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Metabolism Flashcards

1
Q

Kinase

A

Catalyses phosphate transfer

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2
Q

Where does glycolysis occur

A

Cytoplasm

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3
Q

Preparative phase of glycolysis

A

Glucose
Glucose-6-phosphate
Fructose-6-phosphate
Fructose-1,6-bisphosphate
Dihydroxyacetone phosphate AND glyceraldehyde-3-phosphate

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4
Q

Preparative phase of glycolysis enzymes

A

Hexokinase
Phosphoglucoisomerase
Phosphofructokinase (PFK1)
Adolase
Isomerase

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5
Q

Rate limiting step of glycolysis

A

PFK-1
fructose-6-phosphate to fructose-1,6-bisphosphate

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6
Q

ATP generating phase of glycolysis

A

Glyceraldehyde-3-phosphate
1,3-bisphossphoglycerate
3-phosphoglycerate
2-phosphoglycerate
Phosphenol pyruvate
Pyruvate

OCCURS TWICE PER GLUCOSE MOLECULE

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7
Q

ATP generating phase of glycolysis enzymes

A

Triose phosphate dehydrogenase
Phosphoglycerate kinase
Phosphoglycerate mutase
Enolase
Pyruvate kinase

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8
Q

Anaerobic respiration

A

Pyruvate —> lactate

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9
Q

Anaerobic respiration enzyme

A

Lactate dehydrogenase

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10
Q

Purpose of anaerobic respiration

A

Regenerate NAD+ from NADH when no O2

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11
Q

What amplifies PFK1

A

AMP

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12
Q

Allosteric regulation of PFK-1

A

Fructose-2,6-bisphosphate
Citrate
ATP
Phosphoenol pyruvate

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13
Q

Inhibitor of pyruvate kinase

A

ATP

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14
Q

Amplifiers of pyruvate kinase

A

AMP
fructose-1,6-bisphosphate

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15
Q

Where does the link reaction occur

A

Mitochondrial matrix

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16
Q

Link reaction

A

Pyruvate —> acetyl CoA

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17
Q

Link reaction enzyme

A

Pyruvate dehydrogenase

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18
Q

Inhibitors of pyruvate dehydrogenase

A

Acetyl-CoA
ATP

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19
Q

Amplifier of pyruvate dehydrogenase

A

AMP

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20
Q

What is produced during link reaction

A

NADH + H+ + CO2

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21
Q

Ketogenesis in the liver

A

2 acetyl-CoA
Acetoacetyl-CoA
HMG-CoA
Acetoacetate
Beta-hydroxybutyrate and acetone

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22
Q

Enzyme converts acetyl-CoA to acetoacetyl-CoA

A
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23
Q

Ketones produced by ketogenesis

A

Acetoacetate
Acetone
Beta-hydroxybutyrate

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24
Q

What does 1 pyruvate molecule produce

A

3 NADH
1 FADH2
2 CO2
1 GTP

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25
Q

What is the kreb’s cycle inhibited by

A

NADH
ATP

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26
Q

What is the kreb’s cycle stimulated by

A

ADP

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27
Q

Where does the kreb’s cycle occur

A

Mitochondrial matrix

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28
Q

Kreb’s cycle

A

Acetyl-CoA
Citrate
Isocitrate
Alpha-ketoglutarate
Succinylcholine-CoA
Succinct
Fumarate
Maleate
Oxaloacetate

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29
Q

Rate limiting enzyme of kreb’s cycle

A

Isocitrate dehydrogenase

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30
Q

Enzymes of the kreb’s cycle

A

Citrate synthase
Aconitase
Isocitrate dehydrogenase
Alpha-ketoglutarate dehydrogenase
Succinyl-CoA synthase
Succinct dehydrogenase
Fumarate hydratase (fumarase)
Maleate dehydrogenase

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31
Q

Number of ATP produced per glucose molecule

A

38 ATP

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32
Q

Number of ATP produced per pyruvate molecule

A

19

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33
Q

ATP produced by glycolysis

A

2 ATP directly (4 ATP made and 2 ATP used)
6 ATP produced by 2NADH2 (3 each)

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34
Q

ATP produced by Kreb’s cycle per pyruvate

A

9 ATP produced by 3 NADH2 (3 each)
2 ATP produced by FADH2 (2 each)

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35
Q

Number of ATP produced by NADH2

A

3

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36
Q

Number of ATP produced by FADH2

A

2

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37
Q

Metabolism

A

Sum of chemical reactions that occur within each cell of an organism

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38
Q

Anabolic

A

Forming large molecules from small molecules, requires energy

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39
Q

Catabolic

A

Breaking down large molecules into smaller ones, creates energy

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40
Q

Kcal/g released by protein

A

4

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41
Q

Kcal/g released by carbohydrate

A

4

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42
Q

Kcal/g released by alcohol

A

7

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43
Q

Kcal/g released by lipid

A

9

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44
Q

Kcal/unit of alcohol

A

56
7 kcal/g x 8g (10ml=1unit) = 56 kcal/unit

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45
Q

Basal metabolic rate

A

Energy required to maintain non-exercise bodily functions (homeostasis)

