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Esa 1 > Metabolism > Flashcards

Metabolism Flashcards

0
Q

Describe the relationship between catabolism and anabolism

A

Catabolism produces reducing agents and energy for anabolism to take place.

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1
Q

Define metabolism

A

The processes which derive energy and raw materials from food stuffs and use them to support repair, growth and activity of tissues of the body.

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2
Q

Define homeostasis and what is its importance?

A

The control of the internal environment within set limits and it is a dynamic equilibrium. Failure of homeostasis leads to disease.

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3
Q

What is BMI? How is it calculated?

A

A simple way to estimate desirable weight. It stands for Body Mass Index. Calculated by weight (kg)/(height(m))^2

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4
Q

How do you interpret BMI results

A 
Underweight=18.5 or lower
Desirable= 18.5-24.9
Overweight= 25-29.9
Obese= 30-34.9
Severely obese= 35 or over
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5
Q

Define daily energy expenditure

A

Energy required for:

  1. BMR
  2. Voluntary physical activity
  3. Energy required to process food (diet-induced thermogenesis)
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6
Q

Define basal metabolic rate (BMR)

A

Measure of basal energy required to maintain life and functioning of tissues at physical, emotional and digestive rest.

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7
Q

What are the percentages associated with BMR?

A

Skeletal muscle= 30%
Central nervous system= 20%
Liver= 20%
Heart= 10%

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8
Q

How do you get a rough estimate for BMR?

A

A very rough estimate for BMR is the weight (kg) X 100
So 70kg man= about 7000kJ
And 58kJ woman= about 5800kJ

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9
Q

What are approximate value of daily energy requirement?

A

A 70 kg man at normal activity level will need about 12000kJ (2800kcal) to support BMR, voluntary physical activity and processing of food.

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10
Q

What does voluntary physical activity encompass?

A

Reflects the energy demands of skeletal muscles, heart muscle and respiratory muscles.
The energy required will vary dependant on intensity and duration of activity.

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11
Q

What are rough values of energy required at different energy levels in voluntary physical activity?

A

Sedentary person- 30kJ/Kg/day
Moderate activity- 65KJ/Kg/day
Very active- 100kJ/Kg/day

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12
Q

What are the energy levels available from different foods?

A

Carbohydrate- 17000kJ/kg
Protein- 17000kJ/kg
Lipid- 37000kJ/kg
Alcohol- 29000kJ/day

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13
Q

What are the essential components of the diet?

A 
Carbohydrates
Protein
Fat
Vitamins and minerals
Water
Fibre
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14
Q

What do the essential components of the diet provide us with?

A 
Carbohydrate- mostly energy
Protein- energy and amino acids
Fat- energy and essential fatty acids
Vitamins and minerals- essential for life
Water- maintains hydration 
Fibre- necessary for normal GI function
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15
Q

How is energy intake linked to body weight?

A
  • If energy intake is equal to expenditure then body weight will be stable
  • if energy intake exceeds expenditure then energy stores will increase (body weight increase)
  • if expenditure is greater than intake first energy will deplete then other body components (protein) will be utilised to provide energy (body weight decreases)
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16
Q

What is energy needed for?

A

1-Biosynthetic work (synthesis of cellular components (anabolism))
2-Transport work (membranes a- maintenance of ion gradients
b- nutrient uptake)
3-Specialised functions:
-mechanical work- muscle contraction
-electrical work- nervous impulse conduction
-osmotic work- kidney

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17
Q

Give examples of major carrier molecules

A

Nicotinamide adenine dinucleotide (oxidised form:NAD+, reduced form:NADH + H+)
Nicotinamide adenine dinucleotide phosphate. (oxidised form:NADP+, NADPH + H+)
Flavin adenine dinucleotide (oxidised form:FAD, reduced form:FADH2)

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18
Q

What are high and low energy signals and how do they regulate pathways?

A

When ATP is HIGH, anabolic pathways are activated

When ATP is LOW, and ATP and AMP are HIGH, catabolic pathways are activated

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19
Q

What is creatine phosphate used for?

A

Can provide a short time boost to ATP levels when levels fall. This is because the creatine is converted to creatine phosphate when ATP levels are high and this reaction is reversed to release a phosphate group on the ADP when needed.

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20
Q

What enzyme is associated with creatine phosphate?

