Metabolism

Introduction to Metabolism
1. Define metabolism1
2. What are the endings for processes involving catabolism and anabolism respectively?2
3. Are ATP and NADH used in anabolic or catabolic processes?3
4. Name the umbrella terms for the pathways used to convert the following into Acetyl
CoA: Glucose, Fatty acids, Amino acids4
5. Whereabouts does b-oxidation of fatty acyl CoA into acetyl CoA occur? 5
6. What is the name of the enzyme which converts pyruvate into Acetyl CoA 6
7. What are the three components of an ATP molecule?7
8. What does hydrolysis mean?8
9. What are the two main uses of ATP in the human body?9
10.What is an allosteric enzyme? 10

Glycolysis
1. Where does glycolysis occur?11
2. Name all 4 stages of glycolysis12

Series of enzyme reactions within cells for converting fuel molecules into useful energy

Catabolic processes (breakdown) end in lysis e.g. glycolysis, Anabolic processes end in genesis

Anabolic, NADH is used to add H+ and ATP used to add phosphate

Glucose is converted into pyruvate and then Acetyl-CoA by glycolysis, Fatty acids into Acetyl-CoA by beta
oxidation and Amino acids by transamination
5In

the mitochondria, it is transported there by carnitine

6Coenzyme

Ribose sugar, adenine unit, 3 phosphate chain

Cleavage of chemical bonds by the addition of water

Na/K ATPase and Muscle contraction

10

Multiple binding sites. Enzyme changes shape on binding (other than active site) which allows regulation

11

Cytosol

12

Investment/Activation Stage, Splitting of 6C into 2x 3C, Oxidation Step, ATP Synthesis (x2)

3. Name all 10 products in glycolysis13

4. What enzymes are used at each stage? 14
5. Which steps use ATP and give off ADP?15
6. Which steps synthesise ATP from ADP?16
7. In situations of oxygen depravation, what happens to excess pyruvate which cannot be
converted into CO2?17
8. In the presence of oxygen, in human tissue, pyruvate is converted into?18
9. Rate of glycolysis is at its highest under what conditions?19
10. Rate of glycolysis is lowest under what conditions?20
11. Which step is targeted by an allosteric protein/enzyme to inhibit the metabolic
pathway? 21
12. If pyruvate is converted into lactate in the muscles, where does the reverse occur?22
13. What is the enzyme used to catalyse the conversion of pyruvate into lactate? 23
14. Why do RBC undergo a comparatively large amount of glycolysis?24

Glycogen Synthesis & Degradation

13

Glucose, Glucose 6 phosphate, Fructose 6 phosphate, Fructose 1,6, phosphate (Activation Stage)
Dihyrdoxyacetate phosphate, Glyceraldehyde 3 phosphate (Splitting of 6C to 3C), 3 Biphosphoglycerate,
(oxidation step) 3 phosphoglycerate, 2 phosphoglycerate, phosphoenolpyruvate, pyruvate (ATP Synthesis)
14

Hexokinase, Phosphoglutonate isomerase, phosphofructokinase, fructose biphosphate aldolase,

triphosphate isomerase, glyceraldehyde phosphate dehydrogenase, phosphoglycerate kinase,
phosphoglycerate mutase, enolase, pyruvate kinase
15

Glucose to Glucose-6-phosphate, Fructose 6 phosphate to fructose 1,6, diphosphate

16

3 Biphosphoglycerate to 3 phosphoglycerate, Phosphenolpyruvate to pyruvate

17

Pyruvate is converted into lactate (a.k.a. lactic acid)

18

Acetyl CoA

19

During exercise or after high carb meal (high levels of insulin)

20

Fasting state - because there are high levels of circulating glucagon. Glucagon converts glycogen into
glucose but also inhibits glycolysis via the 2nd ATP using step in the activation stage
21

Within the activation stage, phosphofructokinase which converts fructose-6-phosphate into fructose 1-6biphosphate can be inhibited to slow metabolism
22

