 categories

A

Glucogenic
Ketogenic
(Some are both)

189
Q

What can glucogenic amino acids form

A

Glucose- eg pyruvate, oxeloacetate, alpha ketoglutarate succinyl

190
Q

How many amino acids are glucogenic?

A

14

191
Q

What are the ketogenic only amino acids

A

Leucine

Lysine

192
Q

What can ketogenic amino acids make?

A

Ketone bodes and fatty acids- eg Acetyl coa

193
Q

What amino acids are both glucogenic and ketogenic

A

Isoleucine
Tyrosine
Phenylalanine
Tryptophan

194
Q

What stimulates transamination

A

Cortisol

195
Q

What do most amino acids use as the keto acid in transamination

A

Alpha ketoglutarate

196
Q

What is the general formula of transamination?

A

Amino acid + keto acid -Aminotransferase-> keto acid+ amino acid

197
Q

If alpha ketoglutarate is the keto acid being used in by an aminotrasferase, what is the resultant amino acid. And what happens to that amino acid?

A

Glutamate

Either re-used or deammination

198
Q

What transaminase differs in that it does use alpha ketoglutarate at keto acid 1?
What does it use?
What amino acid does it produce?

A

Aspartate aminotransferase
Uses oxaloacetate
Amino acid produced is aspartate

199
Q

What are the 2 transaminases commonly measured?

A

ALT

AST

200
Q

What is deamminaton

A

Removal of NH2- from amino as Nh3+

201
Q

What enzymes do we possess that deamminate

A

L and D amino oxidisas

202
Q

Why do we have lots of D amino acid oxidases?

A

We don’t use D amino acids in protein synthesis but they need to be processed.

203
Q

What enzyme is responsible for deamination of glutamine?

What does it produce?

A

Glutaminase

Glutamate and NH3+

204
Q

Glutamate (deaminated from glutamine) is processed further how?
What is the direction of this reaction determined by?

A

Glutamate dehydrogenase converts it to alpha ketoglutarate and Nh4+
The direction is determined by the relative concentrations

205
Q

At what level is ammonia kept at in the body?
What is particularly sensitive to hyperammonia?
What symptoms are associated?

A

25-40nmol
CNS
Blurred vision, tremors, slurred speech, coma, death

206
Q

How is ammonia mostly processed?

A

Detoxification in the liver by either converting it to urea or using it in N compound synthesis

207
Q

What is ammonia mainly converted to(N compound)?

A

Glutamine

208
Q

How does the liver convert ammonia to glutamine?
(Additional compounds needed)
(Enzyme)

A

Nh4+ + glutamate + ATP -> Glutamine + ADP + Pi

Glutamine synthase

209
Q

Once glutamine synthase has made glutamine from ammonia and glutamate, what happens to it?
What enzyme is involved

A

It’s transported to the kidney to make urea

Glutaminase converts it to NH4 and glutamate.

210
Q

Why is urea so damn good as a method of excreting nitrogen

A

It’s inert and 47% nitrogen

211
Q

Is the urea cycle subject to feedback inhibition?

A

No but it does become induced. High protein diet=more enzymes

212
Q

What is refeeding syndrome? What happens

A

Due to low protein diet the urea cycle is induced to having low levels of enzymes to make urea
Sudden increase results in hyperammonia

213
Q

What cycle does the urea cycle overlap with

A

TCA

214
Q

After glycogen stores are depleted what does the body need to do?

A

Gluconeogenesis

215
Q

What can be used in gluconeogenesis

A

Pyruvate
Lactate
Glycerol
Essential and non essential amino acids

216
Q

What cant be used in gluconeogenesis? Why?

A

Acetly Coa

PDH is irreversible

217
Q

How many steps of glycolysis are reversible?

A

7

218
Q

What steps of glycolysis are not reversible and therefore need a seperate mechanism in gluconeogenesis?

A

1, 3 and 10

219
Q

How is reaction 1 altered in gluconeogenesis?
Enzyme
Regulation

A

G6P+ H20 -> glucose
Glucose 6 phosphotase
Thermodynamically spontaneous

220
Q

How is reaction 3 of glycolysis altered in gluconeogenesis?
Enzyme
Method

A

Fructose 1,6 bisphosphate + H20-> fructose 6 phosphate
Fructose 1,6 bisphosphotase
Thermodynamically spontaneous

221
Q

What does pyruvate need to be converted to first before step 10 of glycolysis? What enzyme is needed? What else is needed?