A

Creatine kinase

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21
Q

What is the presence of a particular isoform of creatine kinase in the blood used to diagnose?

A

MI, the isoform is released from cardiac myocytes (cells) when damaged, in a myocardial infarction. It appears in the blood after few hours.

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22
Q

What is creatinine?

A

Produced by a spontaneous reaction at a constant rate unless the muscle is wasting. It is a breakdown product of creatine (and creatine phosphate)

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23
Q

What does creatinine excretion over 24h show?

A

It is proportional to muscle mass of the individual

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24
Q

What does creatinine concentration in urine show?

A

It is a marker of urine dilution so can be used as a benchmark for measuring other concentrations in the urine

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25
Q

How is reducing power converted to ATP?

A

Oxidative phosphorylation

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26
Q

Give an overview of stage 1 catabolism

A 
Breakdown of large molecules to building block molecules
Extra cellular (GI tract)
No energy produced
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27
Q

Give an overview of stage 2 catabolism

A

Intercellular (cyotosolic and mitochondrial)
Building block molecules (many) to simple molecules (few)
Oxidative (coenzymes are reduced e.g. NAD+ to NADH)
Some energy produced

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28
Q

Give an overview of stage 3 catabolism

A 
Mitochondrial
Single pathway- tricarbxylic acid cycle (TCA or Krebs cycle)
Oxidative requires NAD+ and FAD
Some energy produced directly
Acetyl converted to 2 CO2
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29
Q

Give an overview of stage 4 catabolism

A 
Mitochondrial
Electron transport and ATP synthesis
NAD and FAD2H re-oxidised
O2 required (reduced to H2O) 
Large amounts of ATP produced
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30
Q

What are carbohydrates?

A 
General formula (CH2O)n
Contain aldehyde (-CHO) or keto (-C=O) group
Multiple -OH groups
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31
Q

What is a polymer of glucose and where is it found in animals?

A

Glycogen
Major store of energy in mammals
Highly branched 1-4 and 1-6 bonds

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32
Q

What is a polymer of glucose (plants)?

A

Starch
Less branched than glycogen
GI tract enzymes release glucose and maltose

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33
Q

Describe details of cellulose

A

Structural polymer of glucose found in plants
Beta 1-4 linkages
No GI enzymes to digest linkages
Dietary fibre important for GI function

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34
Q

Give a example of a stage 1catabolism enzyme

A

Amylase
Found in saliva and pancreas
Breaks down glucose polymers

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35
Q

What is the stage 2 catabolism called?

A

Glycolysis

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36
Q

What are the key feature of glycolysis?

A

Exergontic, oxidative
C6 to C3 (no loss of CO2)
With only one more enzyme, glycolysis is the only pathway that can operate anaerbically (no oxygen)

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37
Q

What charge is glucose given during stage 1 of glycolysis?

A

Negative (anionic)

This prevents passage back across the plasma membrane

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38
Q

How many moles of ATP are require to convert glucose to fructose 1,6 bis phosphate?

A

2 moles of ATP per mole of glucose

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39
Q

What is the first committing step that commits glucose to metabolism via glycolysis?

A

The conversion of fructose 6 phosphate to fructose 1,6 bis phosphate with a molecule of ATP

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40
Q

What happens to glucose during the first step of glycolysis?

A

It is phosphorylated to fructose 1,6 bis phosphate with the addition of 2 ATP

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41
Q

How many units is the fructose 1,6 bis phosphate cleaved into?

A

2
3 carbon units
The units are inter convertible

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42
Q

How many molecules of NADH are produced during glycolysis?

A

2 molecules

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43
Q

What are the end products of glycolysis?

A 
2 molecules of pyruvate 
2 molecules of ATP
2 molecules of NADH
2 H+
2 H2O
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44
Q

What is another name associated with glycolysis?

A

Substrate level phosphorylation

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45
Q

Name an important intermediate in glycolysis

A
  • DHAP which is converted to glycerol phosphate in the adipose tissue and the liver
  • 1,3 bis phosphate glycerate which is converted to 2,3 bis phosphate glycerate in RBC
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46
Q

What does 2,3- bis phosphate glycerate regulate?

A

It is a regulator of O2 affinity of haemoglobin (tense form)
Found in RBC at same molar concentration as haemoglobin (about 5mM)

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47
Q

Why is glycerol phosphate important?