Lactate can be converted back into pyruvate in the liver

23

Lactate dehydrogenase, because NADH is returned to NAD+ (dehydrogenated)

24

Because they dont contain mitochondria so cannot use TCA cycle/ETC

1. What are the respective weights of blood plasma glucose and glycogen stores in the
body of a typical 70kg adult25
2. What is the pathway for conversion of glycogen into glucose in the blood?26
3. What configuration of glycoside links connect glucose monomers in a straight chain of
glycogen and what form the branch junctions?27
4. Which enzymes are associated with forming these bonds? 28
5. What is the reaction pathway which transfers glucose into the first glucose-protein
primer which kickstarts glycogen formation?29
6. How is glycogen synthase activated and deactivated?30
7. How is glycogen phosphatase activated and deactivated? 31
8. Which hormone stimulates release of protein phosphatase and so glycogen buildup?32
9. Which hormones stimulate release of protein kinase and so glycogen breakdown?33
10.Name the diseases associated with defective glucose-6-phosphate, lysosomal
glycosidase and glycogen phosphorylase.34

Aerobic Respiration
1. What are the respective pathways for obtaining acetyl-CoA from: glucose, fatty acids
and amino acids?35
25

10g glucose in blood plasma, 120g glycogen stored in liver, 400g in muscle

26

Glycogen--> Glucose 6 phosphate --> Glucose

27

1,4 glycosidic bond are the chains, 1,6 glycosidic bonds make the branches

28

Glycogen synthase for straight 1,4 bonds, branching enzyme for 1,6 branch junctions

29

Glucose ---> glucose-6-phosphate ---> glucose-1-phosphate ---> UDP glucose

30

Activated by protein phosphatase cleaving a phosphate, deactivated by protein kinase and ATP adding a
phosphate
31

Activated by protein kinase & ATP adding a phosphate, deactivated by protein phosphatase removing
phosphate
32

Insulin (secreted by pancreas, acts in liver, muscle and fat tissue)

33

Glucagon (secreted by pancreas, acts in liver only), Adrenaline (secreted by adrenal gland, acts in muscle
and liver)
34

Von Gierkes = glucose-6-phosphatase, Pompes = lysosomal glycosidase, McArdles = glycogen

phosphorylase
35

Glucose = glycolysis to pyruvate and then acetyl CoA, fatty acid beta oxidation, amino acids by
transamination

2. Which unit out of glucose, fatty acids or amino acids produce the most acetate
molecules per molecule of themselves and therefore highest energy per unit weight? 36
3. Is acetyl CoA reduced or oxidised during the TCA cycle? 37
4. Where does the TCA cycle take place within the cell/organelles?38
5. Why do red blood cells not make extensive use of the TCA cycle for respiration?39
6. How many carbons are there in acetyl-CoA? 40
7. Name all 9 compounds which are the subject of the TCA cycle in order41
8. Which steps produce CO2 having cleaved it off the molecules involved?42
9. What is the name for a chemical pathway which cleaves a bond due to the addition of
water? (e.g. conversion of malate into oxaloacetate)43
10.What is the function of coenzyme A in the citric acid cycle?44
11.What part of the coenzyme A molecule is the active bit in this reaction and what type of
bonds does it form? 45
12.Which steps produce NADH from NAD+ during oxidation of compounds involved? 46
13.How many carbons are there in succinyl-CoA 47
14.Which reaction step produced GTP? 48
36

Fatty acids

37

oxidised to produce CO2 and H2O

38

in the mitochondrial matrix

39

RBC contain very few mitochondria

40

41

Acetyl-CoA, Citrate, isocitrate, alpha ketoglutarate, succinyl CoA, succinyl, fumarate, malate, oxaloacetate