A

Oxaloacetate
Pyruvate carboxylase
ATP + CO2

222
Q

How is step 10 reversed in gluconeogenesis. Pyruvate has already been converted to oxaloacetate using pyruvate carboxylase. What next?
End product
Enzyme
Require components

A

Oxaloacetate-> phosphenolpyruvate +CO2
Phosphoenolpyruvate carboxykinase PEPCK
GTP drives it

223
Q

What mainly controls rate of gluconeogenesis?

A

Hormonal control (glucagon and insulin)

224
Q

What inhibits PEPCK and fructose 1,6 bisphosphotase?

A

Insulin

225
Q

What stimulates PEPCK and fructose 1,6 bisphosphotase

A

Glucagon

226
Q

In diabetes, what is the outcome of gluconeogenesis?

A

No insulin means gluconeogenesis is stimulated, contributing to hyperglycaemia

227
Q

The TCA cycle occurs where

A

Mitochondria

228
Q

What is the Acetly coa converted into by going through the TCA cycle

A

2 CO2

229
Q

What does the TCA produce?

A

Some ATP, some NADH, FADH2,GTP

Precursors for biosynthesis

230
Q

What does the TCA not function without

A

O2

231
Q

How many ATP are directly produced from TCA

A

2

232
Q

After the TCA how many net molecules of ATP have been produced?

A

4

233
Q

In the TCA Acetly Coa is converted into what by getting added on to what?

A

Acetyl coa (c2) + oxaloacetate (c4)-> citrate (c6)

234
Q

Citrate is converted into ISO citrate in the TCA. What is the next step?
Enzyme
Products

A

Isocitrate(C6)-> alpha ketoglutarate (C5)+CO2
Isocitrate dehydrogenase
NAD+ -> NADH

235
Q

Alpha ketoglutarate (C5) in the TCA (converted form iso-citrate) goes on to form what?
Enzyme
Products

A

Alpha ketoglutarate (C5) + CoA -> Succinyl-CoA (C4) + CO2
Alpha ketoglutarate dehydrogenase
NAD+ -> NADH

236
Q 
Succinylcholine CoA (C4)(in TCA) is converted to what
What are the products
A

Succinate (C4)+ CoA

GDP-> GTP

237
Q

What is converted to oxaloacetate in the TCA

A

Malate

238
Q

In the TCA what molecules are precursors for amino acids (and where amino acids can feed into TCA)

A

Malate
Oxaloacetate
Alpha ketoglutarate
Succinate

239
Q

What molecule in the TCA goes on in the synthesis of haem?

A

Succinate

240
Q

What molecule in TCA goes on to form fatty acids?

A

Citrate

241
Q

At the end of TCA what has happened to the original glucose molecule

A

All C-C bonds broken
All C atoms oxidised to CO2
All C-H bonds broken
H atoms transferrred to NADH or similar

242
Q

What is the electron transport chains purpose?

A

Released energy providing free energy to drive ATP synthesis with oxidative phosphorylation

243
Q

What do PTCs set up in the ETC

A

The proton motive force

244
Q

What is the proton motive force?

A

Electrochemical gradient of protons on the intermembrane space, wanting to move to the inner membrane

245
Q

Once the PTC have set up the PMF, what happens

A

ATP synthase provides the only route back. It drives the synthesis of ATP

246
Q

How much energy is actually used in moving the H+ across the membrane? What happens to the rest

A

30% the rest is lost as heat

247
Q

How is the ETC regulated?

A

If atp is high there is no substrate (ADP) for atp synthase to use, this increases the H+ in the intermembrane space, this stops the H+ pump (reverse with low atp)

248
Q

What do uncouplers do in relation to the ETC

A

Increase permeability of the mitochondrial membrane to protons, dissipating the PMF

249
Q

What does brown adipose tissue have to generate heat

A

Thermogenin (ETC uncoupler)

250
Q

What is creatine phosphate

A

Small energy store in cardiac and skeletal muscle

251
Q

When is creatine phosphate production favoured/

A

When atp is high

252
Q

How is creatine phosphate produced

Enzyme

A

Creatine + ATP-> creatine phosphate and adp

Creatine kinase

253
Q

What is creatinine?
How’s it made
What do its levels indicate

A

It’s a breakdown product of creatine and creatine phosphate
Non enzymatic change
High levels seen when muscle breakdown levels high (could be due to large muscle mass or pathological)

254
Q

What does a high blood creatine and a low urine creatine indicate?

A

Impaired kidney function

255
Q

What is iron stored in the liver as?

A

Ferritin and haemosiderin

256
Q

What is ferritin?

A

Protein with capacity of about 4500 iron ions

257
Q

The iron stored as a complex in haemosiderin differs from ferritin stored iron how?

A

It is physiologically acitive

258
Q

What is ferritin?