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46
Q

Units of BMR

A

Kcal expended/hr/m^2

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47
Q

Henry equation

A

Estimates BMR based on age, weight and gender

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48
Q

Factors that increase BMR

A

Male (increased muscle mass)
Regular exercise
Caffeine
Young age (growing)
Temperature extreme
Disease
Hyperthyroidism
Pregnancy and lactation
Infection and chronic disease

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49
Q

Factors that decrease BMR

A

Starvation/ dieting
Old age (decreased muscle mass)
Hypothyroidism

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50
Q

BMI

A

Weight (kg)/ height (m^2)

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51
Q

When is O2 consumption measured to calculate BMR

A

When awake, rested and fasted for 12hrs

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52
Q

BMI normal weight range

A

18.5-25

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53
Q

BMI underweight range

A

0-18.5

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54
Q

BMI overweight range

A

25-30

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55
Q

BMI obese range

A

30-40

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56
Q

4 main pathways that dietary components are metabolised

A

• biosynthetic
• fuel storage
• oxidative processes
• waste disposal

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57
Q

Essential fatty acids

A

linoleic (omega 6) and alpha-linolenic (omega 3) series

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58
Q

Essential amino acids

A

lysine, isoleucine, leucine, threonine, valine, tryptophan, phenylalanine, methionine, and histidine.

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59
Q

Which substrates are formed by the splitting of fructose-1,6-bisphosphate

A

Glyceraldehyde-3-phosphate
Dihydroxyacetone phosphate

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60
Q

Which enzyme catalyses the third reaction in the glycolysis pathway

A

Phosphofructokinase

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61
Q

Triacylglycerol

A

3 fatty acids esterified to one glycerol moiety (group)

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62
Q

Kcal requirement for an average hospital patient

A

25-35 kcal/day/kg

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63
Q

Dietary components

A

fuels, essential amino acids, essential fatty acids, vitamins, minerals, water, xerobiotics (foreign substances eg drugs)

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64
Q

Storage of excess fat

A

adipose tissue (only 15% water) as triglycerides (for 70kg man approx. 15kg)

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65
Q

Amount of fat stored in average 70kg man

A

15kg

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66
Q

Storage of excess carbohydrates

A

glycogen in liver (for 70kg man up to 200g) and muscles (70kg man- 150g)

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67
Q

Average amount of glycogen stored in liver for 70kg man

A

200g

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68
Q

Average amount of glycogen stored in muscles for 70kg man

A

150g

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69
Q

Storage of excess protein

A

muscle (80% water) (for 70kg man approx. 6kg)

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70
Q

Average amount of protein stored as muscle in 70kg man

A

6kg

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71
Q

What percentage of muscle is water

A

80%

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72
Q

What percentage of adipose tissue is water

A

15%

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73
Q

How many kJ is 1 Kcal

A

4.18 kJ

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74
Q

BMI severely obese range

A

40+

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75
Q

Rough estimate of BMR

A

1 kcal/kg body mass/hour

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76
Q

What is BMR proportional to

A

Amount of metabolically active tissue (including the major organs) and the lean (or fat free) body mass

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77
Q

How is BMR measured

A

CO2 produced

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78
Q

When does BMR apply

A

• post-absorptive (12 hour fast)
• lying still at physical and mental rest
• Thermo-neutral environment ( 27 -29°C)
• No tea/coffee/nicotine/alcohol in previous 12 hours
• no heavy physical activity in previous 24 hours
• establish steady state (30 mins)

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79
Q

Why is BMR generally higher in children

A

Greater proportion of metabolically active tissue

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80
Q

Why is BMR usually lower in women than men

A

More adipose tissue and less muscle mass

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81
Q

Resting metabolic rate

A

30% higher than basal metabolic weight for a very sedentary person and a value of 60% to 70% of the BMR (per day) for a person who engages in about 2 hours of moderate physical activity per day A value of 100% or more of the BMR is used for a person who does several hours of vigorous physical activity per day.

