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MEH Sem 1 > Lecture 2 - Carbohydrates > Flashcards

Lecture 2 - Carbohydrates Flashcards

1
Q

What are the 4 different stages of catabolism?

A
  1. Breakdown of nutrients to forms that can be absorbed by cells (a.a/monosaccharides/f.a)
    [no energy released]
  2. Degradation of block molecules to organic precursors
    [energy released]
  3. Krebs cycle
  4. Oxidative Phosphorylation
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2
Q

What is the general structure of carbohydrates?

A
  • General formula (CH2O)n
  • Contain aldehyde or keto- group
  • Split into mono-/di-/oligo-/poly-
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3
Q

What are cells that have absolute requirement for glucose?

A
  • RBC
  • WBC
  • Cells of kidney medulla
  • Lens of the eye

N.B Brain & CNS prefer glucose but can metabolise ketone bodies in starvation state

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4
Q

Where does stage 1 of catabolism, the breakdown of nutrients occur?

A

GI tract

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5
Q

Describe the stages of carbohydrate digestion in the body (location, enzymes)

A
  1. Saliva = Amylase (starch –> glycogen)
  2. Pancreas - Amylase
  3. Small intestine = Lactase, Sucrase, Isomaltase, Amylase
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6
Q

Why can’t cellulose be digested?

A

No enzyme in body to break down β-1,4 link

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7
Q

What are some primary and secondary causes of lactase deficiency?

A

Primary:

  • Absence of lactase persistence allele
  • Adults

Secondary:

  • Caused by injury to small intestine (Crohn’s disease, Coeliac disease)
  • Adults and infants
  • Reversible

Congenital lactase deficiency {extremely rare}
- Autosomal recessive defect in lactase gene

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8
Q

What are some symptoms of lactase deficiency?

A
  • Bloating/cramps
  • Flatulence
  • Diarrhoea
  • Vomitting
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9
Q

Why does diarrhoea and bloating occur in lactase deficient patients?

A

Bacteria in gut digests lactose –> lactase –> osmotic effect –> draws water into gut –> diarrhoea AND produce H2, CO2 –> bloating

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10
Q

How are sugars absorbed by the body?

A
  1. Active transport
  2. Passive transport (GLUT 2)
  3. Facilitated diffusion by target cells
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11
Q

What does stage 2 of metabolism involve?

Where does it occur?

A
  • Breakdown of metabolic intermediates
  • Glycolysis –> NADH, ATP
  • Occur in cytoplasm
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12
Q

What is the function of glycolysis?

*occurs in all tissues (cytosolic)

A
  • Oxidation of glucose: produce C6 and C3 intermediates
  • Produce: x2 NADH, X2ATP, X2 Pyruvate (C3, END)
    [per mole of glucose]
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13
Q

What are some features of glycolysis?

A
  • Central pathway of C metabolism
  • Occurs in all tissues (cytosolic)
  • Exergonic (irreversible)
  • C6 –> X2 C3
  • Enzyme LDH only way to do it anaerobically
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14
Q

What are the enzymes involved in glycolysis? What reactions do they catalyse? x3

A
  1. Glucose –> Glucose-6-phosphate
    [Hexokinase/Glucokinase (liver)]
    [1 mole of ATP used]
  2. Fructose-6-P –> Fructose 1,6- bis-P
    [Phosphofructokinase]
    [1 mole of ATP used]
  3. Phosphoenolpyruvate –> Pyruvate
    [Pyruvate kinase]
    [1 mole ATP released]

N.B: ALL STEPS ARE IRREVERSIBLE

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15
Q

Why are so many enzymes involved in glycolysis?

A
  • Efficient energy conservation
  • Allows for fine control
  • Useful intermediates formed
  • Allows for reverse reactions
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16
Q

Why does the phosphorylation of glucose to glucose-6-P occur?

A
  • Makes glucose negatively-charged: prevent travel across membrane
  • Increase reactivity of glucose
  • Uses 2 mole of ATP
  • Large G value, irreversible
17
Q

Which reaction is committing step of glycolysis?

A

Fructose-6-P –> Fructose -1,6- bis-P

[Phosphofructokinase]

18
Q

Which 2 steps produce ATP in glycolysis? What type of phosphorylation is this?

A
  • 1,3-bis-phosphoglycerate –> 3-phosphoglycerate
  • Phosphoenolpyruvate –> Pyruvate
    [Pyruvate Kinase]
  • Sub- level P
19
Q

1,3-bisphosphoglycerate is catalysed into a by b. What is the function of a?