A

Protein with capacity of about 4500 iron ions

259
Q

What’s DMT1

A

Duodenal metal transformer 1- transports ferrous iron

260
Q

Where calcitonin produced?

A

Parafollicular cells of the thyroid

261
Q

What does calcitonin do?

A

Reduce blood calcium levels, opposing parathyroid hormone

262
Q

What’s fatty acyl synthase?

A

Multi enzyme protein that catalyses fatty acid synthesis

263
Q

What surgery is used for pituatry tumours?

A

Transphonoidal

264
Q

When is blood cortisol tested?

A

Midnight

265
Q

What is TAILS in reference to microcytic anaemia causes?

A 
Thalassaemia
Anaemia of chronic disease (can be normo)
Iron defficent anaemia
Lead poisoning
Sideroblastic anaemia
266
Q

What are the endocrine cells of the pancreas?

A

Islets of langerhann

267
Q

What phosphate is hydrolysed for work in atp

A

Y

268
Q

What is the action of metformin?

A

Inhibit hepatic gluconeogenesis lowering plasma glucose

269
Q

What are the 4proteins of the RBC cell membrane

A

Ankyrin, spectrin, protein 4.2 and band 3

270
Q

What vitamin protects against lipid peroxidation?

A

Vitamin E

271
Q

What’s a broken fragmented rbc called

A

Schistocyte

272
Q

If Gibbs free energy is below 0 the reaction is what?

A

Exergonic

273
Q

Equation for BMI

A

Kg/ height in M squared

274
Q

Where is the energy bond in ATP

A

Between beta and gamma phosphate

275
Q

10 calories is how many kilojoules?

A

42 (x4.2)

276
Q

What’s carbohydrates general formula?

A

(CH2O)n

277
Q

What is the formulae for aldehyde?

What is it for keto group?

A

C=OH aldehyde

C=O keto

278
Q

What are the disaccharides sucrose, maltose and lactose made up of?

A

Sucrose- glucose and fructose
Maltose glucose x2
Lactose- galactose and glucose

279
Q

What are routine maintainance iv fluids made up of?

A

1mmol/kg/day of Na+, K+ and Cl-

30ml/kg/day of water

280
Q

A deficency in vitamin a results in what?

A

Xerophthalmia

281
Q

Deficency in vit d results in what

A

Rickets

282
Q

Deficency in vit E results in what?

A

Neurological abnormalities

283
Q

Deficency in vitamin K results in what

A

Clotting abnormalities

284
Q

Examples of dietary fibre include?

A

Cellulose, lignin, pectins, gums

285
Q

Cellulose is a polymer of what?

A

Glucose with beta 1,4 bonds

286
Q

What’s the RDI fibre

A

18g

287
Q

What are some risks of low dietary fibre

A

Constipation, bowel cancer.

High fibre decreases cholesterol

288
Q

What is daily energy expenditure comprised of?

A

BMR+ diet induced thermogenesis + Physical activity

289
Q

What’s BMR

A

Energy required to maintain cellular function

290
Q

What’s BMI

A

Kg/M2

291
Q

What’s an alternative measure to BMI

A

Waist hip ratio

292
Q

What’s kwashiorkor disease

A

Low protein dietary resulting in insufficient plasma oncotic pressure and oedema

293
Q

What is pancreatic amylases role when a disaccharide attaches to the brush border?

A

Breaking alpha 1,4 glycosidic bonds

294
Q

What’s isomaltases role when a dissacharide attaches to the brush border?

A

Breaking alpha 1,6 glycosidic bonds

295
Q

What is primary lactase deficency likely due to/

A

Absence in lactate persistence allele

296
Q

What’s secondary lactase deficency likely due to?

A

Injury to the small intestine eg crohns or ulcerative colitis

297
Q

How is glucose absorbed into intestinal epithelial cells?

A

Sodium dependent glucose transporter 1 SDGL1

298
Q

Once the sodium dependent glucose transporter has taken glucose into the cell what puts it into the blood supply?

A

GLUT 2

299
Q

GLUT2 receptors for glucose are located were? What’s important about them?

A

Kidney
Liver
Pancreatic
Small intestine

They arent regulated by insulin

300
Q

GLUT4 receptors are found where for glucose?

A

Striated muscle and adipose tissue

301
Q

What are some cells that have an absolute glucose requirement? And why is that?

A

RBC- no mitochondria
Neutrophil- mitochondria needed for resp burst
Inner kidney medulla- low o2
Lens of eye

302
Q

What does the CNS use for energy

A

Primarily glucose, also ketone bodies

303
Q

Where does glycolysis take place?