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82
Q

Malnutrition

A

a state of nutrition with a deficiency, excess or imbalance of energy, protein or other nutrients, causing measure adverse effects on tissue/body shape/size/composition, body function and clinical outcome

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83
Q

Starvation

A

• Overnight fast - decreases insulin secretion → glycogenolysis (break down glycogen to produce glucose)
Brain requires approx 150g glucose/day. After an overnight fast, liver has about 80g glycogen
• Longer fasts necessitate gluconeogenesis (uses lactate, amino acids (muscle, intestine, skin breakdown) and glycerol (fat breakdown))- decrease insulin secretion and increased cortisol secretion - lipolysis and proteolysis
• >4 days- liver creates ketones from fatty acids, brain adapts to using ketones (ketones are acidic so excess causes blood pH to fall- ketoacidosis- prevent enzyme function), BMR falls (accommodation)

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84
Q

DEE

A

Daily energy expenditure

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85
Q

What does complete oxidation of proteins produce

A

CO2, H2O, NH4+

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86
Q

Why does lipid oxidation produce the most energy

A

more reduced so can oxidise more to produce more energy

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87
Q

Name of vitamin A

A

Retinol

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88
Q

Name of vitamin D

A

Calciferol

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89
Q

Name of vitamin E

A

Tocopherol

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90
Q

Name of vitamin K

A

Phylloquinone, Menaphthone

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91
Q

Name of vitamin C

A

Ascorbic acid

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92
Q

Name of vitamin B12

A

Cobalamin

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93
Q

Name of vitamin B1

A

Thiamin

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94
Q

Name of vitamin B2

A

Riboflavin

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95
Q

Name of vitamin B3

A

Niacin

96
Q

B vitamins

A

B1, B2, B3, pantothenic acid, B6, biotin, folate, B12

97
Q

Vitamin C

A

ascorbic acid, fruit and vegetables, heat labile, collagen synthesis, improve iron absorption, antioxidant

Destroyed by heat

Lack of vitamin C = Scurvy

98
Q

Vitamin B12

A

cobalamin, protein synthesis, DNA synthesis, regenerate folate, fatty acid synthesis, energy production

Broken down in stomach with cofactor
Absorbed in terminal ileum

99
Q

How long does carbohydrate provide energy for

A

glycogen to sustain energy levels for 12 hours

100
Q

How long does fats provide energy for

A

provide energy for up to 12 weeks

101
Q

When is protein used as an energy source

A

used when muscle glycogen stores fail

102
Q

The prudent diet

A

• 5+ servings of fruit/vegetables
• Base meals around starchy (complex) carbohydrates
• No more than 5% energy should come from free sugars (glucose, fructose)
• 0.8 g/kg/day protein
• Saturated fat: no more than 30g/day for men & 20g/day for women
• No more than 2.4g/day of sodium (6g salt)
• No more than 14 units alcohol / week (over at least 3 days)
• Adequate calcium

103
Q

How much protein should we consume according to the prudent diet

A

0.8g/kg/day

104
Q

How much sodium should we consume according to the prudent diet

A

2.4 g/day (6g salt)

105
Q

How much saturated fat should we consume according to the prudent diet

A

No more than 30g per day for men
No more than 20g per day for women

106
Q

How much energy should come from free sugars (glucose, fructose) according to the prudent diet

A

No more than 5%

107
Q

Major minerals required in the diet

A

Sodium
Potassium
Calcium
Chloride
Phosphorus
Magnesium

108
Q

Kinase enzymes

A

Moves phosphate group

109
Q

ATP

A

currency of metabolic energy- a high energy molecule composed of adenine, ribose and 3 phosphate groups
Hydrolysis of ATP to ADP and Pi

energy is stored in phosphate bonds

110
Q

Need for glycolysis

A

• emergency energy producing pathway when oxygen is limiting (erythrocytes and exercising skeletal muscle)
• Generates precursors for biosynthesis:
• Glucose-6-Phosphate converted to ribose-5-P (nucleotides) via pentose phosphate pathway and G-1-P for glycogen synthesis
• Pyruvate- transaminated to alanine, substrate for fatty acid synthesis
• Glycerol-3-P is backbone of triglycerides

111
Q

Which enzyme phosphorylates glucose to glucose-6-phosphate

A

Hexokinase using ATP

112
Q

Which enzyme isomerises glucose-6-phosphate to fructose-6-phosphate

A

Phosphoglucose isomerase

113
Q

Which enzyme phosphorylates fructose-6-phosphate to form fructose-1,6-bisphosphate