42

Isocitrate to alpha ketoglutarate and alpha ketoglutarate to succinyl CoA

43

hydrolysis

44

Oxidation of pyruvate to form acetyl CoA

45

The SH at the end of the Coenzyme A forms thioester bonds with carboxylic acids (e.g. citric acid). The
CoA on acetyl CoA is a thioester bond. (thiol = sulphur-carbon compound)
46

Isocitrate to Alpha-Ketoglutarate, Alpha-Ketoglutarate to Succinyl-CoA and Malate to Oxaloacetate

47

4, with citrate having lost two to CO2 during an earlier step

48

GDP and Pi are converted into GTP (a similar compound to ATP) in the step between succinyl CoA and
succinate

15.Which reaction step produces FADH2 from FAD during an oxidation reaction? 49
16.Where is the electron transport chain?50
17.Roughly how many ATP are synthesized per molecule of NADH in the ETC?51
18.Which side is more acidic, the mitochondrial matrix or inter-membrane space? 52
19.What are the proton pumps powered by? 53
20.How many ATP are produced by glycolysis and TCA cycle respectively? 54
21.Which steps in the TCA cycle are irreversible? 55
22. Which substances can be produced by transamination?56
23.How many ATP are effectively produced by the products of the TCA cycle?57

Fat as Fuel
1. Name the functions of lipids/sterols in the cell membrane58
2. Where do triglycerides get their name from? 59
3. What is the typical weight of fat at triglyceride on a 70kg adult? 60

49

Succinate to fumarate

50

Proteins on the inner mitochondrial membrane

51

Around three molecules of ATP are synthesized per molecule of NADH in the electron transport chain

52

A proton gradient is generated by proton pumps on the inner membrane, these pump H+ (protons)
released by oxidation in the TCA cycle out of the mitochondrial matrix (inside the mitochondria) into the intermembrane space. This makes the inter-membrane space more acidic and leaves the matrix more alkaline
53

Release of energy (electrons) from NADH to NAD+

54

Net yield of 2 ATP in glycolysis and 10-12 from TCA cycle

55

Isocitrate dehydrogenase, ketoglutarate dehydrogenase and citrate synthetase

56

Transamination of amino acids can produce either alpha ketoglutarate (from glutamate/glutamine) or
oxaloacetate (from aspartate)
57

Per Cycle = (1 GTP = 1 ATP, 3NADH = 2.5, 1 FADH2=1.5)x2 = total 10 ATP

58

Phospholipids and cholesterols in the membrane are precursors of hormones. Protein complexes may
cleave off parts of these lipid molecules which become second messengers in the cell.
59

Because they contain 3 fatty acids (tri) attached to a glycerol molecule

60

Around 11kg stored as triglycerol fat droplets

4. In order, which of the following produces the most energy per weight basis and which is
the least? And why? Fatty acids, glucose and amino acids 61
5. Name 3 common fatty acids62
6. Out of these, which are saturated and which are unsaturated? 63
7. Why do double bonds in unsaturated fatty acids make membranes more fluid?64
8. What is an ester bond? 65
9. Describe the series of breakdown steps to turn triacylglycerol into building blocks which
are free to travel in the blood? 66
10.What types of enzyme are used in this breakdown reaction?67
11.What protein do individual fatty acids bind to to travel in the bloodstream? 68
12.What it the name of the process for converting glyerol (glycerol not glycogen) into
glucose in the starvation state? 69
13.Where does glycerol enter glycolysis under normal conditions in most tissues? 70
14.Whereabouts in the cell/organelles does fatty acid beta oxidation take place? 71

61

Fat produces the most, followed by protein, and carbohydrate the least. The reason is that fats are more
reduced than protein and carbs. (i.e. fats have more H+ contained within them, saturated with H)
62

Any of palmitic acid, stearic acid, oleic acid linoleic acid or linolenic acid

63

palmitic and stearic acid contain no double bonds, oleic = 1, linoleic = 2, and linolenic = 3

64

Because the double bonds make a kink in the physical shape of the molecule, so the membrane is not as
tightly packed and easier to squeeze through
65

