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POM > MBC - Cell metabolism I&II > Flashcards

MBC - Cell metabolism I&II Flashcards

1
Q

What do enzymes that end with KINASE do?

A

Carry out group transfer/ phosphorylation reaction

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2
Q

What are two main concepts of Glycolysis ?

A

Formation and Splitting of ATP

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3
Q

What are the 6 types of reactions that define metabolism?

A 
Redox
Ligation with ATP cleavage
Isomerization
Group transfer
Hydrolytic
Addition/removal of functional groups
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4
Q

How many ATP per molecule of glucose is synthesised in complete oxidation?

A

36-38

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5
Q

How does glucose metabolism happen? (Cellular oxidation for glucose)

A

Small activation energy overcome by enzymes and body temp - process is broken down to several discrete steps

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6
Q

How does glucose combustion happen?

A

Large activation energy as heat given to glucose - produce CO2 and water

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7
Q

What is oxidative phosphorylation?

A

Mitochondrial process that reduces oxygen to produce ATP

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8
Q

What is glycolysis?

A

Anaerobic cytoplasmic process that oxidises glucose to produce ATP, NADH and pyruvate

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9
Q

What is the TCA cycle?

A

Mitochondrial process that oxidises small molecules to generate ATP, NADH, FADH2 - Tricarboxylic Acids (Kreb’s) Cycle

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10
Q

What are the 3 main stages of cellular metabolism?

A
  1. Glycolysis
  2. TCA cycle
  3. Oxidative phosphorylation
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11
Q

Catabolic pathways

A

Metabolic pathways that release energy by breaking down complex molecules into simpler compounds

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12
Q

Anabolic pathways

A

Metabolic pathways that consume energy to build complicated molecules from simpler ones

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13
Q

Glucose to glucose-6-phosphate + H+

A

Hexokinase transfer phosphate group, ATP hydrolysed to ADP

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14
Q

Why is step one (G to G6P) of glycolysis irreversible?

A

Glucose charged, cannot leave by transporters

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15
Q

Step 2: Glucose 6-phosphate to fructose 6-phosphate

A

Phosphoglucose isomerase (isomerization - rearrange compound)

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16
Q

Step 3: Fructose 6-phosphate ——–> ?

A

Fructose-1,6-bisphosphate by phosphofructokinase

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17
Q

Why isomerise G6P to F6P?

A

Create symmetry when cleaved

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18
Q

Step 4: Fructose 1,6-BP to G3P and DHAP

A

Glyceraldehyde-3-phosphate and Dihydroxyacetone phosphate (high energy compounds) by Aldolase in hydrolytic reaction

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19
Q

Why regulate phosphofructokinase?

A

To control entry of sugars into glycolysis pathway by negative feedback

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20
Q

Dihydroxyacetone phosphate (DHAP) to G3P

A

Triose phosphate isomerase (TPI)

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21
Q

Why deficiency in TPI is fatal? (Glycolytic enzymopathy)

A

Shortage of RBC (Haemolytic anaemia)

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22
Q

Where does the second half - the splitting for ATP begin?

A

after glyceraldehyde-3- phosphate (G3P) is produced

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23
Q

(2) Step 6: what are used in the redox and group transfer of G3P to 1,3-bisphosphoglycerate? (3)

A

Glyceraldehyde-3-phosphate dehydrogenase and cofactor NAD + Pi

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24
Q

(2) Step 7: What happens from 1,3-bisphosphoglycerate to 3-phosphoglycerate?

A

Phosphoglycerate kinase phosphorylyse ADP to ATP (phosphate) group transfer

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25
Q

(2) Step 8: 3-phosphoglycerate to 2-phosphoglycerate

A

Phosphoglycerate mutase isomerization

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26
Q

(2) Step 9: 2-phosphoglycerate to phosphoenolpyruvate + H2O

A

Enolase (group removal/Dehydration)

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27
Q

(2) Step 10: Phosphoenolpyruvate ———–> ?

