Cell metabolism Flashcards
1
Q
What are the 6 types of reactions?
A
Oxidation-reduction, Ligation requiring ATP cleavage, Isomerization, Group transfer, Hydrolytic, Addition or removal of functional groups.
2
Q
What is oxidation-reduction?
A
Electron transfer.
3
Q
What is ligation?
A
Formation of covalent bonds.
4
Q
What is isomerization?
A
Rearrangement of atoms.
5
Q
What is group transfer?
A
Transfer of a functional group from one molecule to another.
6
Q
What is hydrolytic?
A
Cleavage of bonds by the addition of water.
7
Q
What is addition or removal of functional groups?
A
Addition of functional group to double bond or removal of functional group to form double bond.
8
Q
What are the two phases of glycolysis?
A
Energy consuming phase and energy producing phase.
9
Q
What is a kinase?
A
An enzyme that catalyses the transfer of a phosphate group from one molecule to another.
10
Q
Why can’t glucose-6-phosphate diffuse out of cell?
A
Cause of the negative phosphate group. Makes molecule more reactive and can’t bind to glucose carriers.
11
Q
What key enzyme regulates entry of sugars into glycolysis pathway?
A
Phosphofructokinase.
12
Q
Deficiency in what glycolytic enzyme is fatal?
A
Triose phosphate isomerase.
13
Q
What is an isomerase?
A
An enzyme that catalyses the rearrangement of bonds within a single molecule.
14
Q
What is a dehydrogenase enzyme?
A
An enzyme that catalyses the oxidation of a molecule by removing a hydride ion.
15
Q
What is a mutase enzyme?
A
Catalyses the shift of a chemical group from one position to another within a molecule.
16
Q
Why is glycolysis described as substrate level phosphorylation?
A
Phosphate group is directly being transferred from a substrate (sugar intermediate) to ADP.
17
Q
What is fermentation?
A
Breakdown of sugar in absence of oxygen.
18
Q
Why is pyruvate converted to lactate? What enzyme converts it?
A
Allows continuation of glycolysis as NAD+ is regenerated by converting pyruvate into lactate and oxidising NADH to produce NAD+. Lactate dehydrogenase.
19
Q
Where is NAD+ needed in glycolysis?
A
Dehydrogenation of glyceraldehyde 3-phosphate into 1,3-bisphosphoglycerate.
20
Q
Which is the high energy intermediates in glycolysis?
A
1,3-bisphosphoglycerate and phosphoenolpyruvate.
21
Q
Why are molecules called high energy intermediates?
A
Hydrolysis of phosphate bond has high delta G. Very energetically favourable.
22
Q
How is pyruvate converted to acetyl CoA?
A
Decarboxylation. Addition of co enzyme A. NADH produced.
23
Q
What catalyses pyruvate to acetyl CoA?
A
pyruvate dehydrogenase complex
24
Q
How many carbons is a fatty acid chain shortened by to produce a molecule of acetyl CoA?
A
2 carbons.
25
Where are fatty acids converted into acetyl CoA?
Mitochondrial matrix.
26
What else is produced in the conversion of fatty acids to acetyl CoA?
One molecule of FADH2 and NADH.
27
Where do the oxygen atoms to make CO2 in the krebs cycle come from?
Hydrolysis of three water molecules.
28
What does one turn of the krebs cycle produce?
Three NADH molecules, One GTP molecule, one molecule of FADH2 and two molecules of CO2.
29
What molecules can be formed from the intermediates from glycolysis and citric acid cycle?
Amino acids, lipids, nucleotides and other small organic molecules.
30
What is produced from glycolysis?
Two molecules of pyruvate, 2 molecules of ATP and 2 molecules of NADH.
31
What does creatine phosphate do?
Acts as a buffer for demand for phosphate.
32
Why do people take creatine as a supplement?
To increase creatine phosphate.
33
What allows acetyl CoA to donate the acetate group?
High energy thioester bond (C-S Bond) so it is readily hydrolysed.
34
Pyruvate to acetyl CoA products?
Acetyl CoA, NADH and CO2.
35
3 key glycolysis enzymes?
TPI, PFK and PDH
36
What biochemical pathway does beri beri affect?
Conversion of pyruvate to Acetyl CoA.
37
What results in Beri Beri?
Lack of thiamine which results in poor pyruvate dehydrogenase function.
38
Beri Beri symptoms?
Damage to peripheral nervous system, weakness of musculature and reduced cardiac output.
39
Why is thiamine required for proper PDH function?
Required for thiamine pyrophosphate which is a cofactor in PDH.
40
What is transamination?
Amine group is transferred from amino acid to keto acid forming a new pair of amino acid and keto acid.
41
Why does NADH high energy electrons need to enter the matrix of the mitochondria?
