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MCBG > S5 Carbohydrate Metabolism > Flashcards

S5 Carbohydrate Metabolism Flashcards

1
Q

What are the 4 main stages of carbohydrate metabolism?

A

1) break down of fuel molecules (proteins, carbs, lipids) to monomers (monosaccharides i.e. glucose)
2) Break down to metabolic intermediates: glycolysis + link reaction
3. ) Tricarboxylic acid (Krebs) cycle
4. ) Oxidative phosphorylation

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2
Q

Where in the body does stage 1 of carb metabolism occur?

A
  • extracellular in the GI tract

- building block molecules are absorbed from GI tract into circulation

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3
Q

What enzymes are involved in stage 1 and what do they do/where?

A
  • Salivary Amylases- break down starch, glycogen in saliva to dextrin
  • Pancreatic amylases- break down carbs to monosaccharides
  • In the small intestine:
    —> Lactase (breaks down lactose into glucose and galactose)
    —> sucrase (breaks down sucrose into fructose and glucose)
    —> pancreatic amylase (breaks alpha 1-4 bonds)
    —> isomaltase (breaks alpha 1-6 bonds)
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4
Q

Why can’t cellulose be digested by humans?

A

Humans do not have enzymes to break down the B,1-4 linkages in dietary fibres
BETA Bonds are diff to alpha bonds
(I.e. no cellulase)

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5
Q 
A) What molecules make up lactose?
B) what is lactose intolerance + how is it caused?
C) what foods contain lactose?
D) symptoms?
E) types of lactose intolerance?
A

A) Glucose and galactose
B) inability to break down lactose- small intestine stops making enough of lactase to digest and break down the lactose
C) Milk, cream, yoghurt, cheese
D) bloating/cramps, flatten each, diarrhoea, vomiting, rumbling stomach
E) - primary lactase deficiency: absence of lactase persistence allele (adults only)
- secondary lactase deficiency: caused by injury to SI (gastroenteritis, coeliac, crohns)
- congenital lactase deficiency: autosomal recessive defect in lactase gene, cannot digest breast milk

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6
Q

How are monosaccharides, such as glucose, absorbed into circulation?

A
  • using ion transporters
    1. Active transport into intestinal epithelial cells by sodium dependent glucose transporter 1 (SGLT1)
    2. Passive transport of glucose via GLUT 2 into blood
  • the NA pump generates a gradient
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7
Q

A) What is the rough conc of glucose in the blood?
B) what tissues require glucose?
C) what does the brain use in times of starvation?

A

A) 5mM
B) RBC, neutrophils, innermost of kidney medulla and lens of the eye
C) ketone bodies

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8
Q

A) Where does glycolysis occur
B) characteristics of glycolysis
C) Functions/what does it produce?

A

A) occurs in all tissues and in the cytosol
B) - it is an exergonic and oxidative process
C) - oxidation of glucose
- NADH production (2 per glucose)
- 2 net ATP produced per glucose
- produces c6 and c3 intermediates

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9
Q

A) How many steps is glycolysis?

B) why so many steps?

A 
A) 10
B) - conserves energy
- fine control
- interconnections with other pathways
- intermediates produced 
- some parts reversible
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10
Q

What are the most important enzymes to remember in glycolysis and what do they do and what step is each involved in?

A
  • In step 1: hexokinase- phosphorylation of glucose to Glucose-6-P
  • In step 3: phosphofructokinase-1: Fructose-6-P to Fructose 1,6-bis-P: first committing step
  • in step 10: Pyruvate kinase: catalyses transfer of po4 from PEP to ADP- producing ATP and pyruvate
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11
Q

A) Why is glucose phosphorylated in glycolysis?
B) what step does this occur in
C) what enzyme catalyses this

A

A) makes glucose more negatively charged so that it cannot pass back across membrane and makes it more reactive
B) step 1
C) hexokinase

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12
Q

What are the products of glycolysis and where does each go?

A
  • 2 pyruvate: to link reaction
  • 2 NADH: to ETC
  • 2 net gain ATP (4 produced but 2 lost at start)
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13
Q

What are the two important intermediates produced in glycolysis?

