carbs 2 Flashcards

1
Q

metabolic regulation of glycolysis

A

high NADH concentration= high energy levels
causes product inhibit of step 6
inhibits glycolysis

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2
Q

step 6 of glycolysis

A

2 moles of NADH produced per mole of glucose so the pathway needs NAD+. this is regenerated from nada in stage 4 of metabolism. however in cells that lack mitochondria or have an adequate absence of oxygen NADH is converted back to NAD+ via the lactate dehydrogenase reaction.
NADH + H+ +pyruvate NAD+ + lactate

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3
Q

hyperlactaemia

A

2-5 mM of plasma lactate
below renal threshold
no change in blood pH

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4
Q

lactic acidosis

A

above 5 mM of plasma lactate
above renal threshold
blood pH lowered

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5
Q

how can enzymes be regulated

A

1) allosteric- activator/inhibitor binds at ‘another’ site.

2) covalent modification- phosphorylation/dephosphorylation

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6
Q

regulation of phosphofructokinase (PFK)

A
allosteric regulation(muscle)- inhibited by high ATP. stimulated by high AMP.
hormonal regulation(liver)- stimulated by insulin. stimulated by glucagon.
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7
Q

describe fructose metabolism

A

metabolised in liver
fructose becomes fructose-1P via fructokinase
fructose-1P becomes glyceraldehyde/DHAP via aldolase
becomes glyceraldehyde-3-P

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8
Q

what is essential fructosuria

A

fructokinase missing
fructose in urine
no clinical sign

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9
Q

what is fructose intolerance

A

aldolase missing so fructose-1-P accumulates in liver leading to liver damage.

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10
Q

what are the enzymes involved in galactose metabolism

A

galactokinase
galactose-1-P urdidyl transferase
UDP- galactose 4’-epimerase

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11
Q

cause of galactosaemia

A

individuals can’t utilise galactose obtained from diet because of lack of kinase(galactose accumulates)/transferase(galactose & galactose-1-P accumulate) enzyme
transferase deficiency is more common

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12
Q

issues associated with galactosaemia

A

accumulation of galactose leads to its reduction into galactitol by the activity of the enzyme aldose reductase
this reaction requires NADPH so depletes tissues from it.
prevents maintenance of free sulphydryl groups on proteins
inappropriate disulphide bond formation
loss of structural and functional integrity of some proteins that depend on free -SH groups

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13
Q

effects of galactosaemia on eyes

A

in the eye the lens is structure is damaged(cross linking of lens proteins by -S-S bond formation) causing cataracts.
there also might be non-enzymatic glycosylation of the lens protein due to the accumulation of galactose also contributing to cataract formation.
accumulation of galactitol and galactose may lead to glaucoma which could lead to blindness.

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14
Q

why is the pentose phosphate pathway used

A

if energy levels, glycolysis is inhibited so levels of G-6-P will rise and feed out into the pentose phosphate pathway.

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15
Q

what does the pentose phosphate pathway do

A

converts G-6-P from glycolysis to 5C sugar phosphates, providing NADPH.
requires Glucose-6-Phosphate dehydrogenase.

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16
Q

what is the importance of NADPH provided by pentose phosphate pathway

A

helps the antioxidant molecule glutathione (GSH) to remain in its active state.
GSH prevents damage caused by ROS.
Glutathione reduces disulphide bonds formed within cytoplasmic proteins to cysteines by serving as an electron donor. In the process, glutathione is converted to its oxidized form, glutathione disulphide (GSSG). To be converted back to GSH, NADPH is required as an electron donor.
GlSH helps to maintain proteins in their correct structure by keeping the SH groups in their reduced state.

17
Q

what happens in G-6-P dehydrogenase deficiency

A

reduced NADPH production
inappropriate disulphide bonds can form causing proteins to aggregate.
e.g damage of reactive oxygen species in red blood cells causes Heinz bodies(denatured haemoglobin)——–> haemolysis

18
Q

what are the 5C-sugar ribose made in the pentose phosphate pathway required for?

A

synthesis of nucleotides

DNA & RNA