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MCBG > Carbohydrates Energy Production Lec 2,3,4 > Flashcards

Carbohydrates Energy Production Lec 2,3,4 Flashcards

1
Q

What is the general formula for carbohydrates and what functional groups do they contain.

A

(CH20)n

Contains aldehyde or keto groups

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2
Q

Give 4 examples of cells that can only metabolise glucose

A 
RBC
Neutrophils
Innermost cells of the kidney medulla
Lens of the eye
CNS (brain) prefers glucose as fuel
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3
Q

Why cant cellulose be digested and why is this important?

A

Amylase cant bind to beta sheets in cellulose which is important because cellulose makes up fibre in our body.

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4
Q

What is the difference between primary lactase and secondary deficiency?

A

All are due to an absence of lactase. Primary is due to absence of lactase allele whereas secondary is due to small intestine injury eg gastroenteritis. Primary usually just affects adults whereas secondary affects booth children and adults. Secondary is usually reversible whereas primary usually is not.

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5
Q

What are some symptoms of lactose intolerance?

A 
Vomiting 
Flatulence 
Bloating
Diarrhea 
Rumbling stomach
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6
Q

How is glucose taken up into the cells from the blood?

A

Via facilitated diffusion using transport proteins GLU1- GLU5

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7
Q

What are the 4 main functions of glycolysis?

A

Oxidation of glucose
Synthesis of ATP from ADP
NADH production
Produces C3 from C6

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8
Q

What are the key features of glycolysis

A

It is the central pathway for all carb catabolism
Occurs in all tissues
Exergonic, oxidative
With addition of LDH it is the only pathway that can operate anaerobically
Irreversible pathway

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9
Q

What is the function of hexokinase?

A

Phosphorylation glucose into Glucose-6-P using ATP

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10
Q

What is the function of Phosphofructokinase-1

A

Converts Fructose-6-P into Fructose 1,6-Bis-P using ATP

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11
Q

What is the function of pyruvate kinase?

A

Converts phosphoenolpyruvate into pyruvate producing ATP

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12
Q

What is the purpose of phosphorylation of glucose to glucose-6-P in the first stage of glycolysis?

A
  • Makes it negatively charged (anionic) so it cannot pass back through the plasma membrane.
  • Increases reactivity of glucose for subsequent steps
  • This reaction (reaction 1) and also reaction 3 are irreversible as they have very large negative delta G values
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13
Q

What is a committing step? What is it in glycolysis?

A

A committing step is the step at which the molecules are ‘committed’ to the pathway and will ultimately end up in the pathways final product. In glycolysis this is step 3 the phosphorylation of fructose -6-P to fructose 1,6-biphosphate using ATP

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14
Q

What is the net gain of ATP from glycolysis?

A

2 ATP are invested and 4 produced so net gain of 2 ATP

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15
Q

What is the benefit of having many steps in glycolysis?

A
  • Efficient energy conservation
  • Gives versatility-allows interconnections with different pathways
  • Can be controlled
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16
Q

How could the rate of glycolysis be used as a clinical indicator of cancer?

A

Rate of glycolysis is much higher in cancerous cells. Patient given radioactive glucose mimicking substrate which can be tracked using a PET scan

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17
Q

What is glycerol phosphate? How is it derived? Why is it important? Where is it produced?

A

It is a metabolite which is produced when Fructose 1,6-Bisphosphate is cleaved to form dihydroxyacetone or glyceraldehyde 3-P converts to dihydroxyacetone-P. Dihydroxyacetone-P then is converted to Glycerol phosphate by glycerol 3-phosphate dehydrogenase and by the oxidation of NADH to NAD.
It important in triglyceride and phospholipid biosynthesis. It is produced in adipose and liver

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18
Q

What is 2,3-biphosphoglycerate? How and where is it produced?

A

It is an important metabolite which allows oxygen to be released from Hb (it’s a regulator of Hb affinity for oxygen). It is produced in RBC. It is produced by the conversion of 1,3- bisphosphate glycerate using the enzyme Bisphosphate glycerate mutate.

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19
Q

What are the reactants and products in the reaction involving the enzyme lactate dehydrogenase (LDH)?

