L7- Glycolysis Flashcards

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1
Q

glycolysis simple

A
  • Oxidises glucose (6C) to produce 2NADH, 2ATP and 2 pyruvate (2 x 3C)
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2
Q

what type of pathway is glycolysis

A

irreversible

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3
Q

glycolysis is not isolated and has important intermediates that get fed into other pathways e.g.

A

Dihydroxyacetone- P

2,3- Bis phosphoglycerate

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4
Q

Dihydroxyacetone- P comes from

A

comes from the 5th enzyme of glycolysis (glyceraldehyde-3-P)

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5
Q

Dihydroxyacetone- P is converted into ………. by …….

A

glycerol phosphate by glycerol-3-phosphate dehydrogenase via oxidation of NADH ==> NADH+

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6
Q

glycerol phosphate important

A

in triglyceride and phospholipid biosynthesis

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7
Q

where is GP produced

A

adipose and liver

lipid synthesis in adipose requires glycolysis

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8
Q

2,3-bisphosphate (2,3 BP)comes from …….. by ……

A

1,3- bisphosphoglycerate by 2,3-bisphosphoglycerate mutase

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9
Q

where is 2,3-bisphosphate (2,3 BP)produced

A

RBC

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10
Q

what is 2,3-bisphosphate (2,3 BP) a regulator of

A

haemoglobin O2 affinity

  • promotes release of O2 to tissue
  • present in RBC at same molar conc as Hb (5mM)
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11
Q

what is GP produced from

A

DHAP found in adipose and liver

  • liver can phosphorylate glycerol directly
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12
Q

glycolysis requires

A

NAD+ to produce pyruvate

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13
Q

total [NAD+ and NADH] is

A

constant in the cell

o Glycolysis would stop when all NAD+ is converted to NADH
o Normally, NAD+ is regenerated from NADH in stage 4 of metabolism

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14
Q

glycolysis in RBC

A

have now stage 3 or 4 of metabolism (no mitochondria)

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15
Q

stage 4 (ETC) needs

A

oxygen

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16
Q

supply of O2 to muscles and gut is often

A

reudced

- therefore need way of regretted NADh by some other route

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17
Q

RBC, muscles and gut need way of

A

regenerating NAD+

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18
Q

what alternative pathway can use to to regenerate NAD+ int issue which lack oxygen/ cells which have no ETC

A

Lactate dehydrogenase (LDH)

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19
Q

lactate dehydrogenase

A

converts NADH + H + pyruvate –> NAD+ and lactae

  • regenerating NAD+ source to be used in glycolysis
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20
Q

lactate is produced from

A

glucose and alanine via pyruvate

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21
Q

without major exercise (lactate production)

A

o 40-50g/24 hours

 RBC, skin, brain, skeletal muscle, GI tract

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22
Q

strenuous exercise (lactate production)

A

o 30g/5 mins
 Plasma levels x 10 in 2-5 min
 Back to normal by 90 mins

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23
Q

pathological situations v

A

o High
 Shock
 Congestive heart disease

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24
Q

LDH is produced by

A

RBC and skeletal muscle, skin, brain, GI (need lots of oxygenp- storage of NAD+)

25
Q

LDH is released into blood and metabolised by

A

liver nad heart

26
Q

liver and heard need NAD+ to be

A

regenerated efficiently- well supplied with oxygen

27
Q

in low o2 conditions pyruvate con Crete duo

A

lactate instead of stage 4 of metabolism (which enquires oxygen) by lactate dehydrogenase

28
Q

in the liver and kidney LDH converts lactate to

A

pyruvate

29
Q

plasma conc of lactate determined by

A
  1. rate of production
  2. rate of utilisation (liver, RBC, heart, muscle)
  3. rate of disposal (kidney)
30
Q

hyperlactaemia

A
  • 2-5 mM
  • below renal threshold
  • no change in blood pH (buffering capacity)
31
Q

lactic acidosis

A

above 5mM

  • above renal threshold
  • blood pH lowered
32
Q

normal conc of lactate

A

,1mM

33
Q

lactose acidosis is a critical markers of

A

acutely unwell patient

34
Q

metabolism of other sugars e.g.

A

fructose and galactose

35
Q

fructose

A

Found in fruit (monosaccharide)- forms sucrose disaccharide with glucose (2xC3)
- Metabolised in liver in human

36
Q

fructose enters glycolysis as

A

G-3-P

as opposed to glucose which enters as G-6-P

37
Q

clinical important of fructose metabolism

A
  1. essential fructosuria

2. fructose intolerance

38
Q

essential fructosuria

A

o Fructose kinase missing

o Fructose found in urine no clinical signs

39
Q

fructose intolerance

A

o Aldolase missing
o Fructose-1-P accumulates in liver
- Leading to liver damage

40
Q

treatment of fructose intolerance

A

Treatment- remove fructose from diet

41
Q

galactose

A

monosaccharide that can form a disaccharide with glucose to form lactose

42
Q

lactose is a

A

disaccharide found in milke

43
Q

deficiency in which three main enzymes (only one needs to be deficient) causes galactosaemia

A
  • galactokinase
  • UDP- galactose epimerase
  • Uridyl transferase
44
Q

galactosaemia causes how many deaths

A

1 in 30,000

45
Q

galactokinase deficiency is

A

rare

46
Q

what does galactokinase deficiency cause

A

galactose accumulates

47
Q

transferase deficiency is

A

common

48
Q

what does transferase deficiency cause

A

galactose 1-p accumulate

49
Q

problem with galactose accumulation

A

depletes NADPH levels

50
Q

lens related problem with depletion of NADPH

A

o Prevents maintenance of free sulfhydryl groups on proteins
o Inappropriate disulphide bond formation
o Loss of structural and functional integrity of some proteins that depend on free -SH groups
 Cataracts

51
Q

accumulation of galactose 1-p affects

A

liver, kdineha nd rbain

52
Q

treatment of galactosaemia

A

no lactose in diet

53
Q

the pentose pathway role

A

providing NADPH to maintain SH groups of proteins in a reduced state
- Structural integrity and functional activity of some proteins depends on free-SH groups

54
Q

pentose phosphate pathway starts from

A

glucose-6- phosphate

55
Q

lentos phosphate pathway important

A
  • Important source of NADPH required for
    o Reducing power for biosynthesis (NADPH)
    o Maintenance of GSH levels
    o Detoxification reactions
  • Produces C5-sugar ribose required for synthesis of:
    o Nucleotides
    o DNA and RNA
56
Q

glucose- 6- phosphate dehydrogenase deficiency (G6PDH)

A

is v common inherited defect
o E.g. in RBC, reduced NADPH  inappropriate disulphide bonds formed  aggregated proteins (Heinz bodies)  haemolysis e.g. lens of eye

57
Q

glucose- 6- phosphate dehydrogenase is a …. enzyme

A

rate limiting

58
Q

product to pentose phosphate pathway

A

5C sugar ribose, NADPH, CO2

59
Q

is ATP produced in PPP

A

no