A

Pyruvate by pyruvate kinase

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28
Q

Net ATP after Glycolysis

A

Loss 2 ATP to gain 4 ATP = 2 ATP (+2NADH)

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29
Q

What are the 3 fates of pyruvate?

A

Ethanol (Alcoholic fermentation)
Lactate
Acetyl-CoA

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30
Q

How does alcoholic fermentation happen?

A

Pyruvate decarboxylase removes carboxyl group, alcohol dehydrogenase reduces acetaldehyde to ethanol

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31
Q

How to generate lactate from pyruvate?

A

Pyruvate reduced by lactate dehydrogenase

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32
Q

What purpose do alcoholic fermentation and lactate production serve?

A

Allow cofactor NADH is oxidised to NAD+ (use in glycolysis when oxygen deprived)

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33
Q

What does creatine kinase do?

A

Catalyses the breakdown of creative phosphate into creatine and ATP by phosphorylation of ADP

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34
Q

What acts as a buffer for phosphate demands?

A

Creatine phosphate

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35
Q

How long does creatine phosphate extend when cell is independent of respiration?

A

Double the time, allow longer muscle contraction

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36
Q

Where and how is acetyl CoA generated from pyruvate? (Link reaction)

A

Mitochondrial process where pyruvate dehydrogenase complex PDH (series of enzymes) and cofactors HS-CoA and NAD+ –> NADH (carbonyl group lost [decarboxylation], rest [dehydrogenated] ligated to enzyme CoA)

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37
Q

What is Acetyl CoA?

A

Molecule with thioester bond readily hydrolysed to donate acetate (2C) to Krebs cycle

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38
Q

What results from poor PDH function?

PDH catalyses reaction of pyruvate forming acetyl CoA

A

Beri-Beri, damage to PNS

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39
Q

What and how many molecules are produced in one turn of Krebs cycle?

A

3 NADH, 1 GTP, 1 FADH2, 2CO2

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40
Q

Where is the TCA cycle located?

A

mitochondria matrix

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41
Q

Why does the TCA cycle only operate in aerobic conditions?

A

Need sufficient oxygen for oxidative phosphorylation to re-oxidise the reduced cofactors to generate bulk of ATP

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42
Q

What are the two forms amino acids enter the TCA cycle?

A

Glucogenic and Ketogenic

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43
Q

What do glucogenic amino acids form in the TCA cycle?

A

Glucose

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44
Q

What is the general strategy of amino acid degradation?

A

Remove amino group (excreted as urea)

Carbon skeleton into production of glucose or Krebs cycle to produce ATP

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45
Q

How many molecules/skeletons of the degradation of 20 amino acid give rise to?

A

7 *constituents of TCA cycle

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46
Q

What does transamination reaction do?

A

Get Keto acid to enter TCA with enzyme transaminas

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47
Q

How does transamination work?

A

Switch amino groups of the amino acid (1) and Keto acid (1) to form Keto acid (2) and amino acid (2)

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48
Q

How does NADH produced in glycolysis enter mitochondria from cytosol?

A

By 2 shuttles:

The Glycerol-phosphate shuttle
The Malate-aspartate shuttle

49
Q

Where are the glycerol-phosphate shuttles?

A

Skeletal muscle, brain

50
Q

Where are the Malate-aspartate shuttle?

A

Liver, kidney, heart

51
Q

How does the glycerol-phosphate shuttle work?

A
  1. Cytoplasmic G3P dehydrogenase transfer e- from NADH to DHAP to generate G3P
  2. Membrane-bound G3P dehydrogenase transfer e- to FAD
  3. FAD –> Co-enzyme Q (ETC)
52
Q

How does the Malate-aspartate shuttle work?

