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Sem 1 - MCBG > Energy Production: Carbohydrates > Flashcards

Energy Production: Carbohydrates Flashcards

1
Q

what is the point of convergence during catabolism?

A

Acetyl Coenzyme-A

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2
Q

What is the first step of catabolism?

A

This is the breakdown of macromolecules eg Carbs, Proteins, Lipids to smaller molecules for absorption.
This involves short pathways where the C-N and C-O bonds get broken. No energy is released here.

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3
Q

What happens in the second stage of catabolism?

A

This is when these small molecules get broken down to metabolic intermediates via many pathways.
It is oxidative so it releases ‘reducing power’ (NADH) and ‘energy’ (ATP).
C-C binds are broken here.

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4
Q

What happens in the Krebs cycle?

A

This is the first stage that is the same for all forms of catabolism.
It is oxidative. This releases ‘reducing power’ (NADH, FAD2H) and some energy (GTP and ATP)
Acetyl CoA is also oxidised to CO2.
This cycle also produces some precursors for biosynthesis.

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5
Q

What is the final stage of catabolism?

A 
Oxidative phosphorylation (electro transport chain and ATP synthesis). This is the conversion of 'reducing power' into ATP so lots of energy is released and NADH and FADH2 are deoxidised here.
Oxygen is required to be reduced to H2O.
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6
Q

What is the purpose of the first stage of catabolism?

A

To convert nutrients to a form that can be taken up into cells.
Short pathways
Breakage of C–N and C–O bonds (not C–C)
NO USABLE ENERGY PRODUCED.

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7
Q

Where does the first stage of catabolism occur?

A

Extracellularly or in the GI tract. After, the molecules are absorbed from the GI tract into circulation.

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8
Q

Why is our carbohydrate intake lots more than the percentage of carbohydrates in our body?

A

Because Carbohydrates are our primary energy source.

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9
Q

What is the general formula of carbohydrates?

A

(CH2O)n They also contain an aldehyde (aldose) or keto (-C=O) group (ketose)

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10
Q

How many carbon are present in each oft these monosaccharides?
Triose?
Pentose?
Hexose?

A

3
5
6

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11
Q

How many single sugar units in a disaccharide?

A

2 units eg Sucrose which is disaccharide of glucose and fructose

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12
Q

How many single sugar units in an oligosaccharide?

A

3-12 units eg Dextrins

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13
Q

How many single sugar units in a polysaccharide?

A

10-1000s of units

eg Glycogen, Starch or Cellulose.

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14
Q

What are the three main dietary monosaccharides?

A

Glucose
Fructose
Galactose

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15
Q

What is minimum circulating glucose concentration? Why?

A

About 4.5-5mM.

To create a conc gradient so that a supply can be created to tissues.

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16
Q

What types of cells have an absolute requirement for glucose?

A

RBCs- as no stage 3/4 metabolism as no mitochondria
Neutrophils
Innermost cells of kidney medulla
Lens of eye
Brain (although, in times of starvation and if given time to adapt, it can use ketone bodies for some energy requirements)

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17
Q

How are carbohydrates first broken down?

A

Silivary Amylase -breaks starch and glycogen into dextrin

Pancreatic amylase - turns dextrins into monosaccharides.

Small intestine -disaccharidases attached to brush border membrane of epithelial cells break down disaccharides.
Lactase (breaks down lactose)
Sucrase (breaks down sucrose)
Pancreatic Amylase (breaks a 1-4 bonds)
Isomaltase (breaks a 1-6 bonds)
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18
Q

Why isn’t cellulose digested?

Why do we eat it?

A

Cellulose is not digested as it made form B rather than a glucose. and a and B glycosidic bonds are different.
However, we eat it because it increases the surface area for digestion.

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19
Q

What is Primary lactase deficiency?

A

This is the absence of lactase persistence allele

There is the highest prevalence in northwest Europe and it only occurs in adults.

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20
Q

What is secondary lactase deficiency?

A 
Something happens in bowel (small intestine) to disrupt epithelia layer. Occur through: 
Gastroenteritis 
Coeliac disease
Crohn's disease 
Ulcerative colitis

Occurs in both infants and adults and it is generally reversible.

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21
Q

What is Congenital lactase deficiency?

A

Very Rare!!

But, this is autosomal recessive defect in lactase gene where children cannot digest breast milk.