An ester is a compound containing a carbonyl (a carbon double bonded to an oxygen) bonded to an ether
(an oxygen molecule next to two alkyls) (alkyl = a saturated hydrocarbon)
66

Triacylglycerol-->(fatty acid given off)-->diacylglycerol---> (fatty acid given off)--->monoacylglycerol-->

(fatty acid given off)-->glycerol. The 3 fatty acids and glycerol as separate products are freely diffusible in the
bloodstream
67

Lipases

68

Albumin

69

In conditions of starvation (when glucagon inhibits glycolysis) glycerol from triglyceride breakdown can be
converted into glucose for used in glycolysis by the process of gluconeogenesis.
70

Converted into pyruvate in glycolysis then enters the TCA cycle

71

In the mitochondrial matrix (fully inside the mitochondria, inside both membranes of the double membrane)

15.Where/how do fatty acids (not glycerol) enter the metabolism pathway (i.e. glycolysis/
TCA and which step)? 72
16.What substance does fatty acyl-CoA couple with to enter the mitochondrial
membranes?73
17.What four reactions are the core of B-oxidation?74
18.If a carbon-carbon double bond is added to a compound during a reaction step what
type of reaction is this likely to be?75
19.Name the products of the degradation of fatty acyl-CoA into acetyl-CoA 76
20.How many repeats of the B-oxidation pathway will a fatty acid with 24 carbon atoms
pass through and how many acetyl CoA molecules will be generated before the fatty
acid is completely broken down? 77
21.If a particular fatty acid produces 10 acetyl-CoA molecules, how many ATP are
produced from metabolism of this molecule? 78
22.The lipase enzyme which breaks down fatty acids is activated by which substances? 79
23.How is fatty acid metabolism regulated other than by these substances? 80
24.Which organ in the body relies almost entirely on glucose for fuel (and hence cannot
metabolize fat, which goes direct to acetyl-CoA)81

Skeletal Muscle: Regulation of contraction

72

Although citrate (6c) can be converted into fatty acids if needed, fatty acids may only enter the TCA cycle
via acetyl CoA. Fatty acids are converted into fatty acyl CoA by activating enzyme using ATP to AMP and PPi
73

Carnitine

74

Removal of 2H atoms, addition of water, removal of 2H atoms and removal of 2C unit

75

An oxidation reaction because oxidation is loss of H+

76

Fatty acyl CoA (chain) --> Enoyl-CoA --> 3-L-Hydroxyacyl-CoA --> B-ketoacyl-CoA --> Fatty acyl CoA
(remaining chain) and Acetyl CoA (2C unit which enters TCA cycle)
77

Because a 2C unit is cleaved with each cycle it will take 11 cycles of B-oxidation to fully break down the
fatty acid, a 2C unit will be remaining at the end of the 11th cycle so there will be 12 acetyl CoA (2C) units
produced in total
78

11 acetyl CoA = 10 repeats of the TCA cycle (10x11=110 ATP). As far as beta oxidation is concerned, 10
NADH (2.5 ATP x 10 = 25) and 7 FADH (1.5 ATP x 10 = 15) are produced per cycle so 150 ATP in total
79

adrenaline and glucagon, these are released when the body needs energy

80

Rate of entry into mitochondria (via carnitine shuttle) and rate of reoxidation of NADH and FADH2

81

The brain, only glucose can cross the blood-brain barrier

1. What are the three main stages involved in controlling muscle contraction from AP in
axon hillock to muscle movement? 82
2. What is the name of the main neurotransmitter at the neuromuscular junction of skeletal
muscle?83
3. What is the first thing that happens when Acetylcholine binds to nicotinic receptors on
the post synaptic membrane? 84
4. What features of the muscle fibre allow the AP to dive into the centre of the fibre?85
5. What happens when the AP reaches a triad in one of these features? 86
6. What is the difference between an electrotonic potential and an action potential? 87
7. How does relaxation of the muscle occur?88
8. What causes bound troponin to change its shape and initiate muscle contraction? 89
9. Name the three troponin subunits, which one does calcium bond to? 90
10.Why is the twitch in skeletal muscle much longer than the AP which triggered it? 91