A

This reaction regenerates NAD+ .

NADH + H+ + pyruvate ————-> NAD+ + Lactate

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20
Q

What is happens to glucose in the tissue in anaerobic conditions?

A

It is converted to pyruvate in glycolysis and then pyruvate is converted to lactate by LDH and the oxidation do NADH to NAD+

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21
Q

What happens to the lactate that was produced in the tissue from glucose anaerobic conditions?

A

The lactate travels into the blood and into either the heart or liver and kidney. In the heart it can be converted back to pyruvate by LDH and the reduction of NAD+ to NADH which can be used to release energy. In the liver and kidney it can undergo this process and the pyruvate can be used to release energy or it can undergo gluconeogenesis to produce glucose which can travel into the blood.

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22
Q

In what cases is the conversion of lactate in the liver and kidney impaired?

A

Liver disease
Vitamin deficiency
High alcohol levels- Alcohol uses up NAD+ converting it to NADH therefore there is a lack of NAD+
Enzyme deficiency

23
Q

What 3 things determine lactate plasma concentrations?

A
  1. Production
  2. Utilisation - Heart, muscle and liver
  3. Disposal- Kidney
24
Q

What is and what can cause Hyperlactaemia?

A

Hyperlactaemia is when the levels of lactate in the blood Plasma are higher than normal but there is no change in blood pH levels and it is below the renal threshold. Exercise can cause this.