A

Phosphofructokinase-1 using ATP

114
Q

Which enzymes cleaves fructose-1,6-bisphosphate to form glyceraldehyde-3-phosphate and dihydroxyacetone phosphate

A

Adolase

115
Q

Which enzyme isomerises dihydroxyacetone phosphate to glyceraldehyde-3-phosphate

A

Triose phosphate isomerase

116
Q

Which enzyme oxidises glyceraldehyde-3-phosphate to 1,3-bisphosphoglycerate

A

Triose phosphate dehydrogenase

117
Q

What is produced when Triose phosphate dehydrogenase oxidises glyceraldehyde-3-phosphate to 1,3-bisphosphoglycerate

A

2 molecules of NADH

118
Q

Which steps of glycolysis require ATP

A

Glucose —> glucose-6-phosphate
Fructose-6-phosphate —> fructose-1,6-bisphosphate

119
Q

Which enzyme converts 1,3-bisphosphoglycerate to 3-phosphoglycerate

A

Phosphoglycerokinase

120
Q

Which enzymes isomerises 3-phosphoglycerate to form 2-phosphoglycerate

A

Phosphoglyceromutase

121
Q

Which enzyme isomerises and dehydrates 2-phosphoglycerate to form phosphoenolpyruvate

A

Enolase

122
Q

Which enzyme produces pyruvate from phosphoenolpyruvate

A

Pyruvate kinase

123
Q

Which 2 stages of glycolysis produce 2 ATP molecules by substrate-level phosphorylation

A

1,3-bisphosphoglycerate —> 3-phosphoglycerate
Phosphoenolpyruvate—> Pyruvate

124
Q

How is ATP produced during glycolysis

A

Substrate level phosphorylation

125
Q

Which are irreversible phases of glycolysis

A

Glucose —>glucose-6-phosphate
Fructose-6-phosphate —>fructose-1,6-bisphosphate
Phosphoenolpyruvate—> pyruvate

126
Q

Allosteric regulation of glycolysis

A

molecule binds to a non-catalytic site, conformational change which changes affinity for the substrate

127
Q

What does ATP inhibit in glycolysis

A

PFK1
(Reduces energy wastage)

128
Q

What does AMP activate in glycolysis

A

activator of PFK1, when ATP is used up, ADP accumulates and is converted to AMP by adenylate kinase reaction to generate ATP 2ADP = ATP + AMP

129
Q

What does citrate inhibit in glycolysis

A

inhibits PFK1 so a signal cycle does not need more fuel

130
Q

What does fructose-2,6-bisphosphate inhibit in glycolysis

A

generates from fructose-6-phosphate, inhibitor of PFK1, mediates
effect of insulin and glucagon

131
Q

How does acidosis affect glycolysis

A

Inhibits PFK1

132
Q

Hormonal regulation of glycolysis

A

insulin and glucagon. Indirect route through affecting regulatory molecules (eg kinases or phosphatases)
Increases or decreases gene expression for the enzyme
Increase or decrease enzyme activity

133
Q

Fate of pyruvate- anaerobic conditions

A

lactate formation catalysed by lactate dehydrogenase. Regeneration of NAD+ by oxidation
Important to allow glycolysis to continue so it can produce one ATP in low O2 conditions or erythrocytes
Glucose + 2ADP + 2Pi → 2 lactate + 2 ATP + 2H2O + 2H+

134
Q

Cori cycle

A

prevent build up of lactic acid and muscle fatigue

135
Q

Gluconeogenesis of lactate

A

In liver, gluconeogenesis of lactate to glucose through lactate dehydrogenase
In hepatocytes

136
Q

Fate of pyruvate - aerobic conditions

A

enters mictochondria and converted to Acetyl CoA and CO2 by pyruvate dehydrogenase in a decarboxylation reaction (link reaction). Acetyl CoA can enter Kreb’s cycle for more energy production .
Inhibited allosterically by its products Acetyl CoA, ATP and NADH when in high concentrations, and products indirectly act by activating a kinase that phosphorylates and inhibits PDH
Decarboxylation of pyruvate to Acetyl-CoA is irreversible
Pyruvate + CoA + NAD+ → Acetyl-CoA + CO2 + NADH + H+

137
Q

Which enzyme converts pyruvate to Acetyl CoA

A

Pyruvate dehydrogenase

138
Q

Inhibition of link reaction

A

allosterically by its products Acetyl CoA, ATP and NADH when in high concentrations, and products indirectly act by activating a kinase that phosphorylates and inhibits PDH