82

CONDUCTION - AP set up in axon hillock of a motor neuron and propagated along the axon to its
termnals, NEUROMUSCULAR TRANSMISSION - chemical transmission at the neuromuscular junction to
set up an AP in the muscle fibres, EXCITATION-CONTRACTION COUPLING - process by which muscle AP
causes rise of intracellular Ca2+ and actin-myosin interaction
83

Acetylcholine

84

Causes opening of integral cation channel, leading to Na+ influx resulting in a local depolarisation called
end plate potential, this causes an action potential which moves along the muscle fibre away from the NMJ
85

T-tubules

86

When the AP reaches a triad, it is detected by voltage sensors which cause calcium release channels in
the sarcoplasmic reticulum to open. Calcium leaves the SR. Calcium ions bind to the thin filament allowing
the 3rd stage (cross bridge cycling) to start.
87

Electrotonic potentials rely on charge diffusion across a wide area of the cell away from the Na+ gate
where the potential originates from. In an action potential, voltage gated ion channels are used which takes
longer and uses energy but allows the potential to cover a long distance.
88

When the Calcium ions are pumped back into the sarcoplasmic reticulum

89

Release of calcium from the SR which binds to troponin when in high concentration and changes its
configuration. This moves the tropomyosin out of the way so myosin can bind to actin filaments.
90
91

Tnl, TnC and TnT, Ca2+ binds to TnC

Time is needed for various steps to occur which do not occur in the AP (e.g. SR Ca channels to open and
Ca to diffuse out, Ca to bind to troponin TnC subunit and change troponin configuration allowing cross
bridges to start interacting with thin filaments and physical tightening of elastic structures,

11.What are the relative lengths of time taken to twitch by a short twitch and long twich
fibres?92
12.Why do fast fibres shorten faster than short twitch fibres?93
13.What types of muscle fibre would be most common in (i) a marathon runner and (ii) a
sprinter?94
14.What is a tetanus? 95
15.Apart from short and long twitch, how else might types of muscle fibres be classified? 96
16.Out of training for endurance, strength or speed which is the least effective in terms of
recruitment of specific kinds of muscle fibre?97
17.How do muscle fibres adapt to an increase in length?98
18.What happens to muscle fibres when they are regenerating after damage?99

Nutrition and Health

1. What makes a fatty acid or amino acid essential in the diet? 100
2. Which of the following only contains one dietary component (macronutrient)?: Egg,
pasta, beef, cake, butter, champagne 101
3. What are the main factors considered in the creation of Dietary Reference Values? 102

92

Short twitch = 0.12s, long twitch = 0.32s

93

They have a faster ATPase which allows them to repolarise quicker and get through more cross bridge
cycles per second
94

Marathon runner would have mainly slow twitch and a sprinter mainly fast twitch

95

When a group twitches occur in such quick succession that they overlap

96

By how they generate most of their ATP, aerobic/oxidative (slow) vs glycotic/anaerobic (fast)

97

Strength can be improved by increasing muscle hypertropy and cross sectional area in training, endurance
can be improved by increasing oxidative metabolism by increasing capillary supply and number of
mitochondria. Speed, however is difficult to train for as it is hard to alter the proportion of fast muscle fibres.
98

Adding (if longer) or deleting sarcomeres (if shorter) to maintain optimum sarcomere length at new length

99

Satellite cells are activated and begin to divide, fusion of daughter myoblast cells and synthesis of new
fibre.
100

Those which cannot be synthesized in metabolism (e.g. alanine can be synthesized from pyruvate in the
TCA cycle
101
102

Butter (only contains fatty acids)

Look at intake of substance in people with no deficiency vs with deficiency, intakes that would cure clinical
deficiency and (low) intakes associated with a marker of nutritional adequacy (enzyme saturation and tissue
concentration)