A

1) Glycerol phosphate
- produced from DHAP in step 4
- important to triglyceride and phospholipid biosynthesis
- produced from DHAP in adipose tissue and liver

2) 2,3-Bisphosphoglycerate (2,3-BPG)
- produced from 1,3-bisphosphoglycerate in step 6
- in RBC
- important regulator of oxygen affinity in HB (promotes its release)
- without it, hb would hold oxygen so tightly that it wouldn’t be released in tissues

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14
Q

a) Why is NAD+ production so important in glycolysis?

B) How is NAD+ regenerated?

A

A) - Needed to produce NADH in step 6
- NAD+ and NADH concentration is constant, glycolysis would stop if it all was converted to NADH
B)- NAD+ is regenerated from stage 4 (OP) which requires Oxygen
- RBC don’t have stage 4 ALSO if there was no oxygen NAD+ needs to be regenerated via another route —> lactate dehydrogenase

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15
Q

a) Outline how anaerobic glycolysis is carried out

B) equation

C) what enzyme catalyses this

A

a) - lactate is produced from glucose and alanine via pyruvate
- reversible
- nad+ regenerated

B) NADH + H+ + pyruvate NAD+ + Lactate
(Catalysed by Lactate dehydrogenase)

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16
Q

How is plasma concentration of lactate controlled?

A

it is produced (i.e. via red blood cells or in low o2) released into the blood and is then metabolised by the liver, heart and muscles and then disposed of in kidneys

17
Q

A) what is the normal concentration of plasma lactate?
B) What is:Hyperlactaemia
C) what is: Lactic acidosis

A

A) <1mM
B) plasma lactate conc: 2-5mM, no change in blood pH as below renal threshold
c) plasma lactate conc above 5mM, Blood ph is lowered as it is above renal threshold and is removed in urine

18
Q

What is substrate level phosphorylation?

A

Production of atp without ETC, but involving transfer of a Phosphate from a highly reactive substance,

19
Q

A) where is galactose metabolised?

B) what is galactosaemia

A

A) liver and red blood cells
B) Inability to utilise galactose due to a deficiency in any of the enzymes, it is inherited (caused by a mutation) and lead a to the toxic accumulation of an intermediate compound.

20
Q

A) A new born presents with cataracts, Jaundice, hepatomegaly (enlarged liver), renal failure, vomiting and brain damage- which enzyme would you suspect is deficient in this patient and why?

A

A) Uridyl transferase

  • leads to the accumulation of both galactose-1-phosphate and galactose
  • galactose enters another pathway to form galactitol- forms cataracts
  • galactose-1-phosphate affects the liver function: hence leads to hepatomegaly, jaundice etc.
  • most common type of galactosaemia and most severed side affects
21
Q

Why do galactosaemia patients have jaundice?

A
  • deficiency of the transferase enzyme leads to build up of toxic galactose-1-P
  • this affects liver function
  • one function of the liver is to breakdown old RBC into bilirubin, which is then conjugated and excreted
  • build up of unconjugated bilirubin in blood gives skin a yellow colour
22
Q

Why do galactosaemia patients have cataracts?

A
  • build up of galactose, allowing galactose to enter other pathways e.g. galactose forms galactitol
  • depletes NADPH levels
  • these NADPH were needed to maintain the structure of disulphide bonds in proteins
  • leads to inappropriate disulphide bond formation which affects the structure and hence function of proteins
  • in the eye the crystalline protein is denatured leading to cataracts
23
Q

What is the treatment for galactosaemia?

A
  • exclude galactose from diet
  • no milk or dairy
  • antibiotics, IV fluid
24
Q

What are the 3 important enzymes involved in galactose metabolism?

A
  • galactokinase
  • Uridyl transferase
  • UDP-galactose epimerase
25
Q

A) what is fructosia?

B) what is fructose intolerance?