A

Cytosol

304
Q

What are the 2 stages of glycolysis

A

Investment -2atp

Payback +4 atp

305
Q

What’s the difference between hexokinase and glucokinase

A

Hexokinase is not in the liver and is inhibited by its product G6P

306
Q

What happens to glucose uptake in cancer cells? Why is that relevant?

A

Increases up to 200x

Imaging with radioactive hexokinase

307
Q

How is PFK regulated?

A

Allosterically in muscle by ATP: ADP ratio

Hormonally in liver by insulin: glucagon ratio

308
Q

What is glycerol 3 phosphates role?

A

Convert dihydroxyacetone-P to glycerol phosphate for TAG synthesis

309
Q

What is BPG mutase role?

A

Conver 1-3 BPG to 2-3 BPG

310
Q

What is the purpose of lactate production?

A

Regenerate NAD+

311
Q

When is the conversion of lactate back to pyruvate by LDH impaired?

A

Alcohol metabolism
Liver disease
Thiamine defficency

312
Q

A lactate of 2-5mm is what? What happens?

A

Hyperlactaemia, no change in PH due to buffering capacity of blood

313
Q

When lactate exceeds 5 mmol what happens

A

PH change of blood

314
Q

What are the 3 enzymes of galactose metabolism

A

Galactokinase
Uridyl transferase
UDP galactose epimerase

315
Q

What enzymes are involved in fructose metabolism? What do there defficencies result in?

A

Fructokinase (fructosemia)

Aldolase ( F1P accumulation and liver damage)

316
Q

What is the role of the PPP

A

Produce C5 intermediate

Source of NADPH for biosynthesis

317
Q

Main enzyme in the PPP

A

G6PDH

318
Q

How is pyruvate kinase controlled in glycolysis

A

Insulin:glucagon ratio

319
Q

How else is glycolysis controlled, not at an enzymatic level?

A

Metabolically by NADH;NAD ratio

320
Q

PDH is a large multienzyme complex made of how many enzymes?
What deficency is it sensitive too (req for its cofactors)?
What does it do?

A

5
B1 vitamin
Reduce pyruvate to Acetly coa

321
Q

With a deficency in PDH what is seen in the blood?

A

Lactic acidosis

322
Q

What inhibits PDH, what activate it?

A

Inhibit: Acetly coa, Citrate (forward product), NADH, ATP (high energy)
Stimulate: pyruvate, ADP, NAD+, insulin

323
Q

What does Acetly coA combine with in the TCA to form?

A

Combines with oxeloacetate to form citrate

324
Q

What are the 2 steps in TCA where CO2 is lost? What enzymes facilitate this?

A

Isocitrate-> ketoglutarate (isocitrate dehydrogenase)

Alpha ketoglutarate-> succinyl coa (alpha ketoglutarate dehydorgenase)

325
Q

How many cycles of the TCA for each molecule of glucose?

A

2

326
Q

What are present in the mitochondria to set up the PMF

A

Proton translocating complexes PTC

327
Q

How is the electron transport chain regulated?

A

In high ATP there is less substrate for ATP synthase to use, H+ builds up in the intermembrane and this inhibits the PTC pump

328
Q

What is the difference between an inhibitor of the ETC and an uncoupler?

A

An inhibitor blocks the ETC resulting in no PMF

Uncouplers increase the permeability of the mitochondira to protons resulting in less effective PMF generation

329
Q

What does brown adipose tissue have a lot of for heat production

A

Thermogenin

330
Q

What are some key features of oxidative phosphorylation

A

Requires membrane complexes
Indirect energy coupling
Can’t occur in abscence of oxygen
Minor process in atp generation

331
Q

What are some key features of substrate level phosphorylation

A

Requires enzymes
Direct energy coupling
Can occur without o2
Minor process of atp production

332
Q

What do phospholipids have as well as the carbon, hydrogen and oxygen you would see in a lipid?

A

P and N

333
Q

The average man 70kg would approx how much TAG? How much would an obese 100kg man have roughly?

A

15kg

45kg

334
Q

A chylomicron can go where? Where can it not go?

A

Adipose tissues for storage
Consumer tissue for utilisation of fatty acids
Can’t go RBC, WBC (mitochondria needed) or brain as BBB

335
Q

How can excess glucose be stored as fat?

A

Converted to glycerol 1 p

Combine with fatty acyl coa in esterfication

336
Q

Why are there essential polyunsaturated fats like linolenic acid?

A

Because the body cant synthesise double bonds after c9 compound.