4. What do the DoH recommend as a safe intake for the population?103

5. What is meant by reference nutrient intake (RNI)?104
6. Why is the EAR recommended for energy intake rather than the RNI?105
7. Approximately what percentage of hospital patients are malnourished? 106
8. What percentage of the UK population is overweight or obese and what percentage are
obese? 107
9. In the last 20 years, UK obesity has increased by what percentage?108
10. What percentage of children in the UK eat 5 portions of fruit & vegetables per day? 109

Liver Function 1: Glucose Homeostasis

1. What is the physiological circulating blood glucose in a healthy adult? 110
2. What are the consequences of high blood glucose over an extended period? 111
3. How many ATP are produced from a single molecule of glucose (net)?112
4. What synthetic reactions (synthesis of..) use glucose as a source of a pentose sugar? 113
5. How does glucose cross cell membranes and the blood brain barrier?114
6. Give a disadvantage of using glucose as a metabolic fuel compared to fatty acids?115

103

EAR/RDA plus 2 standard deviations

104

The amount that would satisfy 95% of the population i.e. the average plus 2 SD

105

Because if someone is already overweight and they consumed the EAR then they would get fatter

106

40%

107

66% overweight or obese, 25% are obese

108

300%

109

10%

110

3.9-6.7mM

111

Dehydration, wasting of body tissue and death

112

31

113

In particular synthesis of nucleotides and DNA (contain a pentose sugar in structure)

114

Diffusion - because it is freely soluble in water, unlike fat and protein

115

Glucose produces less ATP per unit weight than fat. Because glucose is freely soluble in water it is
osmotically active and can directly damage cells (e.g. diabetic patient having to have limbs amputated)

7. What is the main function and pathway for glucose metabolism in adipose tissue? 116
8. What is the main function and pathway for glucose in erythrocytes (red blood cells)?117
9. What is gluconeogenesis?118
10.Which enzymes are responsible for the three irreversible steps in glycolysis?119
11.Gluconeogenesis bypasses these steps using different enzymes to the glycolysis
forward reaction, what are they? 120
12.How is gluconeogenesis regulated in terms of enzymes and substrates involved? 121
13.What metabolic by-product is transferred between glycolysis and gluconeogenesis in a
process known as the Cori cycle?122
14.Why is maintaining blood glucose above a certain level crucial to survival? 123
15.What do alpha and beta cells in the Islets of Langerhans in the pancreas secrete? 124

116

The main pathway for glucose metabolism in adipose tissue is glycolysis. The main use of glucose in
adipose is not energy production but production of the glycerol, the basis of a triglyceride fat store molecule
117

Glycolysis and production of energy, RBC have very few mitochondria so largely rely on anaerobic resp.

118

Glycogenesis is a metabolic pathway for the formation of glucose from non-carbohydrate substances
(e.g. pyruvate, lactate, glycerol and amino acids but NOT FATTY ACIDS). It is one of the main mechanisms
in the human body to stop blood glucose levels from dropping too low during carbohydrate fasting
(maintained at 4-5mM/L).
119

Hexokinase/Glucokinase (Step 1), Phosphofructokinase (Step 3) and Pyruvate Kinase (Step 10)

120

In order (reverse to glycolysis because you are going from pyruvate to glucose):
Step 10 uses pyruvate caboxylase enzyme to convert pyruvate into oxaloacetate (using 2CO2, 2ATP and
2H20 and giving off 2ADP and 2Pi). Then it uses phosphenolpyruvate carboxylase to convert oxaloacetate
into phosphenolpyruvate (using 2GTP and giving off 2GDP).
Step 3 uses fructose 1,6 biphosphatase to convert fructose 1,6,biphosphate into fructose 6 phosphate (using
H20 and giving off 1 phosphate molecule).
Step 1 uses glucose 6 phosphatase to convert glucose 6 phosphate into glucose (again using H20 and
giving off 1 phosphate molecule).
121