25
What is lactic acidosis?
When the levels of lactate in the blood plasma exceed a healthy range and blood pH is lowered. It also exceeds the renal threshold meaning lactic acid goes into the urine. It can therefore be used as a clinical marker for acutely unwell patients
26
Which step of metabolism is common in all carbs/ sugars?
Glycolysis
27
Where is fructose metabolised?
Liver
28
What happens when fructokinase is missing from the body?
Fructose cannot be metabolised so is found in the urine. This is called essential fructosuria.
29
What is and what causes Fructose Intolerance? What’s the treatment?
This is when the enzyme aldolase (the enzyme that cleaves Fructose-1-P) is missing. This means that Fructose-1-P accumulates in the liver damaging it. Treatment is to remove fructose from diet.
30
What is the importance of the pentose phosphate pathway?
It produces NADH an important reducing power | Produces the 5 carbon sugar ribose for synthesis of nucleotides
31
What is galactosaema? What occurs in a patient with galatcosaema?
It when people are unable to utilise the galactose taken in in the diet due to an absence of transferase enzyme (more common) or kinase enzyme (rare) . Accumulation of galactose in the tissue leads to it being reduced to galactitol by the enzyme aldose reductase and also the conversion of NADPH to NADP+. This depletes some tissues of NADPH, In the eye the structure is damaged which causes cataracts. Also accumulation of galatitol and galactose in the eye may lead to increase intra-ocular pressure (glaucoma) which if untreated could lead to blindness.
32
What is happens in a person with glucose 6-P dehydrogenase deficiency (G6PD deficiency)?
The gene coding for G6PD is mutated causing it to have low activity levels causing low levels of NADH to be produced. Without NADH glutathione which protects the cell against oxidative damage cant be regenerated. In RBCs the Hb become cross linked by disulphide bonds causing them to aggregate into insoluble formations called Heinz bodies. This leads to premature destruction of RBC and causes haemolysis.
33
Which cells are most affected by G6PD deficiency? Why?
RBC because the pentose sugar pathway is their only source of NADH.
34
What is the effect of covalent modification?
It’s phosphorylation or dephosphorylation usually by kinase enzymes. Adding a bulky negatively charged phosphate group alters the structure and activity of a protein.
35
What are potential sites of regulation?
Irreversible steps are potential sites of regulation. Reversible steps cant be regulated as an inhibitor will not change the amount of product it will just affect the speed at which eqbm is reached.
36
What is the effect of inhibiting the committing step?
It allows substrate to be diverted into other pathway rather than it being wasted or unused.
37
What is the effect of high energy signals on catabolic pathways?
High energy signals eg ATP, NADH inhibit the catabolic pathway
38
What is feed forward pathway regulation?
Production of early substrate signals further down the pathway to activate making it ready.
39
Name the key regulatory enzyme in glycolysis
Phosphofructokinase
40
How is phosphofructokinase regulated?
Allosteric regulation (muscle)- Inhibited by high ATP Stimulated by high AMP Hormonal regulation (liver) Stimulated by insulin Inhibited by glucagon
41
What is the function of pyruvate dehydrogenase (PDH)? Describe the reaction. What is this reaction sensitive to?
PDH converts pyruvate (3C) into Acetyl CoA (2C). This reaction is irreversible (as CO2 is lost) therefore is a key regulatory step. This reaction is sensitive to Vitamin B1 deficiency. Pyruvate + CoA + NAD+ ——-> Acetyl CoA + CO2 + NADH
42
What molecules activate and inhibit Pyruvate Dehydrogenase (PHD)?
Activated by Low Energy Compounds- Pyruvate, ADP, CoA, NAD+, insulin (insulin increases rate of respiration when blood glucose levels are high) Inhibited by High Energy Compounds- ATP, Acetyl CoA, NADH, Citrate
43
What are the key principals of the TCA/ Krebs cycle?
It is oxidative so requires NAD+ and FAD+ meaning reductive steps occur which converts NAD+ to NADH. CO2 is lost Substrate level phosphorylation (ADP converted ATP, GDP converted GTP) Doesn’t function without oxygen
44
What are the regulatory enzymes in TCA/ Krebs cycle?
Isocitrate dehydrogenase | Alpha-ketoglutarate dehydrogenase
45
What inhibits/ activates isocitrate dehydrogenase?
Isocitrate dehydrogenase is inhibited by NADH, ATP | Activated by-ADP
46
What inhibits alpha-ketoglutarate dehydrogenase?
Inhibited by- NADH,ATP, succinyl CoA
47
Can Krebs Cycle function without oxygen? why/why not
No as NAD+ cant be regenerated without oxygen
48
Describe the steps of oxidative phosphorylation
1. FADH2 and NADH carry H+ and e- to the mitochondrial matrix 2. e- Move down the e- transport chain, losing energy at each carrier 3. This energy is used to pump H+ from the mitochondrial matrix into the intermembrane space 4. This forms a electrochemical gradient as the conc of H+ is now higher in the intermembrane space that the mitochondrial matrix 5. H+ moves down the electrochemical gradient back into the matrix via ATP synthase which generates ATP- this is chemiosmosis 6. Oxygen (known as the final e- acceptor) combines with the e- and H+ to form water
49
Describe how high ATP inhibits oxidative phosphorylation
When ATP is high ADP is low, therefore there is no substrate for ATP synthase. Conc. of H+ increases in the intermembrane space and pumping of H+ stops
50
How does cyanide inhibit oxidative phosphorylation?
It mimics O2 preventing the acceptance of e- and therefore blocking the e- transport chain
51
How do uncouplers inhibit oxidative phosphorylation?
Increase the permeability of the membrane to H+ H+ enters the mitochondria without driving ATP synthase No electrochemical gradient No ATP generation
52
What is the uncoupling protein called that’s found in brown adipose tissue?
Thermogenin
53
How does brown adipose tissue regulate body temperature?
In cold temps, noradrenaline activates- 1. Lipase to release fatty acids from triacylglycerol 2.Fatty acids are oxidised which releases NADH and FADH2 which feed into the electron transport chain forming the gradient 3. Fatty acids also activate thermogenin (UCP1) which transports H+ back into the mitochondria So ATP synthesis is uncoupled from electron transport. This means energy from the electron gradient can be released as extra heat
54
Give 4 differences between oxidative and substrate level phosphorylation
1. Oxidative requires membrane associated complexes whereas substrate level requires soluble enzymes 2. Oxidative energy generation occurs indirectly ie the use of a proton gradient whereas in substrate level ATP formation is direct 3. Oxidative cannot occur without oxygen whereas substrate level can occur to a limited extent without oxygen 4. Oxidative produces much more energy/ ATP than substrate level

MCBG (3 decks)

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