139
Q

Fast glycolytic fibres

A

Sparse capillaries
Sparse mitochondria
Sparse myoglobin
Low oxidative capacity/ high glycolytic
Easily fatigued
High ATPase activity
Fast contractions

140
Q

Slow oxidative fibres

A

Abundant capillaries
Abundant mitochondria
Abundant myoglobin
High oxidative capacity
Fatigue resistant
Low ATPase activity
Slow contractions

141
Q

Reason for Kreb’s cycle

A

• Generates lots of energy in form of ATP
• provides final common pathway for oxidation of carbohydrates, fat and protein via Acetyl CoA
• produces intermediates for the synthesis of amino acids, glucose, heme etc
• Sequence of 8 enzymatic reactions
• Acetyl CoA condenses oxaloacetate forming citrate
• Oxaloacetate is regenerated in the last step of the krebs’ cycle and 2 CO2 molecules released
• Energy is harvested in the form of NADH, 2FADH2 and ATP molecules

142
Q

Pneumonic for kreb’s cycle order

A

Citrate Is Krebs’ Starting Substrate For Making Oxaloacetate

143
Q

Which enzyme combines acetyl CoA and oxaloacetate to form citrate

A

Citrate synthase

144
Q

Which enzyme isomerises citrate to isocitrate

A

Aconitase

145
Q

Which enzyme oxidises and dehydrogenates isocitrate to form alpha-ketoglutarate

A

Isocitrate dehydrogenase

146
Q

What is produced when alpha-ketoglutarate is formed

A

CO2 and NADH

147
Q

Which enzyme converts alpha-ketoglutarate to succinyl-CoA

A

Alpha-ketoglutarate dehydrogenase

148
Q

What is produced when succinyl-CoA is formed

A

CO2 and NADH

149
Q

Which enzyme converts succinyl-CoA to succinate

A

Succinate thiokinase

150
Q

What is produced when succinate is formed

A

Phosphorylation of GDP to GTP which is then converted to ATP

151
Q

Which enzyme oxidises succinate to form fumarate

A

Succinate dehydrogenase

152
Q

What is produced when fumarate is formed

A

FADH2

153
Q

Which enzyme converts fumarate to malate

A

Fumarate hydrase (by addition of water)

154
Q

Which enzyme converts malate to oxaloacetate

A

Malate dehydrogenase

155
Q

What is produced when oxaloacetate forms

A

NADH

156
Q

Regulation of kreb’s cycle

A

• rate determined by levels of ATP, NADH, FADH2- high levels inhibit Krebs’ cycle
• Activated by high ADP
• Alpha-ketoglutarate dehydrogenase as activated by Ca2+ (muscle contraction)
• if cycle inhibited, build up of Acetyl CoA so undergoes fatty acid synthesis

157
Q

What inhibits pyruvate dehydrogenase

A

ATP, NADH, Acetyl-CoA

158
Q

What activates pyruvate dehydrogenase

A

ADP

159
Q

What inhibits citrate synthase

A

ATP, NADH, citrate

160
Q

What activates citrate synthase

A

ADP

161
Q

What inhibits isocitrate dehydrogenase

A

ATP, NADH

162
Q

What activates isocitrate dehydrogenase

A

ADP

163
Q

What inhibits alpha-ketoglutarate dehydrogenase

A

ATP, NADH, GTP, succinyl-CoA

164
Q

What activates alpha-ketoglutarate dehydrogenase

A

Ca2+

165
Q

Where does oxidative phosphorylation occur

A

occurs in inner mitochondrial membrane, aerobic conditions

166
Q

Oxidative phosphorylation

A
  1. Components of ETC accept electrons (reduced) and pass them on (oxidised).
  2. Electrons are transferred to final electron acceptor O2 (which is reduced by hydrogen to form water)
  3. Free energy drop as electrons are passed down ETC
  4. Free energy is used to pump H+ across the inner membrane space via the Cytochrome-C oxidase complex, creating a proton motive gradient
  5. ATP synthase contains a proton pore
  6. ATP produced as protons flux in through ATP synthase- energy coupled to chemiosmosis (about 28 ATP molecules)
  7. In the matrix, the H+, electrons and oxygen combine to form water as O2 is the final electron acceptor
    1/2O2 + 2e- + 2H+ → H2O
167
Q

Complex I

A

Removes electrons from NADH

168
Q

Complex II

A

Removes electrons from FADH2 in prescence of coenzyme Q (ubiquinone)

169
Q

Complex III,IV and cytochrome C

A

donate electrons to cytochromes containing iron (anemia and OXPHOS diseases decreases mitochondrial capacity for oxidative phosphorylation)

170
Q

Why must protons move via ATP synthase

A

Inner mitochondrial membrane is impermeable

171
Q

What causes an increased metabolic rate and heat generation - oxidative phosphorylation

A

Proton leakage, chemical uncouplers and regular uncoupling protons

172
Q

What is rate of ETC coupled with

A

rate of ATP synthesis by the transmembrane electrochemical gradient As ATP is used for energy-requiring processes and ADP levels increase, proton influx through the ATP synthase pore generates more ATP, and the electron transport chain responds to restore Δp. In uncoupling, protons return to the matrix by a mechanism that bypasses the ATP synthase pore, and the energy is released as heat.

