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MEH > Energy Production - Carbs 1,2,3 > Flashcards

Energy Production - Carbs 1,2,3 Flashcards

1
Q

What is metabolism?

A

The inter conversion of biological molecules in small chemical steps

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2
Q

Name + define the two types of metabolic pathways

A

Catabolic - oxidative (release H) + the breakdown of large molecules into smaller intermediates + releases large amounts of energy

Anabolic - reductive + the synthesis of larger molecules from smaller intermediates + uses the energy released from catabolism

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3
Q

What types of energy carriers are released in catabolism?

A
  • reducing power - NADH, NADPH, FADH2
  • energy - ATP
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4
Q

How is reducing power converted to ATP?

A

Oxidative phosphorylation

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5
Q

What is the purpose of stage 1 in catabolism?

A

To convert nutrients from a form that can be taken up into cells

e.g. carbs > monosaccharides
Lipids > glycerol + fatty acids
Proteins > amino acids

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6
Q

Where does stage 1 catabolism occur?

A

Extracellularly (GI tract)

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7
Q

Does stage 1 catabolism produce energy?

A

No

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8
Q

What is the purpose of stage 2 catabolism?

A

Degradation of building blocks to small number of organic precursors
Glycolysis occurs here&raquo_space; ATP made

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9
Q

Where does stage 2 catabolism occur?

A

Intracellularly - cytosolic + mitochondrial

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10
Q

Does stage 2 catabolism produce energy?

A

Glycolysis occurs here so yes
Some ATP

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11
Q

What occurs in stage 3 catabolism?

A

Tricarboxylic acid cycle - Kerb’s cycle

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12
Q

Does stage 3 catabolism produce energy?

A

GTP produced

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13
Q

What occurs in catabolism stage 4?

A

Oxidative phosphorylation - ETC + ATP synthesis

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14
Q

What is required for stage 4 catabolism?

A

Oxygen to act as the final electron acceptor

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15
Q

Does stage 4 catabolism produce energy?

A

Lots of ATP - oxidative phosphorylation

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16
Q

What is the general formula for carbs?

A

(CH2O)n

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17
Q

What are the stages of catabolism?

A

Stage 1 - breakdown to monomers
**Stage 2* - breakdown to metabolic intermediates - glycolysis
Stage 3 - tricarboxylic acid cycle
Stage 4 - oxidative phosphorylation

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18
Q

How many units are oligosacharides?

A

3-12

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19
Q

What is sucrose made up of?

A

Glucose-fructose

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20
Q

What is lactose made up of?

A

Galactose-glucose

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21
Q

What is maltose made up of?

A

Glucose-glucose

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22
Q

What is the glucose concentration in blood?

A

5mM

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23
Q

What cells have an absolute requirement for oxygen and why?

A

Red blood cells - no mitochondria
Lens of eye - no mitochondria
Neutrophils - low O2 environment
Innermost cells of kidney medulla - low O2 environment

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24
Q

What enzymes are in your saliva for metabolism of carbs?

A

Amylase

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25
Q

What enzymes are in the pancreas for metabolism of carbs?

A

Amylase

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26
Q

What enzymes are in your small intestine for carb metabolism?

A

Lactase
Sucrose
Pancreatic amylase - a 1-4 bonds
Isomaltase - a 1-6 bonds

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27
Q

What is primary lactase deficiency?

A

Absence of lactase persistence allele - mainly in northwest Europe
Only occurs in adults

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28
Q

What is secondary lactase deficiency?

A

Caused by injury to small intestine:
- gastroenteritis
- coeliac disease
- Crohn’s disease
- ulcerative colitis

In both infants + adults

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29
Q

What is Congential lactase deficiency?

A

Autosomal recessive defect in lactase gene
Cannot digest breast milk

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30
Q

Symptoms of lactose intolerance

A

Bloatin/cramps
Flatulence - accumulation of gas
Diarrhoea
Vomiting
Rumbling stomach

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31
Q

How are monosaccharides absorbed?

A

1- active transport into intestinal epithelial cells by sodium dependent glucose transporter 1 SGLT1
2- passive transport via GLUT2 into blood
3- transported in blood to target cells
4- glucose uptake via facilitated diffusion using GLUT1-5

Na+/K+ ATPase needed to maintain conc. gradient for SGLT1

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32
Q

What role does Na+/K+ ATPase have in the absorption of monosaccharides?