A

Malate and Aspartate go in and leave mitochondria by antiporters

Inside: Malate oxidised to oxaloacetate (keto1) [NAD+ capture e- –> NADH] & transamined to aspartate (amino2)

Outside: Aspartate (amino1) transamined to oxaloacetate (keto2) then reduced [capture e-] to form malate [generate NAD+]

As malate enters, a-keto glutamate (keto1) leaves to reduce aspartate(amino1) to oxaloacetate (keto2)

As Aspartate leaves, glutamate (amino1) enters to oxidise oxaloacetate (keto1) to aspartate (amino2)

53
Q

How many ATP molecules are formed by re-oxidation of NADH and FADH2 respectively?

A

3 and 2

54
Q

What would happen if there were mutation in TCA enzyme genes?

A

Decrease TCA activity

Enhance aerobic glycolysis

55
Q

What is produced in TCA cycle?

A

GTP/ATP and reduced cofactors (NADH, FADH2)

56
Q

What are redox reactions?

A

Electron transfer by dehydrogenases

57
Q

What are isomerization reactions?

A

Rearrangements of atoms to form isomers by isomerases

58
Q

What are ligation reactions?

A

Formation of covalent bond (require ATP cleavage)

59
Q

What are group transfer reactions?

A

Transfer of functional group from one molecule to another by kinases

60
Q

What are hydrolytic reactions?

A

Cleavage of bonds by addition of water

61
Q

What are addition/removal of functional reactions?

A

Addition of group to remove double bond

Removal of group to form double bond

62
Q

What are the amino acids that can be phosphorylated?

A

Serine, Threonine, tyrosine (contain OH- group)

63
Q

How is LDH a diagnostic tool?

A

Elevated levels of LDH could diagnose stroke & myocardial infarction

64
Q

What are the 5 main classes of lipids?

A
  • Free fatty acids
  • Triacyglycerols
  • Phospholopieds
  • Glycolipids
  • Steroids
65
Q

How is fatty acid stored?

A 
As triacyglycerols (3 fatty acid + 1 Glycerol) in the cytoplasm.
The ester linkage help neutralise carboxylic acid groups to keep pH in range
66
Q

What are the ways in which Acetyl CoA is produced?

A

Glycolysis from glucose and Beta-oxidation from fatty acids

67
Q

Where is Acetyl CoA production located?

A

Where ATP is synthesised, in the mitochondria

68
Q

Where are fat derived from? (3)

A
  1. Diet
  2. De novo synthesis (liver) - Lipogenesis
  3. Storage in adipose (only in starvation) - broken down for metabolisation
69
Q

Where are bile salts from?

A

Generated by the liver, stored in gall bladder

70
Q

How does bile salt emulsify fat?

A
  1. Lipophobic outer section dissolves triacylglycerol
  2. Lipophilic (hydrophobic) interior contacting triacyglycerol break it down w/ enzyme pancreatic lipase into fatty acid
71
Q

What happens in a lack of bile salts?

A

Fat passing through undigested/unabsorbed - cause Steatorrhea (fatty stool)

72
Q

What inhibits fat absorption? (Treatment for obesity)

A

Orlistat - inhibits pancreatic lipases

- induce fat to go through undigested

73
Q

What are the different types of lipoprotein?

A 
Chylomicrons
VLDL (very low density)
IDL (intermediate)
LDL (low)
HDL (high)
74
Q

What are chylomicrons for?

A

Dietary fat transport

75
Q

Since lipids are highly hydrophobic, what are they transported in the plasma by?

A

Lipoproteins

76
Q

What are HDLs for?

A

Reverse cholesterol transport (take cholesterol from peripheral tissue back to liver)

77
Q

What are the characteristics of lipoproteins?

A

Monolayer of phospholipids

78
Q

What are chylomicrons made of?

A

Apoprotein, phospholipid, triglyceride

79
Q

What is the process of digestion of fat to tissue?