A

It is important to triglyceride and phospholipid biosynthesis

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48
Q

Where are potential sites of control of glycolysis?

A

Enzymes catalysing irreversible steps are potential sites of control

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49
Q

Name a type of regulation

A

Allosteric (activator/inhibitor binds at a site other than the active site on the enzyme)

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50
Q

What happens when there is no more NAD+ for glycolysis?

A

NAD+ is regenerated by:
NADH + H+ + pyruvate NAD+ + lactate
So lactate and NAD+ are produced from NADH and pyruvate

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51
Q

Where is lactate produced?

A

Lactate is produced by RBC and skeletal muscles (skin, brain, GI)
Released into blood and metabolised by liver and heart

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52
Q

What is the enzyme responsible for the production (and conversion) of lactate?

A

Lactate dehydrogenase (LDH)

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53
Q

What 2 enzymes are required to metabolise fructose?

A

Fructokinase- if missing fructose is present in urine (essential fructosuria) no clinical signs
Aldolase- if missing fructose 1-P accumulates in liver resulting in damage (fructose intolerance) treatment is to remove fructose from diet

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54
Q

Where is galactose metabolised?

A

In the liver

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55
Q

What enzymes are required to metabolise galactose?

A

Galactokinease
Galactose-1-P uridyl transferase
UDP-galactose 4’-epimerase

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56
Q

What is galactose converted to so it can enter glycolysis?

A

Glucose-1-P which is then converted to glucose 6-P

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57
Q

What is galactosaemia?

A

The inability to utilise galactose

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58
Q

What different types of galactosaemia are there?

A
  • Galactokinease deficiency (rare) galactose accumulates

- transferase deficiency (common) galactose and galactose 1-P accumulate

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59
Q

What problems does galactosaemia cause?

A

Galactose enters other pathways
Is converted to galactitol. This also converts NADPH to NADP+
The depletion in levels of NADPH leads to damage to structures in places such as the eye so cataracts form (disulphide bridges)
Accumalation of galactose 1-P affects liver, kidney and brain

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60
Q

What is the treatment of galactosaemia?

A

No lactose in diet (lactose is consists of galactose and glucose)

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61
Q

What is the function of the pentose phosphate pathway?

A

1-to produce NADPH (used as a Biosynthetic reducing power and also to maintain free -SH (cysteine) groups on certain proteins (prevents cataracts))
2-produce C5 sugars for nucleotides for nucleic acid synthesis

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62
Q

What are the effects if the pentose phosphate pathway cannot take place? Lack of the enzyme glucose 6-phosphate dehydrogenase (G6PDH)

A

There will be a lack of NADPH so disulphide bridges will form between cysteine groups on some proteins and this will lead to cataracts in the eyes and heniz bodies in RBC

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63
Q

In general are lipids soluble in water?

A

No,con general they are insoluble (hydrophobic)

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64
Q

Where are triacylglycerols stored?

A

In the adipose tissues which is specialised for this purpose.
They can be used in prolonged exercise or starvation

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65
Q

What are triglycerides converted to?

A

Glycerol and fatty acids in the GI tract

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66
Q

What is type of enzyme responsible for the hydrolysis of lipids?

A

Lipase

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67
Q

Name some fat soluble vitamins

A

A
D
E
K

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68
Q

Where is glycerol metabolised?

A

In the liver

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69
Q

What enzymes are used in glycerol metabolism?

A

Glycerol kinase

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70
Q

What molecules are used in glycerol metabolism?

A

ATP

NAD+

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71
Q

What molecules are produced in glycerol metabolism?

A

ADP
glycerol phosphate (intermediate)
NADH
Dihydroxyacetone phosphate (enters glycolysis)

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72
Q

What is the name of the process that releases energy from fatty acids?

A

Beta oxidation

Occurs in mitochondria

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73
Q

Where does beta oxidation not occur?

A

In red blood cells (do not possess mitochondria)

Cells of the CNS (fatty acids do not readily cross the blood-brain barrier)

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74
Q

Outline fatty acid metabolism

A

1-FA is activated by linking to coenzyme A outside the mitochondrion
2-transported across membrane using carnitine shuttle
3-FA cycles through series of oxidative reactions with C2 removed each cycle

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75
Q

What is used in fatty acid metabolism?