A 
a = 2,3-Bisphosphoglycerate (2,3-BPG)
b = Bisphosphoglycerate mutase
- Function of 2,3-BPG:
i) Produced in RBC
ii) Reduce affinity of Hb to O2 (shift right)
20
Q

Glyceraldehyde 3-P is converted to a then b by c. What is the function of b?

A 
a = Dihydroxyacetone-P (DHAP) 
b = Glycerol phosphate 
c = Glycerol 3-P dehydrogenase 
- Function of b: TAG and phospholipid synthesis
[produced in liver & adipose]
21
Q

What is the clinical application of glycolysis?

A
  • Rate of glycolysis higher in cancer
  • Measure uptake of radioactive modified hexokinase sub. (FDG)
  • Imaging with positron emission tomography (PET)
22
Q

Step 6 of glycolysis (glyceraldehyde 3-P–> 1,3 BPG) is stopped when NADH increases why?

A
  • Ratio of NAD+/NADH is constant –> all glycolysis would stop when all NAD+ converted
23
Q

RBC has no mitochondria but needs to regenerate NAD+ somehow. Suggest a route

A
  • LDH reaction
    (NADH + H+ + Pyruvate —> NAD+ + lactate)
  • Catalysed by LDH
24
Q

How is plasma concentration of lactate controlled?

A
  • Conc. determined by rate of production/utilisation/disposal
  • Normally kept constant < 1mM
25
Q

When is lactate produced?

A
  • W/o major exercise (RBC, skin, brain)
  • Exercise
  • Pathological situations (shock)
26
Q

What ranges are hyperlactatemia and lactic acidosis?

A
  • Hyper:
    i) 2-5mM
    ii) Below renal threshold
    iii) No change in blood pH (buffering capacity)
  • L.A:
    i) Above 5mM
    ii) Above renal threshold
    iii) pH ⬇️
27
Q

Phosphofructokinase, PFK is a key regulator of glycolysis. What are some allosteric/hormonal regulations that controls it?

A

Allosteric:

  • Inhibited by high energy signals (NADH, ATP)
  • Stimulated by low energy signals (AMP, ADP)

Hormonal:

  • Stimulated by insulin
  • Inhibited by glucagon
28
Q

How does glucose-6-P inhibit enzyme hexokinase?

A
  • By allosteric regulation
  • Inhibition in further steps of glycolysis (3 & 6) by high energy signals prevents metabolism of F-6-P —> G-6-P ⬆️–> X hexokinase
29
Q

What reaction does aldolase catalyse? And what occurs when aldolase is missing and fructokinase is missing?

A
  • Fructose-1-P –> glyceraldehyde + DHAP
  • Fructokinase X = Fructose in urine (fructosuria)
  • Aldolase X = Fructose 1-P ⬆️–> liver damage
    [ Treatment: remove fructose from diet]
30
Q

Describe the enzymes and reactions in galactose metabolism

A
  1. Galactose –> Galactose-1-P
    [Galactokinase]
  2. Galactose-1-P –> Glucose-1-P
    [G-1-P uridyl transferase]
  3. UDP-Galactose –> Galactose-1-P
    [UDP-G epimerase]
31
Q

What does galactokinase deficiency result in and how often is it? Vice versa for transferase. Suggest a treatment.

A
  • Galactokinase X = galactose ⬆️
    [rare]
  • G-1-P transferase X = Galactose-1-P AND galactose ⬆️
  • No galactose in diet
32
Q

What happens when galactose accumulates?

A
  • Enters different pathway
  • Galactose –> Galactitol
    [Aldose Reductase]
  • Deplete NADPH –> Causes random formation of disulphide bonds –> loss of structural integrity –> lens of eye become cloudy
33
Q

What is the importance of PPP?

A
  • Generate NADPH –> recycle glutathione to reduced form –> protects against oxidative dmg –> no random disulphide bonds form
  • Form C5 sugar: synthesis of DNA & RNA
34
Q

Where does PPP occur and which enzyme catalyses the reaction?

A
  • Occurs in cytosol
  • Enzyme: Glucose-6-dehydrogenase
    [Reaction: G-6-P –> 5C sugars +NADPH+CO2]
35
Q

What are some features of PPP?

enzyme, regulation, products

A

[Reaction: G-6-P –> 5C sugars +NADPH+CO2]

  1. Loss of CO2 = irreversible
  2. No ATP produced
  3. Controlled by NADP+/NADPH ratio
  4. Rate-limiting enzyme = G6PDH
36
Q

Importance of PPP in RBC is? What happens if PPP x occurs?

A
  • Only source of NADPH –> no mitochondria

- If ❌PPP –> NADPH ⬇️ –> disulphide bond forms –> aggregate proteins, Heinz bodies –> haemolytic anaemia

MEH Sem 1 (18 decks)

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