A

Maintains the conc gradient for the SGLT1

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33
Q

Where is GLUT1 present?

A

All cells

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34
Q

Where is GLUT 2 present?

A

Main abdominal organs:
- kidney
- liver
- pancreatic B cells
- small intestine

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35
Q

Where is GLUT3 found?

A

Neurones
Placenta

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36
Q

Where is GLUT4 found?

A

Adipose tissue
Striated muscle

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37
Q

What regulates GLUT4?

A

Insulin

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38
Q

Where is GLUT 5 found?

A

Spermatozoa
Large intestine

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39
Q

What GLUT is in abdominal organs?

A

GLUT2

40
Q

Functions of glycolysis

A

Oxidation of glucose
NADH production
ATP synthesis
Provides biosynthesis precursors for fatty acids

41
Q

Features of glycolysis

A

Central pathway of CHO catabolism
Occurs in all tissues - cytosolic
Exergonic - produces energy
Oxidative
Irreversible

42
Q

What are the key enzymes in glycolysis?

A
  • hexokinase (glucokinase in liver)
  • phosphofructokianse-1
  • pyrivate kinase
43
Q

What is phosphofructokinase-1 regulated by?

A

allosteric
1- inhibited by high ATP + citrate
2- stimulated by high AMP + F2,6,BP

hormonal
1- inhibited by glucagon
2- stimulated by insulin

44
Q

Why are there so many steps in glycosides?

A
  • Easier in smaller steps
  • Efficient energy conservation
  • Gives versatility - intermediates can be used in other pathways
  • Fine control - easier to slowdown/speed up specific parts
45
Q

What is allosteric binding?

A

Binding at another site

46
Q

Why is phosphofructokinase reaction irreversible?

A

Very negative delta G

47
Q

What is the most important enzyme in glycolysis regulation?

A

Phosphofructokinase

48
Q

What activates pyruvate kinase?

A

High insulin:glucagon ratio
(High insulin, low glucagon)

49
Q

How is NAD+ regenerated?

A

Oxidative phosphorylation
Lactate dehydrogenase

50
Q

What is lactate dehydrogenase important for?

A

Regenerating NAD+ when oxygen is low

51
Q

What is plasma lactate concentration determined by?

A

Relative rates of:
- production
- utilisation - liver, heart, muscle
- disposal - kidney

52
Q

What is the normal concentration of plasma lactate?

A

<1mM

53
Q

What is the plasma lactate concentration in hyperlactaemia?

A

2-5mM
Below renal threshold
No change in blood pH

54
Q

What is the plasma lactate concentration in lactic acidosis?

A

> 5mM
Above renal threshold
Blood pH lowered

55
Q

Where is fructose metabolism?

A

Liver

56
Q

Outline fructose metabolism

A

fructokinase aldolase
Fructose > fructose-1P >glyceralaldehyde-3-P

57
Q

Diseases related to fructose metabolism

A

Essential fructosuria - fructokinase missing
Fructose intolerance - aldolase missing

58
Q

What is essential fructosuira?

A

Fructokinase missing
Fructose in urine

59
Q

What is fructose intolerance?

A

Aldolase missing
Fructose-1P accumulates in liver&raquo_space; liver damage
Managed by removing fructose + sucrose in diet

60
Q

A deficiency in fructokinase causes what?

A

Essential fructosuria

61
Q

How is essential fructosuria detected?

A

No clinical signs
Fructose in urine

62
Q

What does a deficiency in aldolase cause?

A

Fructose intolerance

63
Q

Management of fructose intolerance

A

Remove fructose + sucrose from diet

64
Q

Deficiencies in what enzymes cause galactosaemia?

A

Galactokinase
Uridyl transferase
UDP-galactose epimerise

65
Q

What is galactosaemia?

A

Inability to utilise galactose

66
Q

What is the most common cause of galactosaemia?

A

Galactose-1P uridyl transferase deficiency

Galactose + galactose1-P accumulate

67
Q

Complications of galactosaemia

A

Galactose enters other pathways

aldose reductase
Galactose > galactitol

Accumulation of galactose + galactitol cause swelling + protein precipitation
Increased aldose reductase activity uses excess NADPH
- Crystallin protein denatures&raquo_space; Cataract

68
Q

What does build up of galactose 1P cause?