173
Q

Steady energy state of cell

A

balance ATP generation

174
Q

Maintenance of stable blood glucose

A

• Low glucose is damaging to cells/brain
• High glucose is damaging (glycosylation of proteins)
• Maintained through action of anabolic hormones (insulin) and catabolic hormones (glucagon, catecholamines)

175
Q

Normal blood glucose range

A

4.5-5.5 mmol/L

176
Q

Main ketones in body produced by citric acid cycle from Acetyl CoA

A

Acetone
Acetoacetone
Beta-hydroxybutyrate

177
Q

Synthesis of ketones

A

• occurs when high ATP levels which inhibits the Krebs’ cycle and was to a build up Acetyl CoA
• Occurs in cytosol of cell
• But Acetyl CoA cannot cross mitochondrial membrane

178
Q

Fatty acids

A

• carboxylic head group with aliphatic tail
• Long acyl CoA chains
• saturated and unsaturated
• most are derived from triglycerides and phospholipids

179
Q

18 carbon fatty acid

A

Linoleic acid
Oleic acid

180
Q

16 carbon fatty acid

A

Palmitic acid

181
Q

20 carbon fatty acid

A

Arachidonic acid

182
Q

Lipid absorption

A
  1. Bile salts emulsify dietary fats in small intestine, forming mixed micelles
  2. Intestinal lipases degrade triacylglycerols
  3. Fatty acids and other breakdown products are taken up by the intestinal mucosa and converted into triacylglycerols
  4. Triacylglycerols are incorporated with cholesterol and apoproteins into chylomicrons
  5. Chylomicrons move through the lymphatic system and bloodstream to tissues
  6. Lipoprotein lipase, activated by apoC-II in the capillary, releases fatty acids and glycerol
  7. Fatty acids enter cell
  8. Oxidised as fuel or reesterified for storage
183
Q

What is lipoprotein lipase activated by

A

apoC-II in the capillary

184
Q

What forms chylomicrons

A

Triacylglyerols
Cholesterol
Apoproteins

185
Q

Fatty acid activation

A

• must be activated in the cytoplasm before they can be oxidised in the mitochondria
• if the acyl-CoA has < 12 carbons - can diffuse through mitochondrial membrane
• most dietary fatty acids have > 14 carbons - taken through mitochondrial membrane using the carnitine shuttle

Fatty acid → acyl adenylate → acyl CoA
ATP -> PPi. HS-CoA -> AMP

186
Q

Fatty acid activation equation

A

Fatty acid → acyl adenylate → acyl CoA

187
Q

What enzyme converts acyl adenylate to acyl-CoA

A

Acyl-CoA synthase

188
Q

Citrate shuffle

A

• oxaloacetate bonds with Acetyl CoA to produce citrate- can cross mitochondrial membrane into cytosol
• Citrate ligase converts citrate back to oxaloacetate which is then broken down into pyruvate and Acetyl CoA
• Pyruvate recycled back into mitochondria and converted to oxaloacetate so can re-enter Krebs’ cycle
• Acetyl-CoA converted into fatty acids

189
Q

Carnitine shuffle

A

• the acyl-CoA chains are converted and reformed in order to cross the membrane
• Acyl-CoA to acyl carnitine by carnitine acyltransferase 1 (CAT1)- Located on outer mitochondrial membrane
• CoA is recycled
• acyl carnitine is reformed to acyl CoA by cartinine acyltransferase 2 (CAT2)- On interior of membrane
• Cartinine recycled through the outer membrane

190
Q

Fatty acid beta-oxidation

A

Energy derived from fatty acid beta-oxidation
• once acyl-CoA has crossed the membrane it can now be oxidised
• This involves the sequential removal of 2 carbon units by oxidation- the second (hence beta) carbon is cleaves
• Each round produces 1 NADH, 1 FADH2, and 1 Acetyl-CoA
• FADH2 and NAD undergo oxidative phosphorylation
• Acetyl-CoA re-enters the krebs’ cycle
• ATP is produced
• Oxidation →hydration →oxidation →thiolysis