A

FAD
H2O
NAD+

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76
Q

Does beta oxidation produce ATP?

A

No

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77
Q

What does beta oxidation stop in the absence of?

A

Oxygen

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78
Q

What is the main convergence point for catabolic pathways?

A

Acetyl CoA

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79
Q

How many ketone bodies are produced in the body and what are they?

A

3
Acetoacetate
Acetone
Beta-hydroxybutyrate

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80
Q

Where are acetoacetate and beta-hydroxybutyrate synthesised?

A

In the liver from Acetyl CoA

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81
Q

Where does acetone arise from?

A

The spontaneous (non-enzymatic) decarboxylation of acetoacetate

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82
Q

What are the concentrations of ketone bodies in the blood like and how and why do they vary?

A 
Normally low (less than 1 mMol/L)
Increases in starvation (2-10mmol/L) (physiological ketosis)
Increases in untreated type 1 diabetes (over 10 mMol/L) (pathological ketosis)
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83
Q

Why does the breath of untreated diabetes type 1 patients smell of nail polish remover?

A

Acetone is sometimes excreted via the lungs and acetone is nail polish remover

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84
Q

What happens to ketone body synthesis when insulin/glucagon ratio is high? (Fed state)

A

The enzyme lease is inhibited, reductase is activated so cholesterol is synthesised

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85
Q

What happens to ketone body synthesis when insulin/glucagon ratio is low? (Starvation)

A

Lease is activated, reductase inhibited, ketone body synthesis

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86
Q

What are ketone bodies used for?

A

They are important fuel molecules that can be used by all tissues contains mitochondria including the CNS

87
Q

How are ketone bodies used as fuel?

A

They are converted to Acetyl CoA and this is subsequently oxidised via stage 3 of catabolism

88
Q

Why is Acetyl CoA important?

A

It is the main convergence point for catabolic pathways

It is an important intermediate in both catabolic and anabolic pathways

89
Q

Where is pyruvate dehydrogenase found?

A

In the mitochondrial matrix

90
Q

Describe pyruvate dehydrogenase

A

Large multi enzyme complex

Converts pyruvate to Acetyl CoA irreversibly

91
Q

What inhibits pyruvate dehydrogenase?

A

Acetyl CoA
NADH
ATP

92
Q

What activates pyruvate dehydrogenase?

A 
Pyruvate
CoASH
NAD+
ADP 
Insulin
93
Q

Why is the conversion of pyruvate to Acetyl CoA considered irreversible?

A

It involves the irreversible lose of CO2

94
Q

Per glucose molecule how many turns of the Krebs cycle take place?

A

2

As there are 2 C3 compounds produced from 1 glucose molecule

95
Q

Where does the Krebs cycle take place?

A

Inside the mitochondria

96
Q

What happens to Acetyl CoA during the Krebs cycle?

A

The C-C bonds are broken

The carbons oxidise to CO2

97
Q

Does Krebs cycle run in absence of O2?

A

No

98
Q

What is another name for Acetyl CoA?

A

Acetate

99
Q

How many molecules of NADH are produced per turn of the Krebs cycle?

A

3

So 6 for the 2 turns per glucose molecule

100
Q

How many molecules of FAD2H are produced per turn of the Krebs cycle?

A

1

So 2 for the 2 turns for each molecule of glucose

101
Q

How many molecules of GTP (similar to ATP) are produced per turn of the Krebs cycle?

A

1

So 2 for the 2 turns for each molecule of glucose

102
Q

How is the Krebs cycle regulated?

A

ATP/ADP ratio
NADH/NAD+ ratio
Both of these feed back into the Krebs cycle about the rate of ATP use

103
Q

Name an enzyme that is responsible for an early irreversible step in the Krebs cycle and can be allosterically controlled

A

Isocitrate dehydrogenase
Allosterically inhibited by high energy signal NADH
Allosterically activated by the low energy signal ADP

104
Q

What happens to the NADH and FAD2H after the Krebs cycle?

A

They are reoxidised

Requires O2

105
Q

What happens to the H+ and electron lost from NADH and FAD2H?

A

Electrons transferred through series of carrier molecules to O2 with release of energy
H+ moved across membrane into the inter membrane space of the mitochondrion (H+ gradient across membrane is the protein motive force or pmf)

106
Q

What is the pmf used to drive?

