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MEH > Carbohydrates > Flashcards

Carbohydrates Flashcards

1
Q

What is stage 1 of catabolism?

A

Breaking down molecules for absorption

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2
Q

What is stage 2 of catabolism?
What type of reaction?

A

Break down of metabolic intermediates
Oxidative

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3
Q

What is stage 3 of catabolism?
What type of reaction?

A

Krebs cycle
Oxidative

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4
Q

What is stage 4 of catabolism?

A

Oxidative phosphorylation
Converts reducing power into ATP

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5
Q

What is an example of a metabolic intermediate?

A

Acetyl-CoA

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6
Q

Where does stage 1 take place?

A

Extracellular - like the GI tract

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7
Q

What type of bonds are broken in stage 1?
How much energy is produced?

A

C-N C-O no C-C
No energy produced

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8
Q

Where does stage 2 take place?
What is is also known as?

A

Intracellular
Glycolysis

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9
Q

What type of bonds are broken in stage 2?
How much energy is produced?

A

C-C
Some energy as ATP

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10
Q

Where does stage 3 occur?

A

Mitochondria

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11
Q

What reaction can convert energy without O2?

A

Glycolysis

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12
Q

What does stage 4 require?

A

O2

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13
Q

Where does stage 4 occur?

A

Mitochondria

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14
Q

General formula of carbohydrates

A

(CH2O)n

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15
Q

What is sucrose composed of?

A

Glucose
Fructose

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16
Q

What is lactose composed of?

A

Galactose
Glucose

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17
Q

What is maltose composed of?

A

Glucose
Glucose

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18
Q

Which cells can metabolise glucose?

A

All of them

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19
Q

Give three cells that require just glucose
Why?

A

Red blood cells - no mitochondria

Neutrophils (white blood cells) - mitochondria used to produce free radicals

Lens of eye - no capillaries, so no O2

Kidney medulla cells - little O2, as cortex uses it

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20
Q

Where are glucose polymers broken down?
By what?

A

Salvia + pancreas - amylase - starch and glycogen to dextrins
Small intestines - disaccharidases attached to membrane of epithelial cells - break down dextrins

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21
Q

Why can’t cellulose be broken down by humans?

A

No complementary enzyme
Cellulose is Beta - which has a different shape from Alpha

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22
Q

What causes primary lactase deficiency?
Who does it effect?

A

Absence of lactase persistence allele

Adults

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23
Q

What causes secondary lactase deficiency?
Who does it effect?
Key fact

A

Injury to small intestine - coeliacs, chron’s

Infants and adults

Is reversible

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24
Q

What causes congenital lactase deficiency?

A

Autosomal recessive defect in lactase gene

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25
Q

Three stages of monosaccharide absorption

A

Active transport - into intestinal epithelial cells by Na-dependent glucose transporter, from apical side

Passive transport - (high to low) via GLUT2 into blood

Facilitated diffusion - into target cells using transport proteins

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26
Q

Why are there so many steps in glycolysis? (3)

A
  • useful intermediates made
  • can be controlled
  • parts can reverse
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27
Q

Is glucose reduced or oxidised in glycolysis?

A

Oxidised

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28
Q

What is produced in glycolysis?

A

NADH (2 per glucose)
ATP from ADP - net increase of 2
Biosynthetic precursors - used in biosynthetic reaction

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29
Q

In what type of tissue does glycolysis happen?

A

All tissue

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30
Q

Is glycolysis reversible or not?
Exergonic or endergonic?

A

Irreversible
Exergonic

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31
Q

What makes a reaction irreversible?

A

Large negative DELTA G

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32
Q

Is CO2 emitted during glycolysis?

A

No
C6 glucose > 2 C3 pyruvate

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33
Q

Two key enzymes of glycolysis

A

Hexokinase (glucokinase in liver)

Phosphofructokinase-1

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34
Q

What does phosphorylation glucose at the start of glycolysis mean?

A
  • prevents movement back across plasma membrane, as negatively charged
  • increases reactivity
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35
Q

What is the committing step in glycolysis?
What does this mean?

A

fructose 6-phosphate → fructose 1,6- bisphosphate

First step to commit glucose to metabolism

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36
Q

What does cytosolic mean?

A

Occurs in all tissue

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37
Q

What type of steps are potential sites of regulation?

A

Irreversible

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38
Q

What is an allosteric enzyme?

A

The activator or inhibitor binds at another site

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39
Q

What site do substrates bind to on an enzyme?

A

Catalytic site

40
Q

What site do regulatory molecules bind to on an enzyme?

A

Regulatory site

41
Q

What is the enzyme that controls the phosphorylation of fructose-6-P to fructose-1,6-biP?

A

Phosphofructokinase

42
Q

Where does allosteric regulation take place for Phosphofructokinase?

43
Q

Name what inhibits Phosphofructokinase - allosteric

A

High ATP
High citrate

44
Q

Name what stimulates Phosphofructokinase - allosteric

A

High AMP
High F2,6,BP (Fructose 2,6-bisphosphate)

45
Q

Where does hormonal regulation take place for Phosphofructokinase?

46
Q

Name what stimulates Phosphofructokinase - hormonal

47
Q

Name what inhibits Phosphofructokinase - hormonal

48
Q

What molecule is oxidised in glycolysis?

A

NAD+ to NADH

49
Q

Why wouldn’t NADH be converted back to NAD+?