Glycerol (a major substrate in gluconeogenesis) is released from fat breakdown which only happens
during starvation state, so fatty acids can enter the TCA cycle. Muscle protein breakdown in starvation state
releases amino acids (also major substrates of gluconeogenesis). In terms of enzymes, pyruvate
carboxylase (used for converting pyruvate into oxaloacetate) is activated by acetyl-CoA (TCA cycle).
122

Lactate (lactic acid) is produced after glycolysis in the absence of oxygen (where pyruvate cannot be
converted into Acetyl-CoA). Lactate can be transferred to the liver and is turned back into pyruvate before
being broken down into glucose, which is sent back to the tissues. This is known as the Cori cycle.
123

Glucose is the only fuel used by the brain; the body needs glucose to respire in anaerobic conditions

124

Beta cells secrete insulin, alpha cells secrete glucagon

16.Out of insulin and glucagon, which is anabolic and which is catabolic? 125
17.What are the 4 main metabolic effects of insulin on actions within the liver?126
18.What does insulin make the muscle do to glucose?127
19.What are the effects of glycogen on adipose tissue? 128

Liver Function 2: Protein and Nitrogen Metabolism

1. Which of the following three does the body keep least in storage: Glucose, fatty acids,
amino acids?129
2. All proteins have a certain lifespan (half-life) and so need to be replenished at some
point, what is the average protein turnover in a typical adult per day? 130
3. What is the nutritional protein requirement for a typical adult per day?131
4. Name the essential amino acids (Very many hairy little pigs live in the toilet argentine) 132
5. Name three situations in which an individual could have a positive nitrogen balance
(protein uptake of body greater than excretion) and three in which someone could have
a negative nitrogen balance.133
6. Why does the starvation state degrade proteins in the body? 134
7. What are the two main component parts of an amino acid?135

125

Glucagon is catabolic, it promotes breakdown of complex molecules (glycogen) to produce useful fuel.
Insulin is anabolic, it promotes the building up of complex glycogen from glucose monomers in the blood.
126

Inhibition of glucogenesis, activation of glycogen synthesis, increased fatty acid synthesis, increased
amino acid uptake and protein synthesis
127

Increased glucose uptake by increasing glucose transporters (GLUT4)

128

Increased adipose tissue lipolysis (fat breakdown), increased fatty acid oxidation in the liver (to generate
fuel for the TCA cycle)
129

Amino acids, although freely exchangeable with protein, there are only specific stores in the body for
glycogen (glucose storage) and triglycerides (fatty acid storage)
130

Around 300-400g of protein per day

131

Roughly the same as the individuals body weight in kg but in g (e.g. 50g protein for a 50kg person)

132

Valine, Methionine, Histidine, Lysine, Phenylalanine, Leucine, Isoleucine, Threonine, Tryptophan, Arginine

133

Positive balance = pregnant woman, growing child, convalescence after serious illness, negative balance
= starvation, injury and trauma, serious illness.
134

Insulin normally inhibits protein breakdown, so in the state of high glucagon levels, proteins are broken
down to provide amino acids which ultimately enter glyconeogenesis and the TCA cycle
135

An oxo acid (keto acid) e.g. pyruvate, coupled with an NH2 (amine) group

8. What happens to an amino acid during the process of oxidative deamination? 136
9. What happens to an amino acid during the process of transamination?137
10. What is a trans-deamination reaction? 138
11. Which is the only amino acid which can be directly deaminated? 139
12. What is the difference between ketogenic and glucogenic amino acids? 140
13. What substance is excess protein in the liver converted to?141
14. Which amino acid can be synthesized during the urea cycle and is therefore not a
requirement in the diet of a healthy adult with a neutral nitrogen balance? 142
15. What are the four steps within the urea cycle? 143
16. The excretion of creatinine is proportional to the mass of what tissue?144
17. What is the medical term for impaired conversion of NH3 to urea?145
18. What is a normal renal threshold for glucose in mmol/L?146
19. What proportion of the population are affected by diabetes and what proportion of the
healthcare budget is spent on it? 147