A

ATP synthesis from ADP and a phosphate

107
Q

How much energy is required to bind a phosphate onto ADP?

A

+31 kJ/mol

108
Q

How many moles of ATP can be produced from 2 moles of NADH?

A

5

109
Q

How many moles of ATP can be produced from 2 ,olds of FAD2H?

A

3

110
Q

How is energy released from ATP?

A

The hydrolysis of the phosphate bond to form ADP and a phosphate group

111
Q

How is ATP synthesised?

A

ATP synthase allows the return of H+ across the membrane which is favoured energetically by the electrochemical gradient.
This drives ATP synthesis

112
Q

What is the final stage of catabolism called?

A

Oxidative phosphorylation

113
Q

What are the 2 processes involved in oxidative phosphorylation?

A

Electron transport

ATP synthesis

114
Q

How is oxidative phosphorylation regulated?

A

When ATP is high, ADP is low so no substrate for ATP synthase
Therefore inward flow of H+ stops
So concentration of H+ goes up
This prevents further H+ pumping

115
Q

How do inhibitors of oxidative phosphorylation work?

A

They block electron transport (e.g. Cyanide) by preventing acceptance of electrons by O2

116
Q

How do uncouplers of oxidative phosphorylation work?

A

They increase the permeability of the mitochondrial inner membrane to H+ so pmf is reduced so less drive for ATP synthesis

117
Q

What is the purpose of brown adipose tissue?

A

Contains a naturally occurring uncoupling protein
Electron transport is uncoupled from ATP synthesis
The energy of pmf is captured as extra heat

118
Q

How many moles of ATP are produced from one mole of glucose?

A

32

119
Q

Name some tissues that have an absolute requirement for glucose

A

Erythrocytes
Leukocytes
Kidney medulla
Lens of eye

120
Q

What type of fuel does CNS prefer?

A

Glucose

121
Q

What is about a normal blood glucose level?

A

5mM

122
Q

Why is glucose stored as glycogen?

A

It is efficient
Large molecule
Minimal osmotic effect

123
Q

Where is glycogen stored?

A

As granules in:
Liver (up to about 100g)
Skeletal muscle (up to about 300g)

124
Q

What is another name for glycogen synthesis?

A

Glycogenesis

125
Q

What enzyme are involved in glycogenesis?

A

Hexokinase (muscles) /glucokinase (liver)
Phosphoglucomutase
Glycogen synthase

126
Q

What is the first step in glycogenesis?

A

Glucose is phosphorylated
Requires ATP
produces ADP and glucose 6 phosphate

127
Q

What does phosphoglucomutase do?

A

Move the position of the phosphate group on glucose 6-P to make glucose 1-P

128
Q

What does glucose 1-P combine with before it can bind to glycogen?

A

UTP (similar to ATP but a different base)

129
Q

When is glycogen degraded in the skeletal muscles and liver?

A

Skeletal muscles- in response to exercise

Liver- in response to fasting or stress

130
Q

What is the break down of glycogen called?

A

Glycogenolysis

131
Q

Name the enzymes involved in glycogenolysis

A

Glycogen phosphorylase
Phosphoglucomutase
Glucose 6-phosphatase (liver only)

132
Q

What is glycogen from skeletal muscles broken down to?

A

Glucose 6-phosphate (which then enters glycolysis)

133
Q

What is glycogen from the liver broken down into?

A

Glucose (which is then released into the blood)

134
Q

What is the regulatory enzyme in glycogen synthesis?

A

Glycogen synthase

135
Q

What is the regulatory enzyme in glycogen degradation?

A

Glycogen phosphorylase

136
Q

What affect does glucagon and adrenaline have on glycogen synthesis and degradation?

A

Decreased synthesis

Increased degradation

137
Q

What affect does insulin have on glycogen synthesis and degradation?

A

Synthesis increases

Degradation decreased

138
Q

How do glycogen storage diseases arise?

A

Through inherited conditions- inborn errors of metabolism

Deficiency or dysfunction of enzyme involved in glycogen metabolism

139
Q

Give an example of a glycogen storage disease

A

von Gierke’s disease

Deficiency of the enzyme glucose 6-phosphate

140
Q

What does gluconeogenesis mean?

