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Carbohydrate Metabolism Flashcards

0
Q

What different forms of carbohydrates are there?

A

-Mono-, di-, polysaccharides and dextrins

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1
Q

Why are carbohydrates very polar?

A

-Contain lots of aldehyde, ketone and -OH groups

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2
Q

By what type of bonds are disaccharides joined?

A

-Glycosidic

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3
Q

Is lactose a mono,di or polysaccharides?

A

-Disaccharides

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4
Q

Is glucose a mono,di or polysaccharide?

A

-Monosaccharides

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5
Q

What is the basal glucose level in the blood?

A

-5mM

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6
Q

Why can’t glucose readily cross cell membranes?

A

-Hydrophillic so can not cross hydrophobic phosopholipid bilayer

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7
Q

What are the main uses of carbohydrates?

A
  • Main fuel source
  • Energy store -> glycogen
  • In anabolic nucelic acid, glycolipid and glycoprotein synthesis
  • Release energy and reducing power via catabolic pathways
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8
Q

What are the four stages of carbohydrate metabolism?

A
  • Stage 1 -> digestion and absorption
  • Stage 2 -> glycolysis
  • Stage 3 -> TCA/Krebs cycle
  • Stage 4 -> Oxidative phosphorylation
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9
Q

What happens in stage 1 of carb metabolism?

A
  • Carb-> monosaccharides in the lumen of GI tract for absorption
  • Digestion -> salivary amylase (Buccal Cavity), pancreatic amylase, glycosidases and disaccharidases on brush border in duodenum/jejenum
  • Absorption -> Monomers actively transported into blood via GLUT transporters to tissues
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10
Q

How are GLUT transporters representative of glucose requirements?

A

-GLUT1-5 receptors have varied distribution and affinity throughout the tissues of the body which represents the glucose dependancy

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11
Q

Which cells/tissues have an absolute glucose requirement?

A

-RBCs, WBCs, Kindey medulla, lens of the eye (CNS is v.preferential)

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12
Q

What is the purpose of glycolysis?

A
  • Breakdown into intermediate metabolites
  • Release of energy and reducing power
  • Provide building blocks for anabolism
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13
Q

What is the end product of glycolysis?

A

-2 x Pyruvate

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14
Q

Where does glycolysis occur?

A

-In all active tissues intracellularly in the cytoplasm

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15
Q

Which steps in glycolysis are irreversible?

A

-1, 3,7 and 10

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16
Q

Describe phase 1 of glycolysis

A
  • Glucose->G6P (uses ATP,irreversible, anionic so cannot go back across PM,)
  • G6P->F6P (increases reactivity)
  • F6P->F16BP (irreversible, committing step, uses ATP)
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17
Q

What enzyme catalyses step 1 of glycolysis (Glucose-> G6P)?

A

-Hexokinase

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18
Q

What enzyme catalyses step 3 of glycolysis(F6P->F16BP)?

A

-Phosphofrucokinase-1

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19
Q

What are the most important steps of phase 2 glycolysis

A

-Steps 7 and 10 as these are the irreversible steps which both produce ATP (substrate level phosphorylation)

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20
Q

What is the net synthesis of ATP in glycolysis

A

-2 ATP

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21
Q

Why are the intermediates DHAP and G3P important?

A

-G3P is oxidised DHAP which is used in TAG synthesis

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22
Q

Why is the intermediate 1,3-BPG important?

A

-Used to synthesis 2,3-BPG which is important in regulating Hb

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23
Q

What is the an overview pathway of glycolysis?

A
  • C6->C6 (using 2ATP)
  • C6->C3
  • C3-> 2 x pyruvate (Producing 4 ATP and 2NADH)
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24
Q

What is the overall equation for glycolysis?

A

-Glucose + 2ADP + 2Pi +2NAD+-> 2 Pyruvate +2ATP + 2NADH +2H+ +2H2O

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25
Q

Why can humans not digest cellulose?

A

-Linked together by B1-4 glycosidic links and do not possess an enzyme to degrade this strong bond

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26
Q

How is glycolysis under product control?

A
  • High ATP inhibits glycolysis
  • High ATP means high NADH and low NAD+
  • negative feedback inhibition of step 6 where NAD+-> to NADH
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27
Q

What are the two types of enzymatic control of glycolysis?