337
Q

What are the 3 steps in fatty acids metabolism and where are they occuring

A

1- fatty acyl coa synthase links CoA to the fatty acid (outside mito)

  1. Carnitine shuttle transports into mitochondria (inhibited by malonyl coa)
  2. Beta oxidation
338
Q

How can glycerol be utilised? Both anabolically and catabolically.

A
  1. Glycerol kinase enzyme used to make glycerol phosphate in liver
  2. Then can anabolically combine with fatty acids to make tag or be synthesised into DHAP and enter glycolysis
339
Q

How can acetyl CoA be used anabolically and catabolically

A

Catabolic- TCA
Anabolic- fatty acid synthesis (fatty acyl synthase and Acetly coa carboxylase)
Cholesterol/ ketone bodies (HMG CoA +/- reductase or lyase)

340
Q

If insulin is high what is more likely to be formed cholesterol or ketone bodies?

A

Cholesterol

341
Q

If glucagon is high what is more likely to be formed from HMG?

A

Ketone bodies rather than cholesterol

342
Q

What is the target of statins?

A

HMG CoA reductase

343
Q

What are 2 outcomes of high ketone bodies?

A

Ketoacidosis (acetoacetate and beta hydroxybutyrate strong organic acids)
Ketouria (above renal threshold)

344
Q

How are lipids hydrolysed in digestion?

A

Pancreatic lipases

345
Q

Hormone sensitive lipase is upregulated how?

A

Increased glucagon

346
Q

How are fatty acids carried to tissues for utilisation?

A

Bound to albumin as fatty acid complex

347
Q

What is the general formula for esterfication

A

Glycerol 1-P +fatty acyl coA-> TAG

348
Q

What’s the general formula of lysis of a TAG

A

TAG-> fatty acid (bound to albumin in blood)+ Glycerol

349
Q

How is a fatty acid re-esterfied?

A

Conversion to fatty acyl coa

350
Q

Where are ketone bodies synthesised?

A

Liver mitochondira

351
Q

What’s HMG CoA synthase role?

A

To make HMG CoA from Acetly CoA

352
Q

What’s the calorie requirement for the BMR of average person of 70kg

A

1700 (x4.2 for kj)

353
Q

What’s an exergonic reaction?

A

Releases energy, -ve Gibbs

354
Q

Is NAD+ reduced?

A

No its oxidised

355
Q

What is an indicator of muscle breakdown?

A

Creatinine

356
Q

What does creatine kinase enzymatically work on?

A

Conversion of creatine to phosphocreatine

357
Q

What is alcohol broken down into (end product after acetaldehyde dehydrogenase) what is that then used for?

A

Acetate-> acetyl coa for glycolysis or tag synthesis

358
Q

What other things can oxidise alcohol?

A

Cyp450- cypb2e

Catalase in brain

359
Q

How many units of alcohol are recommended per week?
How many in half a pint?
How quickly do we get rid of alcohol

A

14 spread over at least 3 days
1 unit, 8g alcohol
7g per hour

360
Q

What do free radicals damage?

A

Nucleic acids, proteins, lipids.

361
Q

Is hydrogen peroxide a free radical?

A

No but can create hydroxyl radical when it reacts with iron in Fenton reaction

362
Q

How can ROS damage DNA

A

React with base resulting in modified base that can cause mispairing
React with sugar backbone causing strand break

363
Q

How can ROS damage protein

A

Damage backbone causing fragmentation

Damage side chain altering function

364
Q

What bonds can ROS cause?

A

Inappropriate disulphide bonds

365
Q

What effect can ROS have on lipids?

A

Lipid peroxidation

366
Q

What uses resp burst?

What’s released?

A

Neutrophils, macrophages

Superoxide, hydrogen peroxide

367
Q

How does superoxide dismutase and catalase work together to manage ROS

A

Superoxide dismutase converts superoxide to H2O2 and oxygen

Catalase converts H2O2 to H2O and oxygen

368
Q

What does glutathione (GSH) have that makes it an antioxidant?
What enzyme?

A

An electron to donate with the help of enzyme glutathione peroxidase.
It makes a double bond with another GSH to make GSSG

369
Q

How is GSSG converted back to GSH for anti-oxidant properties?
What enzyme
What else does it need and where does it get it from?

A

Glutathione reductase

Needs NADPH from PPP

370
Q

Why do you get Heinz bodies with G6PDH defficency

A

No NADPH to regenerate glutathione resulting in ROS damage to haemoglobin

371
Q

Why do you get damage to the lens of the eye with galactasamia

A

Aldose reductase uses up all NADPH so glutathione regen cant happen and ROS damage lens

372
Q

How do Vit E and Vit C work together as antioxidants

A

Vit E is a free radical scavenger. Vit C regenerates vit E to its active form

373
Q

How is paracetemol normally metabolised? Not in toxic dose

A

Conjugation with glucorinide or sulphate and then excreted

374
Q

What happens when there is toxic levels of paracetemol?