So that they can be used in oxidative phosphorylation and to regenerate NAD+ for glycolysis.
42
How are electrons from NADH produced in cytoplasm transferred across mitochondrial membrane?
Via a shuttle.
43
In the glycerol phosphate shuttle what is the final destination for the electrons transferred to?
FAD and then to co-enzyme Q (part of electron transport chain).
44
Where is the glycerol phosphate shuttle used in the body?
Skeletal muscle and brain
45
Where is the malate aspartate shuttle used?
Liver, Kidney and heart
46
What transports malate and aspartate across the mitochondrial membrane?
Antiporter. (As one molecule goes in another molecule leaves).
47
How many ATP molecules per molecule of NADH?
3
48
How many ATP molecules per molecule of FADH2?
2
49
What is the warburg effect?
Mutations in genes of Fumerase, Succinate, Isocitrate Dehydrogenase, decreases Kreb's Cycle activity which enhances anaerobic glycolysis. Generation of lactate from glucose even in increased O2 availability.
50
Caloric yield of fats compared to carbs?
Fats have 2x the caloric yield.
51
What is the first step of B oxidation?
Fatty acid is converted to acyl CoA.
52
Where does the first step of B oxidation occur?
Outer mitochondrial membrane.
53
How is acyl CoA transported into the mitochondrial matrix?
Carnitine shuttle. Acyl group binds to carnitine and acyl carnitine is transported in via a translocase. Acyl group is then transferred to a CoA molecule and carnitine is transported back out.
54
How many molecules of ATP per acetyl CoA molecule?
12
55
How many B oxidation cycles from a 16 carbon fatty acid?
7 cycles. Last cycle produces 2 acetyl CoA molecules.
56
How many Acetyl CoA molecules produced from a 16 carbon fatty acid chain.
8
57
How many NADH and FADH2 molecules are produced from a 16 carbon fatty acid chain?
7
58
Why is fatty acid oxidation called b oxidation?
Oxidation occurs at beta carbon.
59
Why are ketone bodies made?
Acetyl CoA produced from b oxidation of fatty acids can only be used if there is enough oxaloacetate. The body needs a plan b as oxaloacetate is used in gluconeogenesis and can sometimes be low in quantity. Also brain can't use fatty acids and so they can only use glucose or ketone bodies.
60
When are ketone bodies made?
During fasting.
61
Enzymes in fatty acid synthesis?
Acetyl CoA carboxylase and fatty acid synthase.
62
Where does fatty acid synthesis take place?
Cytoplasm.
63
What carrier is used in b fatty oxidation?
CoA.
64
What carrier is used in fatty acid synthesis?
ACP (Acyl carrier protein).
65
Reducing power in fatty acid synthesis?
NADPH.
66
Reducing power in b fatty oxidation?
FAD/NAD+
67
Where are fatty acids synthesised in the body?
Liver, adipocytes and lactating breast tissue.
68
Where does fatty acid elongation to increase fatty acid chain length above 16 carbons occur?
Mitochondria and endoplasmic reticulum.
69
What class of enzymes catalyses conversion of saturated fatty acids to unsaturated fatty acids?
Desaturases.
70
How to manage MCAD deficiency disease?
High carbohydrate diet and avoid fasting.
71
Why can't red blood cells use ketone bodies?
They don't have mitochondria.
72
What energy sources does muscle rely on?
Carbohydrates and fatty acids.
73
What energy sources does the heart rely on?
Carbohydrates and fatty acids.
74
What energy sources can the brain not use?
Fatty acids.
75
What is used to meet energy demand in light contraction in muscles?
Oxidative phosphorylation.
76
Changes during vigorous muscle contraction?
Glycogen is broken down. Lactate is produced.
77
What organ is the body's made source of glucose?
Liver.
78
What kind of metabolism is the heart designed for?
Aerobic respiration.
79
Can the heart use ketone bodies?
Yes.
80
What is the point of gluconeogenesis?
The brain's is heavily reliant on glucose metabolism. Body wants to avoid hypoglycemia as that can lead to a coma.
81
What are glucogenic amino acids?
Amino acids used to generate glucose via gluconeogenesis.
82
What are ketogenic amino acids?
Amino acids used to generate fatty acids and ketone bodies.
83
What is glycerol used for in gluconeogenesis?
To produce dihydroxyacetone phosphate.
84
How is gluconeogenesis made energetically favourable?
Six phosphoanhydride bonds are broken (atp bonds).
85
During fasting what is acetyl CoA used to produce?
Ketone bodies.
86
What occurs during aerobic exercise?
Increase production of ATP and increase uptake of glucose. Adrenalin increases rate of glycolysis by increasing rate of gluconeogenesis and release of fatty acids from adipocytes.
87
What occurs during anaerobic exercise?