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22
Q

What are the symptoms of lactose intolerance?

A 
Bloating / Cramps
Flatulence
Diarrhoea
Vomiting 
Rumbling stomach
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23
Q

How is glucose moved from the apical side into the intestinal epithelial then into capillaries?

A

Active - (low to high) into intestinal epithelial cells by Na dependant glucose transporter 1 (SGLT1)
THEN.. Passive (high to low) via GLUT2 into blood supply.
(Na conc. kept low in the enthelial cells using NaKATPase)
Glucose is then transported via the blood supply to target tissues.

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24
Q

What are the different glucose transporters?

A

Glucose uptake into cells from the blood is via facilitated diffusion using transport proteins that are hormonally regulated:

GLUT1 - basal uptake. passive uptake.
In Foetal tissies, adult erythrocytes and blood brain barrier
*GLUT2 - inportant for glucose sensing to release insulin from pancreatic B cells. They are also present int he kidney, the liver and the small intestine.
GLUT3
*GLUT4 - in vesicles in cell. Insulin regulated so, when Insulin present, go into membrane and increase glucose uptake. They are also present in adipose tissue and in striated muscle.
GLUT5

(GLUT2 and GLUT4 are the most important ones.

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25
Q

What are the functions of glycolysis?

A
  • Oxidise glucose (hexose) into 2 x Pyruvate (triose)
  • Release a small amount of ATP (2 per glucose via substate level phosphorylation)
  • Produce 2 NADH per glucose,
  • Prodice C6 and C3 intermediates before making pyruvate.
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26
Q

What are the features of glycolysis?

A
  • Central pathways of carbohydrate metabolism
  • Occurs in all tissues (cytosolic)
  • Exergonic, oxidative
  • C6 to 2xC3 (no loss of CO2)
  • Irreversible (as too exergonic to go backwards)
  • With one extra enzyme, it is the only pathways that can operate anaerobically.
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27
Q

What is needed for glycolysis to occur?

A

Required 2x ATP and take some reducing power (but makes 4 so net gain of 2) .

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28
Q

What 3 key enzymes involved in glycolysis? and what is their role?

A

Hexokinase (glucokinase in the liver) - catalyse Glucose to glucose-6-phosphate

Phosphofructokinase-1 - catalyse fructose-6-phosphate to fructose-1-6-bis-phosphate

Pyruvate kinase - catalyse 2-phosphoenolpyruvate to pyruvate (last step).

They catalyse the highly exogenic steps and make the reaction irreversible

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29
Q

Why are there so many steps in glycolysis?

A

Chemistry easier in small steps
Efficient energy conversion
Gives versatility
-allows interconnection with other pathways
-allows production of useful intermediates
-allows part to be used in reverse
Can be finely controlled

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30
Q

When is glycolysis irreversible?

A

after step 3 (The conversion of fructose-6-phosphate to fructose-1-6-bisphosphate catalysed by phosphofructokinase-1)

This is the COMMITTING STEP

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31
Q

How is knowledge of glycolysis clinically useful?

A

Rate of glycolysis is up to 200x faster in cancer.

Can measure uptake of FDG (radioactively modified hexokinase) and the image with PET scan to find out where in the body a tumour is.

Substate concentrated in highly metabolising tissues (cancer) so, can be used clinically to find and diagnose cancer.

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32
Q

What is Glycerol Phosphate?

Why is it important?

A

It is an important intermediate in glycolysis.
Important to triglyceride and phospholipid biosynthesis
Produced from dihydroxyacetone phosphate (DHAP) in adipose tissue and liver.
Therefore, lipid synthesis in liver requires glycolysis (Liver can phosphorylate glycerol directly)

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33
Q

What is 2,3-bisphosphoglycerate?

A

Important glycolysis intermediate.
Produced from 1,3-bisphosphoglycerate in RBCs.
Regulator of Hb O2 affinity (promotes release).
Present in RBC at the same molar conc as Hb (5mM).

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34
Q

What is allosteric regulation?

A

This is when an activator/inhibitor binds away from the active site and affects activity.

Proteins (usually enzymes) have two sites:
Catalytic site where the substrate binds and the regulatory site. This regulatory site allows binding of specify molecules which affect catalytic activity by producing activation or inhibition.

Can also get covalent modification (phosphorylation / dephosphorylation) which affects activity.