A

NADPQ1 accumulates. Direct toxic effect to lipids, proteins, dna.
Also decreases glutathione leading to ROS damage

375
Q

What is given in paracetemol overdose? Why

A

Aceylcysteine to replenish glutathione

376
Q

What is a measure of oxidative Dave

A

Amount of 8-oxo-dog

377
Q

What is chronic granulomatous disease a result of?

A

Genetic defect in NADPH oxidase complex.
No NADPH means no resp burst
Enhances susceptibility to bacterial infection

378
Q

Some symptoms of galactosaemia?

A 
Hepatomegally
Renal failure
Seizures
Hypoglycaemia
Cataracts
379
Q

Name a glucogenic, ketogenic and either type of amino acid

A

Glucogenic- glycine
Ketogenic- leucine
Both- isoleucine

380
Q

What makes up an amino acid?

What bonds do they form?

A

Amine group, carboxyl group and a variable r region

Peptide bonds

381
Q

What coenzyme do aminotransferases from

A

B6 vitamin derivative

382
Q

Why does a UTI smell?

A

Bacteria breakdown releasing ammonia

383
Q

How can high levels of ammonia give us issues?

A

Disrupts cerebral blood flow
Makes ph more alkaline
Interferes with amino acid neurotransmitters

384
Q

What important nitrogen containing compound is found in skeletal muscle?

A

Creatine

385
Q

Why is meat protein a favourable source of amino acids

A

Has all essential aminos

386
Q

What do most amino transferase use as substrate and product? What’s the exception

A

Most use conversion of alpha ketoglutarate to glutamate

Aspartate aminotransferase uses oxaloacetate to aspartate

387
Q

What does ALT do?

What does AST do?

A

ALT- alanine to glutamate

AST- glutamate to aspartate

388
Q

What is deammination?

A

Liberation of amino group as free ammonia

389
Q

What enzymes can deaminate?

A

Amino acid oxidases
Glutaminase
Glutamate dehydrogenase

390
Q

Defects in the urea cycle result in what generally?

A

Hyperammonia

Accumulation or excretion of urea cycle intermediates

391
Q

What are 2 mechanisms for disposal of ammonia from tissues?

A
  1. Combine with glutamate to make glutamine. Travels to liver where glutaminase converts it back. Or to kidney where ammmonia directly excreted
  2. Combine with pyruvate to make alanine. Travel to liver where ALT transaminases it
392
Q

What is phenylketonuria a defficency of?

A

Phenylalanine hydroxylase

393
Q

What is the outcome of phenylketonuria (due to defficent in phenylalanine hydroxylase)

A 
Phenylketones in urine
Less tyrosine (phenylalanine converted product)
394
Q

What’s homocystinuria a defficency in?

A

Cystathione beta synthase

395
Q

In homocystinuria what accumulates?

A

Methionine and homocysteine

396
Q

What’s normal blood glucose level

A

5mmmol/litre

397
Q

What’s a marker for diabetes?

A

Glycated haemaglobin c

398
Q

What’s the central protein in glycogen?

A

Glycogenin

399
Q

What enzyme converts glucose 1 phosphate to UDP glucose for glycogen storage?

A

G1p uridyltransferase

400
Q

How do muscles keep the glucose 6 phosphate within the muscle when it has been broken down from glycogen?

A

Lack of glucose 6 phosphotase enzyme

401
Q

How is muscle glucagon alloserically regulated?

A

AMP an activator of glycogen phosphorylase

402
Q

Importantly what do LDL lack and what does that result in?

A

They lack apoC and apoE. They are not efficiently cleared by the liver.
Longer half life increases susceptibility to oxidative damage and therefore the chance of getting taken up by macrophages to form foam cells.

403
Q

What do cells requiring cholesterol express?

What acts as a ligand for this receptor

A

LDL receptors

ApoB-100 on LDL acts as ligand

404
Q

What is LDL receptor expression controlled by?

A

Cholesterol concentration of the cell

405
Q

What’s the difference between a Micelle and a liposome

A

Micelle is single layer of phospholipid and liposome double

406
Q

What is cholesterol essential for? 3

How is it transported around the body? What enzyme

A

Components of membranes modulating fluidity
Steroid precursor
Bile acid precursor

Transported as cholesterol ester
Enzyme LCAT

407
Q

What does a lipoprotein have?

What are the 5 distinct classes?