136

The amine is split with the acid in the presence of water to produce a keto acid and ammonia (NH3)

137

The ketoacid on the amino acid is displaced by a different ketoacid to form an entirely new amino acid

138

Trans-deamination is a two step process that begins with a transamination reaction which is required to
make an amino acid suitable for deamination. This is the case for degradation of most amino acids except
glutamine/glutamate, which goes directly to alpha ketoglutamate
139

Glutamate/glutamine and aspartate can be directly deaminated

140

Ketogenic amino acids can only be degraded into acetyl-CoA whereas glucogenic may become glucose

141

Urea

142

Arginine can be synthesized from carbamoyl phosphate-->citruline-->argininosuccinate(+ATP-->PPi)-->

arginine
143

(1) Carbamoyl phosphate + Ornithine --> Citruline --> (2) Citruline + aspartate --> (3) argininosuccinate ->
fumarate (connection with TCA cycle) + arginine --> (4) arginine --> UREA + ornithine
144

Muscle

145

Hyperammonaemia

146

10mmol/L (the renal threshold is the blood concentration of a substance above which the substance starts
being removed in urine, i.e. above 10mmol/L glucose is only incompletely reabsorbed in the PCT)
147

3-4% of the population, 5-10% of NHS budget

20. What is the mechanism of action of early onset type 1 diabetes? 148

Despos Questions
1. What is the function of glucagon? 149
2. What processes are activated by insulin?150
3. What is glycogen used for and how? 151
4. What happens to excess protein taken in the diet?152
5. How is blood glucose maintained in fasting? 153
6. What is the function of the TCA cycle? 154
7. How is glucose oxidised?155
8. What are the products of beta oxidation? 156
9. Where does it take place?157

148

Autoimmune destruction of B-cells, hallmarks are hyperglycaemia (high blood sugar) and ketoacidosis,
because ketone bodies are produced in fasting state, dissociated at blood pH and creates lots of H+ ions
Released by the body during the fasting state to stimulate breakdown of glycogen stores in the liver and
muscle tissues releasing glucose for energy. Glycogen also inhibits glycolysis.
149

150

Protein & triglyceride synthesis, production of glycogen from glucose.

151

Glucose store in liver and muscle tissues, compact, branched structure for rapid metabolism when
needed but compact are taken up, not osmotically active
152

Since the body has a relatively small pool of stored amino acid, excess protein is converted either into
urea and excreted in the urine, or it may leave the urea cycle as fumarate and enter the TCA cycle.
153

During the fasting state, glycogen is released which breaks down glycogen stores and releases glucose
from them. Also breaks down triglyceride stores into fatty acids and glycerol, of these, only glycerol may be
broken down into glucose. Glycogen also inhibits glycolysis, so less glucose is used up by glycolysis and
more stays in the blood.
154

Oxidation of Acetyl-CoA and subsequent products to reduce FAD+ to FADH2 and NAD+ to NADH, these
then produce 2.5 ATP and 1.5 ATP respectively in the electron transport chain which are energy for the body,
particularly for muscle contraction and ATPase pumps. One step also makes GTP out of GDP. Also allows
fatty acids and amino acids to be used as energy as they can enter it at various stages.
Glucose is the starting point for glycolysis, it is oxidised into different compounds beginning with
glucose-6-phosphate, fructose-6-phosphate, fructose-1-6-biphosphate etc. reaching Acetly-CoA and going
into the TCA cycle. Every time the reaction overall gives off H+ in the form of H20, or NADH or FADH2 the
reaction is an oxidation reaction. The process of step by step oxidation continues through glycolysis and the
TCA cycle.
155

156

Acetyl-CoA from fatty acyl CoA

157

Inside the mitochondria, fatty acyl-CoA molecules are transported inside by carnitine