A
  1. Fat from diet absorbed by enterocytes
  2. Re-synthesise triglycerides and incorporate into chylomicron
  3. Chylomicron transported via lymphatics out into bloodstream (picking up apoprotein from HDL)
  4. Tissue use content of chylomicron
80
Q

What happens when digesting chylomicrons?

A

Lipoprotein lipase located in capillary endothelial cell lining tissues (adipose, heart, skeletal muscle) recognise the apoprotein and induce degradation & digestion of triacylglyceride to from fatty acid and glycerol

81
Q

Where is fatty acid and glycerol used?

A

Fatty acid - B-oxidation

Glycerol - return to liver for gluconeogenesis

82
Q

What happens to the chylomicron remain?

A
  1. Picked up apoprotein from HDL in order to be recognised and uptake by liver
  2. Used to synthesis other molecules
83
Q

What is the general anatomy of a lipoprotein?

A
  • Phospholipid monolayer containing cholesterol & apoproteins
  • Core of cholesterol esters and triacylglycerols
84
Q

How are cholesterol esters synthesised?

A

In plasma, reaction from cholesterol and acyl chain of lecithin (catalysed by LCAT)
- transfer of acyl group onto cholesterol molecule

85
Q

Why ester cholesterol molecules?

A

Increase hydrophobic so pack more tightly in lipoprotein core

86
Q

Describe life cycle of VLDL, IDL, LDL, HDL

A
  1. VLDL produced from liver, apoprotein recognised by lipase
  2. Breakdown triacylglyceride into FFA & cholesterol (taken up by tissue) & glycerol
  3. Depleted VLDL transfers apoprotein to HDL –> turns into IDL
  4. HDL transfers cholesterol esters to IDL –> turns into LDL
  5. LDL either - content used for production of acetyl CoA,
    then uptake by liver OR uptake by macrophages (PROBLEM: atherosclerosis)
87
Q

What does prolonged elevation of LDL levels lead to?

A

Atherosclerosis

88
Q

What is the difference between HDL and LDL?

A
  • HDL lowers total serum cholesterol

- LDL transports cholesterol synthesised in liver to peripheral tissues

89
Q

How does fatty acid generate acetyl CoA?

A
  1. Fatty acid converted to acyl CoA species
  2. Carnitine shuttle acyl CoA into matrix by translocase
  3. B-oxidation cycle to generate acetyl CoA
90
Q

Where and how does fatty acid convert to acyl CoA species?

A

Outside mitochondria
Fatty acid + ATP + HS-CoA —> Acyl CoA + AMP + PPi
(hydrolyse phosphoanhydride bond to give 2Pi)
ATP–>AMP [2 high energy bond used]

91
Q

How does the carnitine shuttle work?

A
  1. Couple acyl CoA to carnitine to form Acyl carnitine
  2. Translocase imports acyl carnitine and exports carnitine
  3. Enzyme catalyses reverse - CoA displaces carnitine to form acyl CoA in mitochondria
92
Q

What is primary carnitine deficiency?

A

An autosomal recessive disorder, mutation in gene encoding carnitine tranporter
Reduced ability to uptake carnitine
[No FA –> no ATP –> no energy]

93
Q

What happens in the B-oxidation cycle?

A

Acyl CoA undergoes oxidation, hydration, oxidation & thiolysis reactions. Result in a molecule of acetyl CoA and 2C shorter acyl CoA than original.

94
Q

What happens to the Acetyl CoA generated by B-oxidation?

A
  1. Enters TCA cycle when B-oxidation & carbohydrate metabolism are balanced (since oxaloacetate is needed for entry)
  2. Forms ketone bodies (acetoacetate, D-3-hydroxybutyrate, acetone) when fat breakdown dominates during fasting
95
Q

How many acetyl CoA, FADH2 and NADH are formed during the B-oxidation?

A

n+1 : n : n

96
Q

What is important to remember when calculating no. of ATP molecules produced in fatty acid metabolism?