A
  • Allosteric regulation

- Covalent Modification

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28
Q

Describe allosteric activation

A
  • Enzyme does not recognise substrate
  • Allosteric activator binds to enzyme, at a site other than the active site
  • Causes a conformational change
  • Enzyme now recognises substrate
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29
Q

Describe allosteric inhibition

A
  • Enzyme recognises substrate
  • Allosteric inhibitor binds to enzyme, at a site other than the active site
  • Causes a conformational change in the active site
  • Enzyme no longer recognises substrate
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30
Q

Give an example of allosteric inhibition in glycolysis

A
  • Step 1 -> G6P acts as an allosteric inhibitor of hexokinase. As G6P accumulates it binds to hexokinase and inhibits its function
  • Step 3 in skeletal muscle -> High ATP:AMP ratio decreases glycolysis by allosterically binding to phosphofructokinase-1. Low ATP:AMP ratio increases glycolysis as AMP acts as an allosteric activator binding to another site on phosphofructokinase-1
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31
Q

How does insulin:glucagon have an effect on glycolysis?

A

In the liver

  • High Insulin promotes glycolysis as the concentration of glucose is high in the blood
  • High glucagon stops glycolysis as the concentration of glucose is low
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32
Q

How does covalent modification control enzymes in glycolysis?

A

-De/phosphorylation of enzymes will inhibit/activate the enzyme

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33
Q

Why are the irreversible steps unidirectional?

A

-The gibbs free energy is favourable in one direction

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34
Q

Why is lactate dehydrogenase important, particularly in RBCs?

A
  • Regenerates NAD+ from NADH through the pathway Pyruvate +NADH + H+-> Lactate + NAD+
  • Important in RBCs as they have no mitochondria which is where NADH is normally oxidised
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35
Q

Which cells produce lactate?

A
  • RBCs

- Skeletal muscle

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36
Q

What happens to the lactate produced?

A

-Transpotrted to the liver, heart and kidney where it is converted to pyruvate, oxidised to CO2 and converted to glucose

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37
Q

What is hyperlactaemia?

A

-An elevation in blood lactate levels but below 5mM - not significant

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38
Q

Why is an elevation of blood lactate >5mM significant?

A
  • Exceeds renal threshold and begins to effect buffering capacity of the blood
  • Leads to lactic acidosis
39
Q

What may cause an increased production of lactate?

A
  • Shock
  • Hearty eating
  • Strenuous exercise
  • Congestive heart disease
40
Q

What may cause decreased utilisation of lactate?

A
  • Liver disease
  • Thiamine deficiency
  • During alcohol metabolism
  • Enzyme deficiencies
41
Q

What happens in lactose intolerance to cause diaarhoea?

A
  • Lactose persists in colon
  • Increases osmotic pressure in lumen
  • Draws in water
  • Causes diarrhoea
42
Q

Describe normal galactose metabolism

A
  • Galactose -> Galactose-1-P via GALACTOKINASE
  • Galactose-1-P -> Glucose-1-P via GALACTOSE-1-P URIDYL TRANSFERASE
  • Glucose-1-P enters glycolysis
43
Q

How is Glucose made from galactose and why is this mechanism important?

A
  • UDP-galactose gets converted to UDP-glucose by UDP-galactose EPIMERASE
  • Important in lactose intolerance and lactation as it allows lactose to be made as the reaction is reversible, i.e. UDP-glucose can be converted to galactose and allow lactose to be made
44
Q

What are the two causes of galactosaemia?

A
  • Lack of GALACTOKINASE

- Lack of GALACTOSE-1-P URIDYL TRANSFERASE

45
Q

Which galactoseamia enzyme deficiency is rare?

A

-galactokinase deficiency

46
Q

Which galactosemia enzyme deficiency is more severe and why?

A
  • Galactose-1-P uridyl transferase deficience

- Accumulation of Galactose -1-P as well as galactose as galactokinase becomes saturated

47
Q

How can galactosaemia cause cataracts/blindness?

A
  • Galactose accumulates in the lens of the eye
  • Galactose->Galactitol by enzyme aldose reductase
  • Uses NADPH->NADP+ causing a reduction in NADPH
  • NADPH is an oxidative protective mechanism
  • Depletion of NADPH leads to damage to lens of eye
  • Inappropriate DSB formation in crystalline protein in eye due to oxidation of protein (loss of reducing power)
  • Forms cataracts
  • In addition non-enzymatic glycosylation of galactose increases the osmotic pressure and causes swelling of the lens -> can lead to blindness
48
Q

Why is an accumulation of Galactose-1-P in galactosaemia a problem?

A
  • Damage to liver, kidney and brain
  • hepatomegaly due to accumulation -> galactose begins entering pathways it is not usually in
  • hepatocellular damage due to depletion of Pi
  • Depletion of Pi interferes with organs normal function
49
Q

What is the substrate for the pentose phosphate pathway?

A

-G6P

50
Q

How is the pentose phosphate pathway regulated?

A

-By G6P dehydrogenase via NADPH/NADP ratio

51
Q

In which tissues is the pentose phosphate pathway important?