Where there is a high demand for ATP, glucose transport from the blood can't keep up with the high demand for glucose. Glycogen is therefore broken down. Lactate increases to allow continuation of glycolysis. Liver uses lactate to form glucose (gluconeogenesis lactate to pyruvate to glucose).
88
What inhibits hexokinase I activity?
Glucose 6 phosphate.
89
What inhibits hexokinase IV?
Low blood glucose.
90
What is the Michaelis constant?
Concentration of a substrate at which an enzyme works at half its maximal rate.
91
What does insulin do?
Stimulates uptake and use of glucose. Storage as glycogen and fat.
92
What does glucagon do?
Stimulates gluconeogenesis, breakdown of glycogen and fat.
93
What do glucocorticoids do?
Increase the synthesis of metabolic enzymes concerned with glucose availability.
94
Hormone control in fasting state?
An increase in glucagon secretion and a decrease in insulin secretion.
95
What happens during prolonged fasting?
Glucagon/insulin ratio increases further. Adipose tissue hydrolyses triglycerides. TCA Cycle intermediates are reduced so they can be used for gluconeogenesis. Protein is broken down to provide amino acid substrates for gluconeogenesis. Ketone bodies are produced to partially substitute brain requirement for glucose.
96
Where does oxidative phosphorylation take place?
Inner membrane.
97
How is mitochondria adapted for oxidative phosphorylation?
Folds in the cristae provide a larger surface area for the membrane-bound components of the electron transport chain.
98
Why does FADH2 produce less ATP than NADH?
FADH2 bypasses complex I when it is reoxidised. NADH therefore pumps more H+ ions into the intermembrane space and so produces more ATP.
99
What is a redox couple?
A substrate that can exist in both an oxidised and a reduced form. (e.g NAD+ AND NADH).
100
What does cyanide and azide target?
Haem group in cytochrome oxidase complex (Complex IV).
101
Structure of atp synthase?
F0 - membrane bound
F1 - Projecting into matrix space.
102
What part of atp synthases produces atp.
F1 portion. F1 portion rotation produces atp.
103
What determines whether atp synthase produces or consumes atp?
Direction of proton flow.
104
How does cyanide and azide stop ATP production?
Blocks flow of electrons.
105
How does malonate act as a metabolic poison?
Acts as a competitive inhibitor of complex II. Slows flow of electrons from succinate to ubiquinone.
106
What happens during non shivering thermogenesis?
UCP-1 is activated. ATP synthase is bypassed and energy from H+ gradient is released as heat instead of producing ATP.
107
How does Rotenone act as a metabolic poison?
Blocks transfer of electrons from complex I to co enzyme Q. Limits synthesis of ATP.
108
How does oligomycin act as a metabolic poison?
Blocks protons from flowing down ATP synthase and so ATP can't be produced in oxidative phosphorylation.
109
How does DNP act as a metabolic poison?
Can move H+ ions across cell membrane reducing the concentration gradient of H+ ions. Reduces ATP synthesis.
110
Where is succinate dehydrogenase?
In complex II.
111
In the fasting state, what is the main metabolic fuel for the heart?
Fatty acids.
112
In the fasting state, what is the main metabolic fuel for the brain?
Glucose.
113
Where are ketone bodies produced?
Liver.
114
What can increase oxaloacetate production for gluconeogenesis?
Transamination of amino acids.
115
What enzyme does insulin downregulate in adipose tissue?
Lipase.
116
How does ketoacidosis and high triglycerides cause coma?
The levels of ketone bodies (and fatty acids) will significantly lower the plasma pH disrupting ion transport in the CNS, leading to coma.
117
Treatment for hyperglycemic patient?
Injection of insulin and i.v. infusion of saline. High blood [glucose] drives urine production leading to dehydration. The saline will help to rehydrate the body.
118
Why does hyperglycemia lead to coma?
Hyperglycaemia leads to coma as it can make you dehydrated which can cause you to lose consciousness.
119
Uncoupling of respiration from ATP synthesis leads to?
Dissipation of the bulk of the energy within the proton motive force as heat.
120
What is needed for oxygen consumption in oxygen electrode?
Citrate/succinate/malanate, ADP and mitochondrial suspension.
121
What glucose transporter do cancer cells express?
GLUT1.
122
What amino acids give rise to α-ketoglutarate and aspartate in transamination?
Glutamate and oxaloacetate.
123
Which family of enzymes catalyses the first oxidation step in the β-oxidation of fatty acids?
Acyl-CoA-dehydrogenases
124
What are the three ketone bodies?
Acetone, acetoacetate and D-3-Hydroxybutyrate.
125
What enzyme catalyse the irreversible reactions?
Hexokinase, phosphofructokinase and pyruvate kinase.
126
What does it mean if a redox couple has a negative standard redox potential?
More reducing power than hydrogen. Has a tendency to donate electrons.