A

The production of new glucose

Occurs in liver and kidney cortex

141
Q

Name some precursors for gluconeogenesis

A 
Galactose
Fructose
Glycerol (from TAG)
Lactate
Glucogenic amino acids
142
Q

Name some enzymes involved in gluconeogenesis

A 
Fructose 1,6-bisphosphatase
Phosphoenolpyruvate carboxykinase (PEPCK)
143
Q

What is gluconeogenesis regulated in response to?

A

Starvation/fasting
Prolonged exercise
Stress

144
Q

What affect on gluconeogenesis does glucagon and cortisol have?

A

They stimulate it

145
Q

What affect on gluconeogenesis does insulin have?

A

Inhibits gluconeogenesis

146
Q

Approximately how long after feeding does glycogenolysis take place?

A

Up to 8-10 hours

147
Q

Approximately how long after feeding does gluconeogenesis take place?

A

8-10 hours onwards

148
Q

When are triacylglycerols used as a source of energy?

A

Prolonged exercise
Stress
Starvation
During pregnancy

149
Q

Where are triacylglycerols stored?

A

Adipose tissue

150
Q

What is fatty acid synthesis known as?

A

Lipogenesis

151
Q

What are fatty acids synthesised from?

A

Acetyl CoA

Requires ATP and NADPH

152
Q

Where does lipogenesis occur?

A

In the cytoplasm of liver cells

153
Q

Where does the Acetyl CoA for the lipogenesis come from?

A

Mitochondria

154
Q

What does Acetyl CoA bind to to be transported out of the mitochondria?

A

Oxaloacetate to form citrate

155
Q

What is the first step of fatty acid synthesis?

A

Acetyl-CoA is converted to malonyl-CoA

156
Q

What enzyme converts Acetyl-CoA to Malonyl-CoA?

A

Acetyl carboxylase

157
Q

What is added each time to the fatty acid chain kn fatty acid synthesis?

A

C2 (as malonyl-CoA)

158
Q

What enzyme is involved in fatty acid synthesis?

A

fatty acid synthase

multi-enzyme complex

159
Q

What inhibits fatty acid oxidation?

A

insulin

160
Q

What inhibits fatty acid synthesis?

A

Glucagon

Adrenaline

161
Q

What stimulates fatty acid oxidation?

A

Glucagon

Adrenaline

162
Q

What stimulates fatty acid synthesis?

A

Insulin

163
Q

What are fuel stores in the body?

A

Triacylglycerol
Glycogen
Muscle Protein

164
Q

What is the triacylglycerol fuel store used for?

A

It is thee largest energy store

165
Q

What is the glycogen fuel store used for?

A

Vital for glucose requiring tissues

166
Q

What is the muscle protein fuel store used for?

A

Important in prolonged starvation

167
Q

Name some classes of lipids?

A 
triacyl gylcerol
fatty acids
cholesterol
cholesterol esters
phospholipids
168
Q

Name some functions of cholesterol

A 
Major component of membranes
Precursor of steroid hormones
Precursor of bile acids
Some from diet, but mostly synthesised in liver
Can be esterified with a fatty acid
  -Eliminates the only polar part
169
Q

Describe some features of phospholipids

A

Diacylglycerol with phosphate group
Major component of membranes
Phosphate is polar

170
Q

Approximately what percentage of lipids are carried in the blood?

A

2%

carried bound to albumin

171
Q

Of the lipids that are in the blood, what are they mainly composed of?

A

fatty acids

172
Q

How are the rest of the lipids transported in the blood?

A

As lipoprotein particles (small assemblies of lipid molecules surrounded by polar molecules (micelles))

173
Q

Where are lipoprotein particles constructed?

A

In liver

174
Q

What 2 properties of lipoprotein particles mean they can be separated by electrophoresis?

A

They vary in:
Density
Surface

175
Q

What are singular apolipoproteins known as?

A

Apoproteins

176
Q

What is a apolipoprotein composed of?

A

Lipids

Proteins

177
Q

What are lipoproteins particles made of?

A

Apolipoproteins

178
Q

Name some apoproteins

A 
apoA
apoB
apoC
apoD
apoE
apoH
179
Q

What functional roles do apoproteins have?

A

activation of enzymes

recognition of cell surface receptors

180
Q

What are some differenrt classes of lipoprotein particles in order of increasing density?

A

Choylomicrons
Very low density lipoproteins (VLDL)
Low density lipoproteins (LDL)
High density lipoproteins (HDL)

181
Q

Where are chylomicrons fromed?