191
Q

When does fatty acid beta-oxidation occur

A

Occurs in response to decreased blood glucose and high glucagon

192
Q

Fatty acid beta-oxidation molecules

A

Acyl-CoA —> Acetyl-CoA
Following oxidation -> hydration-> oxidation ->thiolysis

193
Q

Which enzyme is involved in first oxidation in fatty acid beta-oxidation

A

Acyl-CoA dehydrogenase

194
Q

Which enzyme is involved in hydration in fatty acid beta-oxidation

A

Enol-CoA hydrase

195
Q

Which enzyme is involved in second oxidation in fatty acid beta-oxidation

A

Hydroxyacyl CoA- dehydrogenase

196
Q

Which enzyme is involved in thiolysis in fatty acid beta-oxidation

A

Thiolase

197
Q

What does each round of fatty acid beta-oxidation produce

A

1 NADH
1 FADH2
1 Acetyl-CoA

198
Q

Utilisation of acetyl-CoA

A

• under normal metabolic conditions most Acetyl-CoA is utilised via the TCA acid cycle to produce glucose
• A small proportion is converted to ketones
• Ketones- molecules produced by the liver from Acetyl-CoA - have a characteristic fruity/nail polish remover-like smell
• during high rates of fatty acid oxidation, large amounts of Acetyl-CoA are generated
• this exceeds the capacity of the krebs’ cycle, which results in ketogenesis

199
Q

Ketones

A

molecules produced by the liver from Acetyl-CoA - have a characteristic fruity (pear drops)/nail polish remover-like smell

200
Q

Causes of respiratory alkalosis

A

hyperventilation in response to hypoxia

201
Q

Causes of metabolic acidosis

A

renal failure, loss of HCO3-, excess H+ production

202
Q

Respiratory acidosis

A

PaCO2 increases leading to an increase in H+ ions and so pH decreases
• CO2 production is greater than CO2 elimination

203
Q

Ketogenesis

A

• acetoacetate can undergo spontaneous decorboxylation to acetone, or be enzymatically converted to beta-hydroxybutyrate
• ketone bodies utilised by extrahepatic tissues through conversion of beta-hydroxybutyrate and acetoacetate to acetoacetyl-CoA
• this requires the enzyme acetoacetate: succinyl-CoA transferase, which is found in all but hepatic tissue
• When glycogen levels in liver are high, beta-hydroxybutyrate production increases

204
Q

Ketogenesis reactions

A

2 acetyl-CoA —> acetoacetyl CoA—> 3-hydroxy-3-methyl glutaryl CoA (HMG CoA)—> acetoacetate —> EITHER alpha-beta-hydroxybutyrate OR acetone

205
Q

Which enzyme converts 2 acetyl CoA to acetoacetyl CoA

A

Thiolase

206
Q

Which enzyme converts acetoacetyl CoA to 3-hydroxy-3-methyl glutaryl CoA

A

HMG CoA synthase

207
Q

Which enzyme converts 3-hydroxy-3-methyl glutaryl CoA to acetoacetone

A

HMG CoA lysase

208
Q

Which enzyme converts acetoacetone to alpha-beta-hydroxybutyrate.

A

Alpha-beta-hydroxybutyrate dehydrogenase

209
Q

Which enzyme converts acetoacetate to acetone

A

NONE
it occurs spontaneously

210
Q

Regulation of ketogenesis affected by

A

• release of free fatty acids from adipose tissue- more fatty acids, more ketones
• a high concentration of glycerol-3-phosphate in the liver results in triglyceride production, whilst a low level results in increased ketone body production
• when demand for ATP is high, Acetyl-CoA is likely to be further oxidised via the TCA cycle to CO2
• fat oxidation is dependent upon the amount of glucagon (activation) or insulin (inhibition) present

211
Q

Clinical significance of ketogenesis

A

• during normal physiological conditions the production of ketones occurs at a low rate
• carbohydrate shortages cause the liver to increase ketone the body production from Acetyl-CoA
• the heart and skeletal muscles preferentially utilise ketone bodies for energy preserving glucose for the brain

212
Q

Ketoacidiosis

A

• occurs in insulin-dependent diabetics when dose is inadequate or because of increased insulin requirement (infection, trauma, acute illness)
• often the presenting feature in newly diagnosed type 1 diabetics
• also occurs in chronic alcohol abuse and starvation
• patients present with hyperventilation and vomiting