A

Used 2 ATP equivalent in step 1 - Fatty acid –> Acyl CoA

97
Q

Fatty acid metabolism vs glucose metabolism

A

FA met. generates significantly more ATP/substrate than glucose met.

98
Q

What are the two enzymes in FA biosynthesis?

A

Acetyl CoA Carboxylase

Fatty acid synthase

99
Q

How is fatty acid synthesised from acetyl-CoA & malonyl-CoA?

A

Elongation by 2C undergoing condensation, reduction, dehydration and reduction

100
Q

How is B-oxidation different to FA biosynthesis?

A

Carrier: Coenzyme A (Beta) vs Acyl Carrier Protein (synth)
Oxidising/reducing power: FAD/NAD+ (Beta) vs NADPH (synth)
Location: Mitochondrial matrix (Beta) vs Cytoplasm (synth)

101
Q

Where does elongation of acyl group to make FA longer than 16 C occur?

A

Occurs separately from palmitate synthesis in the mitochondria and ER

102
Q

What enzyme is needed for fatty acid desaturation?

A

Fatty acyl-CoA desaturases

103
Q

What is the ratio of molecules generated in the synthesis of FA? (Acyl group, CO2, H2O. CoA-SH, NADP+)

A

1 : n : n-1 : n+1 : 2n
Acyl group:CO2:H2O:CoA-SH:NADP+

n=malonyl CoA (C3)

104
Q

What is the enzyme that creates oleic acid and palmitoleic acid from sterate and palmitate?

A

Delta-9 desaturase

105
Q

How does delta-9 desaturase create oleic acid and palmitoleic acid from sterate and palmitate?

A

By generating a double bond 9 carbons from the terminal carboxyl group

106
Q

What body tissue is de novo FA biosynthesis restricted to in adults?

A

Liver
Adipose tissue
Lactating breast

107
Q

How to we target FA synthetase (FASN) in cancer?

A

Use of cerulenin (antifungal antibiotic) to inhibit FASN to reduce tumour growth

108
Q

What do Acyl-CoA-dehydrogenases do?

A

They catayse the initial step in each cycle of fatty acid Beta-oxidation within mitochondria matrix

109
Q

Why are there many types of Acyl-CoA-dehydrogenases?

A

As Acyl CoA chain gets shorter, we need different enzymes to carry out catalysis

110
Q

What are the different types of Acyl-CoA-dehydrogenase?

A

Short-chain (<6)
Medium-chain (6-12)
Long-chain 3-hydroxy (13-21)
Very long chain (>22)

111
Q

What is the disorder of B-oxidation?

A

MCADD - Medium chain acyl CoA dehydrogenase deficiency

112
Q

What is MCADD?

A

An autosomal recessive disorder of B-oxidation that can be fatal (can cause Sudden Infant Death Syndrome SIDS)

  • not good at breaking down fatty acid to generate energy
  • Patients should never go without food for more than 10-12 hours - need CARBohydrate diet
113
Q

What treatment should be given to MCADD patients who have appetite loss or severe vomiting?

A

i.v. glucose to make sure the body is not dependent on fatty acids for energy

114
Q

Why are B-oxidation and FA synthesis in different places?

A

Makes no sense to synthesise something in a location where it could also be readily broken down

115
Q

What is so special about ketone body D-3-hydroxybutylate?

A

It has no keto group, it is simply an acid

116
Q

What happens in the case of an ODD chain FA B-oxidation?

A

Produce Propionyl-CoA (3C) and acetyl CoA (in final cycle oxidation)

117
Q

What does propionyl CoA (3C) do as a building block?

A

It undergoes a series of reaction to become succinyl CoA and enters TCA cycle

118
Q

What is non-esterified FA transported by in the plasma?

A

Albumin - a gobular plasma protein

119
Q

What are MCADD patients advised to do?

A

Go for high carbs diet

Avoid fasting

POM (22 decks)

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