A
  • Liver
  • Adipose tissue
  • RBCs
52
Q

Describe the first phase of the pentose phosphate pathway

A
  • Phase 1-> oxidative decarboxylation - removes CO2 -> irreversible-> G6P + 2NADP+ -> C5 + 2NADPH + 2H+ + CO2
  • Regulated by G6P DEHYDROGENASE and PHOSPHOGLUCONATE DEHYDROGENASE
53
Q

Describe phase 2 of the pentose phophate pathway

A

-Converts unused C5 sugar phophates into intermediates of glycolysis -> F6P and Glyceraldehyde 6P

54
Q

What are the functions of the pentose phosphate pathway?

A
  • Produces C5 sugar pentose for nucleotide synthesis (more active in dividing tissues)
  • In adipose tissue it provides NADPH for lipid synthesis
  • In RBCs provides NADPH to protect RBCs from oxidative damage, preventing DSB formation
55
Q

What is G6P Dehydrogenase deficiency?

A

-Deficiency in the enzyme Glucose 6 Phosphate Dehydrogenase

56
Q

What kind of inheritance pattern does G6PD deficiency have?

A
  • X linked recessive

- affects mainly mediterranean/Black USA males

57
Q

What type of mutation causes G6PD deficiency?

A

-Point mutation

58
Q

What happens in G6PD deficiency?

A
  • Decreased G6PD activity in RBCs
  • Consequently there is a decrease in NADPH as during the pentose phosphate pathway G6PD reduces NADP+ to NADPH
  • Decreased NADPH means reduced oxidative protection in RBCs resulting in DSB formation
  • This causes decreased structural integrity and decreased functional activity of RBCs
  • Coupled with this NADPH reduces oxidised GSSG to GSH to replenish oxidative protection
  • Because there is decreased NADPH, Glutathione becomes saturated
  • Oxidative protection is decreased further, more DSB formation
  • Insoluble Heinz bodies form due to aggregation of Hb
59
Q

Why can G6PD deficiency lead to haemolysis?

A
  • Heinz bodies and decreased structural integrity can potentially cause haemolysis
  • Haemolytic episodes are usually induced after exposure to an oxidative chemical, eg antimalarial drugs
60
Q

Explain the key role of Pyruvate Dehydrogenase in glucose metabolism

A
  • Converts Pyruvate to AcetylCoA for use in stage 3 of catabolism
  • A critical step in the production of energy
  • Irreversible as it involves the removal of CO2
  • Reaction is sensitive to the energy status of the cell, i.e. ATP/NADH inhibit the reaction
61
Q

How is pyruvate dehydrogenase activated?

A
  • High pyruvate
  • high NAD+
  • High CoA
  • insulin through phosphorylation
62
Q

What is the overall equation for Pyruvate to AcetylCoA?

A

-Pyruvate + CoA + NAD+ -> AcetylCoA + NADH + H+ + CO2

63
Q

What enzyme catalyses step 10 in glycolysis?

A

-Pyruvate kinase

64
Q

Where does pyruvate->acetyl coA occur?

A

-Mitochondrial matrix (pyruvate is transferred from the cytoplasm)

65
Q

How many molecules of acetyl coA does one glucose produce?

A

-2

66
Q

What inhibits pyruvate dehydrogenase?

A
  • ATP
  • Acetyl CoA
  • NADH
67
Q

Why does PDH deficiency cause lactic acidosis?

A
  • Lack of PDH
  • No AcetylCoA produced
  • Can not store excess pyruvate
  • excess pyruvate shunted to lactate; lactate increases
  • Lactate decreases pH of the blood leading to lactic acidosis
68
Q

What are the main functions of the TCA cycle?

A
  • To transfer the energy from glucose into chemical bond energy mainly NADH and FADH2 (reducing power)
  • To synthesis intermediates to be used for the synthesis of non-essential a’a, in gluconeogenesis, haem synthesis and FA synthesis
69
Q

Where does the TCA cycle occur?

A

-In the mitochondrial matrix

70
Q

What are the 4 requirements for TCA cycle?

A
  • Acetyl Co A
  • Oxaloacetate
  • NAD+
  • FAD+
71
Q

Which pathways converge at the TCA cycle?

Hint: Which pathways can be fed into the cycle?

A

-Sugar, FA, Ketone bodies, alcohol and a’a metabolism

72
Q

Is the TCA cycle oxidative or reductive?

A

-Oxidative

73
Q

How many unidirectional steps are there in the TCA cycle and why are they irreversible?

A

-2 - loss of CO2

74
Q

What are the products of the TCA cycle per glucose?

A
  • 6NADH
  • 2FADH2
  • 2GTP
75
Q

What are the regulatory factors of the TCA cycle?