213
Q

Consequences of ketoacidosis

A

ketones are relatively strong acids (pKa~ 3.5). Excessive ketones lower blood pH which impairs ability of haemoglobin to bind to oxygen

214
Q

Blood test ketoacidosis

A

pH- low
pO2- high
pCO2- low
HCO3- low

CO2 low as acidic so hyperventilate to remove CO2 from blood to compensate for acidic ketones and lots of O2
HCO3 bicarbonate (base) trying to neutralise blood so low levels left

215
Q

Diabetic ketoacidosis

A

Insulin deficiency:
1. Inhibition of glycolysis and stimulation of glyconeogenesis
2. Glycogen breakdown and inhibition of glycogen synthesis
3. Increased lipolysis (increased free fatty acids)
-1 and 2 lead to hyperglycaemia
-3 leads to Increased acetoacetate and beta-hydroxybutyrate (Can be oxidised as fuels in most tissues (eg skeletal muscle))

216
Q

Treatment of diabetic ketoacidosis

A

• sliding scale of insulin
• IV fluid hydration (10% dextrose and 0.9% saline)
• monitor fluid balance closely
• 40 mmol potassium
• pabrinex: injection containing vitamins C, B1, B2, B3, B6

217
Q

Alcoholic ketoacidosis

A

High blood EtOH concentration
Depleted protein and carbohydrate stores:
1. Impaired gluconeogenesis
2. Decreased insulin and increased glucagon secretion
Increased lipolysis (increased free fatty acids)
Increased ketone production

218
Q

3 biological buffers

A

Protein
Haemoglobin
Bicarbonate

219
Q

Homeostasis

A

Maintenance of a stable internal environment eg temperature, glucose, potassium, blood oxygen, hydrogen ions

220
Q

Normal pH range of body

A

7.35-7.45

221
Q

Endocrine glands

A

Ductless
Release hormones into blood

222
Q

Auto rinse

A

messenger molecules bind with receptors in cell where they are produced eg chemical/secondary messengers

223
Q

Paracrine

A

messengers in ECF eg clotting factors, prostaglandins in childbirth, inflammatory mediators, interleukins signalling in immune system mainly between white blood cells, platelet derived growth factor releases from platelets and regulates cell growth. Signal diffuses across gap between cells. Inactivated locally so doesn’t enter blood stream

224
Q

Endocrine

A

secretions into blood eg insulin

225
Q

Exocrine

A

secrete substances through ducts onto your body surfaces. Exocrine glands secrete sweat, tears, saliva, milk and digestive juices

226
Q

Endocrine organs and glands

A

hypothalamus, pituitary, thyroid, adrenals, pancreas, ovaries, testes, skin, heart

227
Q

Peptide hormones

A

Made of short amino acid chains (some have carbohydrate side chains- glycoproteins)
Hydrophilic so can dissolve in blood
Stored in cell and released when needed/signalled
Binds to a receptor on membrane
Produces a quick response via a secondary messenger cascade (eg cAMP, Ca2+)
Eg insulin, growth hormone, TSH and ADH

228
Q

Amino acid derivatives hormones

A

Synthesised from tyrosine
Acts in same way as peptide hormones
Eg adrenaline (epinephrine), thyroid hormones (T4 and T3)

229
Q

What are all amino acid derivatives synthesised from

A

Tyrosine

230
Q

Steroid hormones

A

Synthesised from cholesterol
Water insoluble and lipid soluble- can cross membranes but requires transport proteins in blood
Intercellular receptor target
Synthesised on demand
Steroid hormone made in cell and diffuses out once made (not stored)
Directly affects DNA and alters transcription/translation- slow response as proteins have to be made
Eg testosterones, oestrogen, cortisol

231
Q

Example of steroid hormone transport proteins

A

Albumin
Sex hormone binding globulin

232
Q

What are all steroid hormones synthesised from

A

Cholesterol

233
Q

Positive feedback loop

A

signal is amplified
• when a deviation from an optimum causes changes that results in an even greater deviation from the normal e.g. During birth oxytocin released due to increased pressure, which causes more contractions, increasing pressure, releasing more oxytocin; action potentials; bone repair (osteocalcin) or hypothermia/hyperthermia

234
Q

Negative feedback loop

A

when the change produced by the control system leads to a change in the stimulus detected by the receptor and turns the system off (system is restored to its original level)
• eg blood glucose

235
Q

When is beta oxidation used

A

Beta oxidation is used in aerobic conditions as fuel when there is increased demand
e.g. during fasting or states of low blood glucose. However it cannot be used as fuel for the nervous system because fatty acids cannot pass the blood-brain barrier

IMMS (6 decks)

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