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35
Q

What steps are best to regulate?

A

Irreversible steps are the best ones to regulate because:

Reduced activity reduces the flux of substrates through the pathway directly which reduces the level of product.

36
Q

Why are reversible steps not regulated?

A

equilibrium occurs so the levels of product are unaffected.

37
Q

What is the key regulator of glycolysis? Why?

A

Phosphofructokinase-2 because it is the enzyme that regulates the committing step.

38
Q

How is PFK allosterically regulated?

A

Using ATP and AMP

When ATP high, it produces feedback to turn off pathway. But when energy levels are low (lots of AMP), the glycolysis pathway is then switched on.

39
Q

How is PFK Hormonally regulated?

A

Hormonal regulation of PFK occurs in the liver.

PFK is stimulated by Insulin (which dephoshorylates it) and inhibited by glucagon (which phosphorylates it).

40
Q

How is glycolysis metabolically regulated?

A

When there is a high conc. of NADH or low NAD, there is a high energy level signal which causes product inhibition of step 6 of glycolysis and therefore, it inhibits glycolysis.

This occurs because this step requires NAD to occur. The amount of NAD and NADH in a cell is constant so, it means that it has all been converted into NADH (and not yet converted back in oxidative phosphorylation).

41
Q

How is Pyruvate kinase regulated?

A

Hormonally! When there is a high Insulin:Glucagon ratio its activity is stimulated.

42
Q

What is LDH?

A

Lactate dehydrogenase! This is the enzyme used to convert NADH + H+ + Pyruvate back to NAD + lactate.

43
Q

Where is LDH produced?

A

Lactate in the liver and the heart (via LDH) is produced by RBCs and skeletal muscle (skin. brain, GI) and then released into blood. This lactate is normally metabolised by the liver and the heart as they need NAD to be regenerated efficiently and are usually well supplied with oxygen.

44
Q

When does lactate production rise?

A 
Strenuous exercise (inc Hearty eating) 
Pathological situations (eg shock and congestive heart disease).
45
Q

How lactase produced?

A

Produced form glucose and alanine via pyruvate.

Lactate by liver and heart (via LDH)
Produced by RBCs and Skeletal Muscle into the blood (in low oxygen conc.). It is normally metabolised by the liver and the heart where the reverse reaction occurs (as heart and liver are highly oxygenated tissues).
This allows NAD to be regenerated efficiently, usually well supplied with oxygen.

46
Q

What prevents the conversion of lactate back to glucose in the liver and kidneys?

A

Impared liver disease
Vitamin deficiency -Thiamine
Alcohol (NAD to NADH)
enzyme deficiencies

47
Q

What determines plasma conc of Lactate?

A

Production
Utilisation (liver, heart, muscle)
Disposal (kidney)

48
Q

What is hyperlactaemia?

A

This is when the plasma conc. of lactose is 2-5mM (usually less than 1mM). This is below the renal threshold so there is no change in blood pH (because of buffering capacity) but, the conc. is still higher than normal.

49
Q

What is lactic acidosis?

A

This is when the plasma conc. of lactose is above 5mM. This is above the renal threshold so blood pH is lowered.
This is a good marker of acutely unwell patients.

50
Q

What occurs in fructose metabolism?

A

Fructose is converted to G-3-P via Fructose-1-P. G-3-P is an intermediate in glycolysis.

51
Q

What occurs in galactose metabolism?

A

Galactose is converted to G-1-P then to G-6-P which is an intermediate in glycolysis.
Or, galactose can be converted into glycogen and stored.

52
Q

What is the clinical Important of fructose metabolism?

A

essential fructosuria- fructokinase missing fructose in urine so there are no clinical signs.

Fructose Intolerance- aldolase missing
Fructose-1-P-accumulates in then liver which leads to liver damage.
Treatment is to remove fructose form diet.

53
Q

What is galactosaemia?

A

This is when you are unable to metabolise galactose.
This is a problem as galactose can accumulate and an alternative pathway can occur.
Convert galactose to galactaicol. Requires NADPH and the enzyme aldose reductase.

54
Q

What three enzymes, if deficient, cause galactosaemia?

A

Glactokinase (rare)
Uridyl transferase (common)
UDP-galactose epimerase (rare)

55
Q

What effect does the depletion of NADPH in galactosaemia have?