A

enterocytes (intestinal absorbing cells0 lining the intestine

182
Q

What are chylomicrons formed from?

A

combining triacylglycerols (from food) with specific apoproteins

183
Q

How long after a meal are chylomicrons normally present in the blood?

A

4-6 hrs

184
Q

Where are VLDLs formed?

A

in the liver

185
Q

What are VLDLs formed from?

A

Triacylglycerols (synthesised in liver) with specific apoproteins

186
Q

Where are LDLs formed?

A

In the liver

187
Q

What are LDLs formed from?

A

cholesterol (synthesised in liver) with specific apoproteins (Apo B100 is important)

188
Q

What does an increase in the levels of LDLs give rise to?

A

A higher risk of atherosclerosis

189
Q

Where are HDLs formed?

A

in the tissues

190
Q

What are HDLs fromed from?

A

Cholesterol (from tissues) combined with specific apoproteins

191
Q

How are triacylglycerols from chylomicrons and VLDLs transferred?

A 
Endothelial cells of capillaries have lipase on outside of membrane
Bind chylomicrons and VLDLs
Cleaves triacylglycerols into:
   -Glycerol
   -fatty acids
192
Q

What is the fate of glycerol from tracylglycerols when they are transferred from chylomicrons and VLDLs?

A

it remains in the circulation

193
Q

What is the fate of fatty acids from tracylglycerols when they are transferred from chylomicrons and VLDLs?

A

enter tissues for metabolism

194
Q

What is the fate of VLDLs remnants from tracylglycerols when they are transferred from chylomicrons and VLDLs?

A

usually removed by liver or converted to other types of lipoprotein particles

195
Q

How is cholesterol transferred from LDL?

A

cells have LDL receptor
complex proteins bind to LDL to create receptor/LDL complex which enters cell by endocytosis
cholesterol ester released and cleaved into cholesterol and fatty acid

197
Q

What controls LDL receptor expression?

A

cholesterol concentration in cell

-uptake stimulated by need

198
Q

What is hyperlipoproteinaemias?

A

Raised levels of one or more lipoprotein classes

199
Q

What causes hyperlipoproteinaemias?

A 
Over-production
Under-removal
Defective
   -Enzymes
   -Receptors
   -Apoproteins
200
Q

Outline the stages of atheroma formation

A 
Oxidised LDL
Macrophages
Foam cells
Accumulate in intima of blood vessle walls
Fatty streak
Atheroma
201
Q

How is hyperlipoproteinaemias treated?

A 
Diet
   -Reduce cholesterol, saturated lipids
Lifestyle
   -Increase exercise
     -Stop smoking to reduce cardiovascular risk
Drugs
   -Statins
202
Q

How do statins work to treat hyperlipoproteinaemias?

A

Reduce cholesterol synthesis by inhibition of HMG CoA reductase enzyme
Increase expression of LDL receptors in hepatocytes
Anti-inflammatory?

203
Q

Name some major nitrogen containing compounds

A

Proteins (amino acids)

Purines and pyramidines (DNA/RNA)

204
Q

How does most nitrogen enter the body?

A

Protein from the diet (amino acids)

205
Q

How is most nitrogen excreted from the body?

A

Urea in the urine

206
Q

Give an example of when the body is in positive nitrogen balance

A

Growth

Pregnancy

207
Q

Give an example of when the body is in negative nitrogen balance

A

Starvation

Tissue wasting diseases

208
Q

What is meant by an essential amino acid?

A

An amino acid that is needed in the diet

209
Q

Name some essential amino acids

A 
Lysine
Isoleucine
Leucine
Threonine 
Valine
Tryptophan 
Phenylalanine 
Methionine
210
Q

What amino acids may become essential under certain conditions?

A

Histidine
Arginine
Tyrosine
Cysteine

211
Q

Name 2 methods of removing toxic amine NO2 groups from the blood

A

Transamination

Deamination

212
Q

What is transamination?

A

The transfer of the amino group

213
Q

What is deamination?

A

The disposal of the amine group

214
Q

During transamination an amino acid+ alpha-ketoglutarate forms what?

A

Glutamate and a keto acid

215
Q

During transamination an amino acid+ oxaloacetate forms what?

A

Aspartate and a keto acid

Esa 1 (1 decks)

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