A

A) if fructokinase is missing, fructose in urine

B) if aldolase is missing, fructose-1-p accumulates in liver and can lead to liver damage, take fructose out of diet

26
Q

A) what is the pentose phosphate pathway?
B) what are the two major steps
C) what is the function of this pathway

A

A)
Produces:
-PENTOSE (5C SUGar): ribose-5-P—> nucleotide biosynthesis for DNA and RNA
- PHOSPHATE: phosphorylated molecule: NADPH —> biosynthetic reducing power for fatty acid synthesis

B) 
1. OXIDATIVE STEP
Glucose-6-P ——> 5C + CO2 
Produces NADPH
Catalysed by: glucose-6-P-dehydrogenase
  1. NON-OXIDATIVE:
    3C5 sugars —-> 2 fructose-6-P and 1 glyceraldehyde-3-P

C)

  1. Produces NADPH- biosynthetic reducing power (FA synthesis) + maintains free cysteine (SH) bonds on proteins
  2. Produces ribose-5-P (5C): nucelotide synthesis for DNA and RNA
  3. Produces glycolysis intermediates via reversible pathways
27
Q

A patient has presented with anaemia and jaundice and you have discovered that they have a glucose-6-phosphate dehydrogenase deficiency. Explain how this would cause the above symptoms?

A
  • would be a reduced production of NADPH
  • NADPH has an important role in maintaining free disulphide bonds to protect the structure and function of proteins
  • mutations in the G6PD gene lead to G6PD deficiencies
  • G6PD helps RBC function properly , with low nadph, inappropriate disulphide bonds will be formed in Red blood cells leading to haemolysis and anaemia and hence jaundice as red blood cells are being broken down into bilirubin at a rate higher than the bilirubin is being excreted
28
Q

What are the steps of oxidative phosphorylation?

A
  1. NADH and FADH2- the hydrogens are removed and split into hydrogen ions (protons) and electrons: 2H+ + 2e-
  2. The electrons are transferred down a series of carriers known as Proton translocating complexes- releasing energy that activates proton pumps
  3. These proton pumps actively What are the steps of oxidative phosphorylation? transport the 2 h+ from the matrix into the inter membrane space, this sets up a proton gradient (proton motive force or pmf)
  4. The protons diffuse down this gradient back to the matrix only via the ATP synthase, releasing energy that is used to phosphorylated ADP+pi into ATP
  5. Oxygen accepts the final electrons, which then combines with the two hydrogen ions to form water
29
Q

Why does NADH activate a different number of PTCS than FADH2 (outline how many)?

A
  • NADH activates 3PTCS as the electrons in it have more energy
  • FADH2 only activates 2PTCS
30
Q

a) What is the pyruvate dehydrogenase reaction?
b) where does it occur?
c) What does it involve?
d) why is it important in carbohydrate metabolism?

A

a) Pyruvate converted into acetyl CoA using the enzyme pyruvate dehydrogenase
b) mitochondrial matrix (pyruvate transproted from cytoplasm across mitochondrial membrane)
c) Requires B1 vitamin
d) It is irreversible, irreversible loss of Carbon dioxide and hence it is subject to regulation

31
Q

a) Where does the Tricarboxylic acid (TCA)/ KREBS cycle occur?
b) for one glucose molecule, what is produced and where does it go?
c) Function of TCA?

A

a)Mitochondria
b) 6NADH (ETC), 4CO2, 2FADH2 (etc), 2GTP
c)
- oxidative: produces NADH and FADH2
- Produces some energy: GTP
- important for catabolism (produces precursors for biosynthesis) of sugars, FA, Ketone bodies, AA and alcohol

32
Q

What are the products of the pyruvate dehydrogenase reaction per molecule of glucose and where do they go?

A
  • 2acetyl coA (tca)
  • 2 NADH (ETC)
  • 2CO2 (excreted)
33
Q

What is stage four of carbohydrate metabolism and what does it involve?

A

Oxidative phosphorylation

  • involves: electrons on NADH and FADH2 transferred through carrier molecules to oxygen
  • oxygen is required (reduced to water)
  • ATP synthesis
  • series of redox reactions
34
Q

Where does oxidative phosphorylation occur?

A

across the inner membrane of the mitochondria

35
Q

Outline the differences between oxidative and substrate level phosphorylation

A

OP:

  • cannot occur without O2
  • requires membrane-associated complexes –> occurs in inner mitochondrial membrane
  • utilises proton gradient (pmf)
  • major process for ATP synthesis

SL:

  • can occur to a limited extent without o2
  • requires soluble enzmes –> occurs in cytoplasmic and mitochondrial matrix
  • phosphoryl-grooup transfer
  • minor process for ATP synthesis

MCBG (16 decks)

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