A

O2 supply insufficient
No mitochondria

50
Q

What enzyme is required to regenerate NAD+ when it doesn’t happen in stage 4?

A

Lactate dehydrogenase

51
Q

What reaction does lactate dehydrogenase catalyse?
Is it reversible?

A

Reduction of pyruvate to lactate
Yes

52
Q

What causes high lactate production?

A

Shock
Congestive heart disease
Major exercise

53
Q

What three factors effect plasma concentration?

A

Production
Utilisation
Disposal

54
Q

What is the condition when the plasma mM is 2-5?
How is the pH effected?

A

Hyperlactaemia
No change

55
Q

What is the condition when the plasma mM is above 5?
How is the pH effected?

A

Lactic acidosis
pH lowered

56
Q

Where is fructose metabolised?

57
Q

What is essential fructosuria?

How would you identify this?

A

No fructokinase

There would be fructose in urine

58
Q

What is fructose intolerance?

How would you manage it?

A

Aldolase missing
Fructose-1P accumulates in liver - causing liver damage

Remove fructose and sucrose from diet

59
Q

What is fructose phosphorilated into?

A

Fructose-1P

60
Q

What enzyme hydrolyses Fructose-1P?

61
Q

Where is galactose metabolised?

62
Q

What is the condition is which you are unable to utilise galactose?

A

Galactosaemia

63
Q

What causes issues like cataracts when you have galactosaemia?

A

Galactose enters other reaction pathways
Using NADPH - depleting the levels
Causing structure damage

64
Q

What is the start reactant in a pentose phosphate pathway?

A

Glucose-6-phosphate

65
Q

What is produced in a pentose phosphate pathway?(3)

A

NADPH
C5-sugar ribose
CO2

No ATP

66
Q

What is NADPH used for?(3)

A

Reducing power for biosynthesis
Maintains levels of GSH
Detoxification reactions

67
Q

What is C5-sugar ribose used for the synthesis of?(3)

A

Nucleotides
DNA
RNAa

68
Q

What is the rate limiting enzyme in a pentose phosphate pathway?

A

Glucose 6-phosphate dehydrogenase

69
Q

What molecule enters the kreb cycle?

A

Acetyl CoA

70
Q

What enzyme catalyses the reaction between pyruvate and CoA to acetylcoA?

What is a key fact about the reaction - what does it mean?

A

Pryruvate dehydrogenase (PDH)

Irreversible - key regulatory step

71
Q

Where is PDH found?
What is the structure?

A

Mitochondrial matrix
Multi-enzyme complex

72
Q

What is PDH regulated and activated by?

A

A: reactants - CoA, NAD+, ADP, Pyruvate
I: acetyl-CoA, NADH, ATP

But the ratio - like NAD+:NADH

73
Q

Where does the Krebs cycle take place?

A

Mitochondria

74
Q

What is acetyl converted to in the Krebs cycle?

75
Q

What do the high energy electrons reduce in the Krebs cycle?

76
Q

What are the products of the Krebs cycle?

A

NADH and FADH2 (reducing powers)
GTP
CO2

Precursors for biosynthesis

77
Q

What is the Krebs cycle also known as?

A

Tricarboxylic acid cycle
TCA

78
Q

Where does a large amount go in the catabolism of glucose?

What does the efficency depend on?

A

Lost as heat

Tightness of coupling

79
Q

Where does oxidative phosphorylation take place?

A

Mitochondria

80
Q

What is the cytoplasm of the mitochondria called?

81
Q

How many moles of ATP do NADH and FADH2 produce?

82
Q

What does a [H+] gradient create?

A

Proton motive force

83
Q

Where is adipose tissue found?
Why?

A

Newborns - maintain heat
Hibernating animals - generate heat

84
Q

Describe how the levels of ATP and ADP would inhibit oxidative phosphorylation

A

High ATP:Low ADP
No substrate for ATP synthase
No inward flow of H+
Conc of H+ in intermitochondrial space increases
Prevents further H+

85
Q

What are dextrins?

A

Small carbohydrate subunits

86
Q

Why are enzyme catalysed steps irreversible in glycolysis?

A

Very negative delta G

87
Q

What is the significance of hexokinase?

A

Makes glucose more negatively charged
Preventing it from passing back through cell membrane

88
Q

What effect does cyanide have on the electron transport chain?

A

Prevents the flow of e- through the e- transport chain

89
Q

What enzymes catalyses acetylCoA form pyruvate?

A

Pyruvate dehydrogenase

90
Q

What is the intermediate in glycolysis that produces glycerol phosphate?

A

dihydroxyacetone phosphate

91
Q

How is NAD+ regenerated in cells containing no mitochondria?

A

Lactate dehydrogenase
Pyruvate to lactate

92
Q

What would cause a decrease in glycolysis?

A

Low conc of NAD+
Due to product inhibitomn

93
Q

What 2 key transporters are required for the absorption of monosaccharides into the blood?
From where to where?
What type of transport is it?

A

SGLT1 - intestinal lumen to intestinal epithelial cell - active

GLUT2 - intestinal epithelial cell to capillary - passive

94
Q

What type of transport is it for glucose from the blood into cells?

A

Facilitated diffusion

95
Q

Where are GLUT2 transporters found?

A

Pancreatic beta cells

96
Q

Where are GLUT4 transporters found?

A

Adipose tissue

MEH (10 decks)

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