A

Phospholipid monolayer
Peripheral and integral apolipoproteins
Cargo- TAG, cholesterol ester, DEAK

VLDL, IDL, LDL, HDL, chylomicron

408
Q

When are chylomicrons normally present in the blood?

A

4-6h after a meal

409
Q

What apolipoproteins are important in VLDL, IDL, LDL and HDL?

A

ApoB in VLDL, IDL, LDL

ApoAI in HDL

410
Q

How does a chylomicron know to deposit its cargo to adipocytes and muscle?

A

ApoC binds to lipoprotein lipase.

411
Q

What apolipoproteins binds to hepatocytes?

A

apoE

412
Q

What is HDL role?

A

Reverse cholesterol transport. Removes cholesterol from cholserol laden cells.
ABCA1 protein within cell facilitates transfer of cholesterol to HDL
Converted to ester with LCAT

413
Q

What is the fate of mature HDL?

A

Taken up by liver
Scavenger receptor on cells requiring cholesterol
Exchange cholesterol for TAG with VLDL via cholesterol exchange transfer protein

414
Q

What do chylomicrons transport?
VLDL
LDL
HDL

A

Chylo- TAG from diet
VLDL- TAG from liver
LDL- cholesterol from liver
HDL- excess cholesterol

415
Q

What are 3 clincal signs of high levels of blood cholesterol?

A

Xanthelasma- yellow eyelid patches
tendon Xanthoma- nodules on tendon
Corneal Arcus- white circle around eye

416
Q

Treatment of hyperlipoproteinaemias ?

A

States- inhibit HMG CoA Reductase
Bile salt sequestrant- forces liver to produce more bile acids using up cholesterol

DIet and exercise

417
Q

What does protein deficency in children results in?

A

Growth failure
Impaired physical development
Impaired mental development
Negative nitrogen balance
Oedema due to lack of albumin
Increased risk of infection due to reduced immunoglobulin
Anaemia due to reduced haemoglobin synthesis
Fatty liver due to reduced Lipoprotein synthesis

418
Q

Why are the CNS and heart particularly succeptible to damage in low energy stages, ie ischaemia

A

Both lack fuel storage therefore require constant supply (CNS specifically glucose and ketone)

419
Q

What would skeletal muscle use in times of anaerobic metabolism?

A

Glycogen as fuel

Myoglobin for oxygen

420
Q

A 30 year old woman presenting with stomach pain and diarrhoea after smashing 15 litres of milk likely has what?

A

Lactase defficency

421
Q

How is lactate processed in the heart compared to the liver?

A

Heart- pyruvate from lactate is oxidised via TCA

Liver- could be oxidised but most pyruvate gets converted to glucose.

422
Q

When raised lactate seen?

A

Raised production- meal, shock, exercise, heart disease

Reduced utilisation- liver disease, thiamine defficency, alcohol metabolism

423
Q

What is the specific need for glycolysis in RBC (apart from energy)

A

Production of 2,3 BPG from 1,3 BPG

424
Q

What is the specific use of glycolysis in adipose cells (not energy production)

A

Glycerol phosphate production from dihydroxyacetone phosphate for esterfication of fatty acids

425
Q

What is PDH relation under control mechanisms for? What does it ensure?

A

Acetyl coa from beta oxidation of fart acids rather than glucose as Acetly coa inhibits it
Enzyme activated when there is plenty of glucose to catabolise (insulin)

Ensures glucose isn’t rapidly used up

426
Q

What is used in the ETC to move protons from the inside to the outside of the inner membrane?

A

Free energy

427
Q

What is required for ketone synthesis

A

Fatty acids available for oxidation following excessive lipolysis
Fall in plasma insulin

428
Q

What is inadequate for fatty acid oxidation in alcohol metabolism?

A

NAD+ as acetaldehyde and alcohol dehydrogenase produce NADH

429
Q

Why do TAGS accumulate with alcohol (in liver)

A

Increased TAG synthesis and a reduced capacity for the liver to export these due to lower lipoprotein synthesis

430
Q

How are superoxide radicals produced in the mitochondria

A

During oxidative phosphorylation about 0.1 - 2% of electrons do not reach the end of the electron transport chain and they prematurely reduce oxygen to from superoxide radicals (O2 -).

431
Q

Name some agents that protect the cell against reactive oxygen species

A 
Superoxide dismutase
Catalase
Glutathione
NADPH
Antioxidant C and E vit
432
Q

What is the relationship between NADPH and glutathione

A

NADPH reduces oxidise glutathione to its reduced form via the enzyme GSH reductase

433
Q

How is the respiritory burst created in leukocytes

A

Produced by a member a bound enzyme complex termed NADPH oxidase

434
Q

What is an early step in the catabolism of amino acids?