A

Prevents maintenance of free sulphydryl (-SH) groups on proteins.
Inappropriate disulphide bond formation.
Loss of structural and functional integrity of some proteins that depend on free -SH groups eg the lease of the eye.

56
Q

What is the pentose phosphate pathway and what is it needed for?

A

A has a series of non-oxidative reactions which convert 5C sugars into 6C and 3C sugars which can then be utilised in glycolysis.

It also makes NADPH reducing equivalents for:
Fatty acid biosynthesis,
Steroid biosynthesis,
GSH regeneration.

Makes Ribose-5-P which is required for:
Nucleotides
DNA
RNA
Coenzymes
57
Q

What gets released during the pentose phosphate pathway? What is the consequence of this?

A
  • CO2 which makes it unidirectional
  • NO ATP in produces.
  • NADPH is also made from NADP -the ratio of NADP:NADPH at G6P dehydrogenase controls this pathway).
58
Q

Functions of the pentose phosphate pathway?

A
  1. Produce NADPH in cytoplasm..
    a) Biosynthetic reducing power: eg lipid synthesis which means it has high activity in liver and adipose tissue.
    b) Maintain free -SH (cysteine) groups in certain proteins which prevent oxidation to S-S (disulphide bonds)

2) Produce 5C sugars for nucleotides needed for nucleic acid synthesis. Therefore, it has high activity in dividing tissues like bone marrow.

59
Q

What happens if there is a glucose-6-phosphate dehydrogenase (G6PDH) deficiency?

A

THIS IS THE RATE LIMITING ENZYME.

NADPH level reduced, So, reduced free -SH groups and more S-S bonds formed. This can cause aggregated proteins.
Eg in RBCs, the aggregated proteins lead to heinz bodies being formed which leads to haemolysis.
It also causes blurred vision in tense of eye.

It is a common inherited defect

60
Q

What is pyruvate dehydrogenase?

A

PDH is a large, multi-enzyme complex that is in the mitochondrial matrix.
These enzymes convert pyruvate to acetyl CoA.
The reaction is irreversible so it is a key regulatory step.
It also involves an irreversible loss of CO2.

61
Q

Why is the PDH reaction described as sensitive to Vitamin B1 deficiency?

A

The different enzyme activities require various co-factors (FAD, thiamine…), B-vitamins provide these so it is sensitive to its deficiency.

62
Q

What does PDH deficiency lead to?

A

Lactic acidosis

63
Q

What is the Tricarboxylic cycle?

A
  • A single pathway
  • Occurs in the mitochondria
  • Acetyl CoA concerted into 2 x CO2
  • Highly oxidative (required NAD and FAD)
  • Some energy produced (ATP/GTP)
  • Also produces precursors for biosynthesis.
64
Q

C6 to C5 (step of TCA)

A

release NADH and CO2

65
Q

C5 to C4 (step of TCA)

A

NAD to NADH
Add CoA
Release CO2

66
Q

C4 to C4 (step of TCA)

A

GDP to GTP
then FAD to FADH2
then H2O
They NAD to NADH

67
Q

C4 to C6 (step of TCA)

A

Add Acetyl CoA

68
Q

What does TCA produce per one glucose?

A

6 NADH
2 FADH2
2 GTP

(as 2 CoA)

69
Q

What is the TCA Regulated by?

A

Regulated by energy availability.

Presence of ADP stimulates isocitrate dehydrogenase and therefore Krebs.
ATP and NADH inhibit cycle as already have lots of energy present.

70
Q

What are other functions of the TCA?

A

Amino acids and fatty acids can be converted into different intermediates in the pathways.
This pathway is central to metabolism.
It is also used to produce some amino acids, fatty acids and haem and glucose.

71
Q

Summarise the TCA

A

Cantral pathway in catabolism of sugars, fatty acids, ketone bodies, amino acids and alcohol.

They produce molecules that readily loose CO2.

Break C-C bond in acetate (acetylCoA) and carbons are oxidised to CO2.

Oxidative -produces NADH and FADH2.

Some energy as GTP produced directly.

Produces precursors for biosynthesis

Does not function in the absence of O2 (as need ETC)

Intermediates act catalytically - no net synthesis or degradation of Krebs cycle intermediates alone.

72
Q

Stage 4..