A
  • Predominantly ATP:ADP ratio -> high ATP-> H+ cannot enter saturated ATPase-> H+ stops translocating -> stops ETC accepting e- ->inhibits glycolysis
  • NADH:NAD+ ratio -> High NADH -> High H+ to drive ATP synthase -> inhibits glycolysis
76
Q

How are the enzymes of the TCA cycle regulated?

A

-High energy signals such as NADH and low energy signals such as ADP allosterically bind to enzymes and inhibit/activate them, respectively

77
Q

Why can the TCA cycle not function in the absence of O2?

A
  • O2 is the final electron acceptor

- Without O2 NAD+ is not regenerated and the cycle cannot function

78
Q

What is the main function of oxidative phosphorylation?

A

-Primary source of energy generation

79
Q

Where and what as is the energy stored which is released from glucose after the TCA cycle?

A
  • Stored as chemical bond energy in NADH, FADH2

- Also ATP from glycolysis and GTP from TCA cycle

80
Q

`Where does oxidative phosphorylation occur?

A

-On the inner mitochondrial membrane

81
Q

What has more chemical bond energy, NADH or FADH2 and why?

A
  • NADH

- Uses 3 ETC complexes whereas FADH2 uses 2

82
Q

What percent of ATP is conserved from NADH and FADH2?

A
  • approx 35% from NADH

- Approx 31% from FADH2

83
Q

What happens to the remaining energy which is not conserved as ATP?

A

-Dissipated as heat to maintain body temperature

84
Q

Describe what happens in oxidative phosphorylation

A
  • NADH is oxidised and H+ and e- release. e- is transferred down a series of complex multicomponent carriers which span the inner mitochondrial membrane
  • This releases a large amount of free energy in a stepwise fashion
  • The final electron acceptor at the end of the ETC is O2
  • The free energy released is used to translocate the H+ across the inner mitochondrial membrane, which is impermeable to H+, into the intermembrane space
  • This forms an electochemical potential difference across the inner membrane which is known as the proton motive force
  • The PMF then drives the H+ ions through an ATPsynthase complex located on the inner membrane, back into the mitochondrial matrix
  • The movement of H+ ions through the ATPsynthase complex drives ATP synthesis causing ATP synthase to catalyse ADP+Pi producing ATP
85
Q

What is the relationship between the amount of PMF and ATP

A

-The greater the PMF the more ATP is produced

86
Q

Compare and contrast oxidative phosphorylation with substrate level phosphorylation

A

Oxidative phosphorylation

  • Requires enzyme complexes
  • Energy generation occurs indirectly through the generation and utilisation of the pmf
  • Cannot occur without O2
  • Major process of ATP synthesis

Substrate level phosphorylation

  • Requires soluble enzymes
  • Energy generation occurs directly through Pi transfer
  • Can occur without O2 - limited
  • Minor process of ATP synthesis
87
Q

Why are ETC and ATP synthesis controlled by the same molecules?

A

-Because they are not mutually exclusive, i.e. they are coupled and must occur at the same time

88
Q

How does High ATP:Low ADP ratio regulate ETC/ATP synthesis?

A
  • Low ADP -> ATPsynthase stops due to low substrate
  • This prevents translocation of H+ back into matrix
  • [H+] increases in the intermembrane space
  • Prevents H+ being pumped out of matrix into intermembrane space
  • Absence of H+ causes electron transport to stop
89
Q

What are uncouplers and how do they work?

A
  • Molecules which cause the ETC to become uncoupled from ATP synthesis
  • Uncouplers increase the inner membranes permeability to H+
  • H+ can now move back into the mitochondrial matrix without passing through the ATPsynthase complex and driving ATP
  • ETC has become uncoupled from ATP synthesis
90
Q

What happens to the PMF during uncoupling?

A

-It is no longer driving ATP synthesis as it is not passing through the ATPase complex and the energy is dissipated as heat

91
Q

How many UCPs are endogenous in the body and where are they found?

A
  • UCP 1-5

- Located on the inner mitochondrial membrane, largely expressed in brown adipose tissue

92
Q

What is non-shivering thermogenesis?

A
  • A process which enable mammals to survive in cold environments
  • UCP-1 causes H+ to be able to leak back across the membrane and be dissipated as heat
93
Q

Where is UCP3 found and why is it important?

A
  • Highly expressed in skeletal muscle

- Involved in modifying FA metabolism and protection against ROS

94
Q

How much of the BMR does proton leack account for

A

-20-25%

95
Q

Give examples of exogenous uncouplers and how they work

A
  • CO/cyanide poisoning
  • Cause NADH/FADH2 not to be oxidised
  • No pmf
  • No ATP synthesis
  • No heat

Metabolism (14 decks)

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