A

Removal of amino group to be converted to uraea

435
Q

What do ketogenic amino acids produce?

A

Acetly Coa

436
Q

What do glucogenic amino acids produce

A

Products that can be used fro glucose synthesis

437
Q

What are L and D amino acid oxidases

A

Enzymes that have low specificity to convert amino acids to keto acids and NH3

438
Q

What is Glutaminase?

A

High specificity enzyme that converts glutamine to glutamate and NH3

439
Q

What is glutamate dehydrogenase?

A

High specificity enzyme that catalyses the reaction of glutamate to alpha ketoglutarate and NH4

440
Q

What precursors can be used for gluconeogenesis

A

Lactate
Pyruvate
Glycerol
Amino acids

441
Q

What enzyme means liver can export glycogen breakdown products but muscle cant?

A

Glucose 6 phosphotase

442
Q

Why are TAG more efficient as energy storage than Glycogen?

A

They are hydrophobic and anhydrous
Whereas glycogen is polar and is stored in water

Also taG more reduced so more energy

443
Q

What is required before beta oxidation can occur of fatty acids

A

Activation by linking to CoA (requires ATP)

Carnitine transporter

444
Q

What are some key benefits of lipogensis and fatty acid degredsation not being simple reversal of each other

A

has more flexibility as different substrates and intermediate
Better controlled as not reciprocal

445
Q

How are TAGS obtained from chylomicrons and VLDLS

A

Extracellular lipoprotein lipase in capillary beds of tissue
Hydrolysis to fatty acid and glycerol
Fatty acid taken up and re-esterfied to TAG using glycerol from glucose metabolism

446
Q

How is cholesterol obtained from LDL

A

Receptor mediated endocytosis

447
Q

Why would an individual with a defect in enzyyme lethicin cholesterol acyltrasnferase produce unstable lipoproteins ?

A

Lipoproteins only stable in spherical shape dependent on ratio of core to surface lipids

Stability restored when suraface lipid converts to core lipid (by LCAT)
Converts cholesterol on surface to cholesterol ester

Deficency results in instability and therefore deposition

448
Q

What is catabolism? Key features

A

Oxidative and exergonic

Generates ATP, reducing power and building blocks

449
Q

What is anabolism?

A

Reductive and endergonic, synthesis of macromolecules

450
Q

What are the bodies normal fuels?

And special fuels?

A

Normal- glucose in the form of circulating glucose and glycogen
Fatty acids stored as TAG
Special- amino acids- ketogenic or glucogenic
Ketone- from fatty acids
Lactate- conversion to glucose via cori cycle

451
Q

What’s an advantage of using lactate for energy? What cycle?

A

Cori cycle

No investment phase as goes in as G6P

452
Q

What are some key points regarding the TCA cycle

A

4 carbon oxaloacetate and 2 carbon pyruvate make 6 carbon citrate
Isocitrate the key enzyme- inhibited by NADPH and acitvated by ADP
NADH and FADH2 are made and GTP made from substrate level

453
Q

What are some key points re the ETC

A

Electrons in intermembrane space to pump H+

Complex 1,3,4 move the H+

454
Q

What are some key points to fatty acid oxidation?

A

Linked to coenzyme A by fatty acyl coa synthase
Carnitine shuttle to inner membrane that is inhibited by malonyl coa (a fatty acid synthesis intermediate)
Produces NADH and FADH2 and acetate that goes on to Acetly coa

455
Q

What are some key points to ketone body production

A

Made in liver mitochondria from acetyl coa

Glucagon activates and insulin inhibits

456
Q

What’s the order in which the body uses up fuels as you go from fed to starvation

A

Glucose-> glycogen->fat-> amino acids, glycerol and lactate-> ketones

457
Q

When glucose is low how is glucose sparred from the muscles?

A

No glut 4 on cell therfore fatty acids used

458
Q

What happens hormonaly in starvation?

A

Glucagon and cortisol released causing breakdown of protein and fat
Reduction of insulin and anti insulin affects (preventing cells using glucose)
Glycerol from fat enters gluconeogensis to spare porotein breakdown

459
Q

In muscles how much to myosin atpase account for atp turnover?

A

70%

460
Q

How would energy systems be used in sprinting

A

Initial creatine phosphate stored

Followed by anaerobic glycolysis and muscle glycogen

461
Q

How does exercising muscle get its glucose?

A

Amp causes glut 4 translocation

462
Q

Fatty acids can sustain exercise for how long? What limits them?

A

48H

Carnitine shuttle

ESA 2 (10 decks)

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