A

Damage to liver, kidney + brain

69
Q

What do Heinz Bodies suggest?

A

G6PDH deficiency

70
Q

What molecule plays an important role in regulating the affinity of haemoglobin for O2?

A

2,3-bisphosphoglycerate

71
Q

What are Heinz bodies caused by?

A

Precipitated haemoglobin aggregates + binds to cell membrane

72
Q

What are Heinz bodies removed by?

A

Spleen

73
Q

What can a deficiency in pyruvate dehydrogenase cause?

A

Lactic acidosis

  • Pyruvate cant be converted to acetyl CoA
  • anaerobic respiration occurs to regenerate NAD+
  • lactate build up
74
Q

What is pyruvate dehydrogenase sensitive to and why?

A

Vitamin B1
Requires coenzymes which are provided by vit B

75
Q

What is pyruvate dehydrogenase activated by?

A

Pyruvate
NAD+
ADP
Insulin

76
Q

What is pyruvate dehydrogenase inhibited by?

A

Acetyl CoA
NADH
ATP
Citrate

77
Q

Outline the intermediates in the TCA cycle?

A

Citrate
Isocitrate
a-ketogluarate
Syccinyl-coA
Succiante
Fumarate
Maleate
Oxaloacetate

78
Q

Net gain from TCA cycle

A

6 NADH
2FADH2
2GTP

79
Q

How is the TCA cycle regulated?

A

Energy availability
Isocitrate dehydrogenase - rate limiting enzyme
a-ketoglutarate dehydrogenase

80
Q

Key features of oxidative phosphorylation

A
  • ETC + ATP synthesis
  • NADH + FADH2 reoxidation
  • lots of ATP produced
  • O2 acts as final electron acceptors
81
Q

Outline oxidative phosphorylation

A

1- NADH + FADH2 get reoxidised
2- energy from this powers proton translocating complexes
3- H+ ions move from matrix to intermembrane space which creates a proton motive force
4- H+ attach to ATP synthase
5- ADP&raquo_space; ATP

82
Q

How does high ATP conc regulate oxidative phosphorylation?

A

Low [ADP] - no substrate for ATP synthase
Inwards H+ flow stops
Increase in H+ in inter membrane space
ETC + ATP synthesis stops

83
Q

Two processes of using reducing power in ATP synthesis

A

1- electron transport - e- from NADH + FADH2 transferred through ETC
2- oxidative phosphorylation - free energy released used to drive ATP synthesis

84
Q

How many molecules of ATP is produced from 1 NADH?

A

2.5ATP

85
Q

How many molecules of ATP are produced from 1FADH2?

A

1.5

86
Q

What proof translocatioing complexes does NADH + FADH2 use?

A

NADH - Complexes I, III, IV
FADH2 - complexes III + IV

87
Q

What effect to inhibitors have on oxidative phosphorylation?

A

Block ETC by blocking O2 acting as FEA

88
Q

Examples of inhibitors

A

Cyanide
Carbon monoxide

89
Q

What effect do uncouplers have on oxidative phosphorylation?

A
  • Increases membrane permeability to H+
  • stops PMF
  • H+ cross membrane without passing through ATP synthase so no ATP synthesis
  • no inhibition of ETC
90
Q

Examples of uncouplers

A

Fatty acids
Dinitrocresol
Dinitrophenol

91
Q

Compare oxidative phosphorylation + substrate level phosphorylation (4 points)

A

Oxidative phosphorylation
- requires membrane-associated complexes
- cannot occur without O2
- major process for ATP synthesis
- energy cooling occurs indirectly through generating + using PMF

Substrate level phosphorylation
- requires soluble enzymes
- can occur to an extent without O2
- minor process for ATP synthesis
- energy coupling occurs directly through formation of high energy of hydrolysis bond

92
Q

How does energy coupling occur in oxidative phosphorylation?

A

Indirectly through generating and using PMF

93
Q

How does energy coupling occur in substrate level phosphorylation?

A

Directly through formation of high energy of hydrolysis bond

94
Q

Symptoms of galactosaemia

A

Cataracts
Hypoglycaemia
Hepatomegaly + cirrhosis
Renal failure
Vomiting
Seizure + brain damage

95
Q

Function of the outer and inner membrane of mitochondria

A

Allows a proton gradient to be formed

MEH (23 decks)

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