A

Mitochondria - Inner mitochondrial membrane

Consists of electron transport and ATP synthesis (oxidative phosphorylation).

NADH and FADH2 are re-oxidised

O2 required (to then be reduced to water)

Large amounts of energy (ATP) produced.

73
Q

What is the electro transport chain?

A

Electrons are transferred through a series of carrier molecules -protein translator complexes (PTC)- (mostly within proteins) to O2, which release energy.

This happens because:

  • The NAD will get oxidised,
  • 2 x H+ will go from mitochondrial matrix to inter membrane space at each PTC to create a H+ gradient (a proton motive force / pmf),
  • H+ will reduce O2 to form water (also combine with the e-)
74
Q

How much energy is used to move H+ across the mitochondrial membrane? What is the use of this energy?

A

30% (lots released as heat)

This heat energy is used to keep body temperature at 37 degrees.

75
Q

What is ATP synthase / Proton Translocating ATPase?

A

It is a protein in the inner mitochondrial membrane which, using hydrogen ion gradient, drives the synthesis of ATP from ADP.

76
Q

How is ATP synthesised?

A

Return of H+ is favoured energetically by the electrochemical potential (electrical and chemical gradient)
-Protons can only return across the membrane via ATP synthase and this drives ATP synthesis.

77
Q

How is electro transport coupled to ATP synthesis?

A

Electrons are transferred from NADH and FADH2 to oxygen in the electro transport chain.
Energy released is used to generate a proton gradient, proton motive force (pmf)
Energy from the dissipation of the proton motive force is coupled to the synthesis of ATP from ADP via ATP synthase.

78
Q

How is oxidative phosphorylation regulated?

A

When the ATP conc is high, there will by no substrate (ADP) for ATP synthase.
Therefore, the inwards flow of H+ stops.
This means that the conc. of H+ in the intermitochondrial space increases which prevents further H+ pumping and prevents ETC.
It is reversed when there is a low conc. of ATP.

79
Q

When is there inhibition of oxidative phosphorylation?

A

Inhibitiors block electron transport eg cyanide prevents acceptance of e- by O2.
CO is also an inhibitor.

This means there is no pmf so, it is lethal.

80
Q

What do uncouplers do?

A

Uncouplers increase the permeability of the inner mitochondrial membrane to protons.

  • This dissipates the H+ gradient as H+ enter without going though ATP synthase, thereby reducing pmf.
  • This means there is no phosphorylation of ADP (to form ATP). But, electron transport continues as this has not been inhibited.
81
Q

What is the role of brown adipose tissue in metabolism?

A

Brown adipose tissue can control the degree of coupling using fatty acids. This allows extra heat generation.

82
Q

How does brown adipose tissue help with thermoregulation?

A

Contains Thermogenine (UCP1). This is a naturally occurring uncoupling protein.
In response to cold, noradrenaline activates:
1. Lipases which release fatty acids from triacylglycerol
2. Fatty acid oxidation which leads to electron transport.
3. Fatty acids activate UCP1
4. UCP1 transports H+ back into mitochondria.

So, if electron transport is uncoupled form ATP synthesis then the energy of pmf is released as extra heat.

83
Q

Where is brown adipose found?

A

Newborns (to maintain heat, particularly around vital organs) and Hibernating animals (to generate heat to maintain body temperature).

84
Q

How many moles of ATP created from each glucose?

A

32 moles of ATP from each glucose.

85
Q

What has more energy, NADH or FADH2?

A

Electro in NADH have more energy than in FADH2. So, NADH uses 3 protein translator complexes where FADH2 only uses 2.

The greater the pmf, the more ATP is synthesised.

2 mol of NADH=5mol of ATP.
2 mol of FADH2 = 3mol of ATP..

86
Q

What is the difference between oxidative and substrate level phosphorylation?

A

Oxidative requires membrane associated complexes whereas substrate level requires soluble enzymes.

Oxidative -energy coupling occurs indirectly through generating and subsequent utilisation of proton gradient whereas, in substate level, energy coupling occurs directly through the formation of high energy hydrolysis bond.

Oxidative cannot occur in the absence of O2 whereas, substate level can occur to a limited extent.

Oxidative is the major process for ATP synthesis in cells which require a large amount of energy. Whereas, substate level is a minor process for ATP synthesis in cells requiring a large amounts of energy.

Sem 1 - MCBG (16 decks)

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