Glycolysis Flashcards

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1
Q

Fate of absorbed glucose - how does glucose in the bloodstream enter cells?

A

via specific transporters (GLUT) by facilitated diffusion!

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2
Q

Where is glucokinase found? what it its Km for glucose?

A

in liver and beta cells of pancrease

km is high (needs way more glucose to get saturated) = which is why its more active when BGL are elevated

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3
Q

what is hexokinases Km for glucose?

A

low Km = high affinity!

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4
Q

after glucose is phosphorylated and becomes glucose-6-phophate, what are the intracellular fates of glucose-6-phosphate in the liver?

A

glycogen
pyruvate
HMP shunt

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5
Q

where are glycolytic enzymes present>

A

in the cytosol

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6
Q

what are the 3 general stages of glycolysis

A

Stage 1: energy investment stage
stage 2: cleavage of 6C sugar to 3C intermediates
stage 3: energy generation phase

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7
Q

How many reactions are involved in stage 1?

A

2 phosphorylation reactions

requires 2 ATP

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8
Q

what is the second irreversible reaction of glycolysis?

A

PFK1 - phosphofructokinase-1

also the most important regulated step (allosteric regulated enzyme)

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9
Q

Where are aldolase A and B found?

A

muscle and liver

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10
Q

how many molecules of pyruvate are formed in glycolysis?

A

2 pyruvate

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11
Q

what does glyceraldehyde-3-phosphate dehydrogenase result in the formation of?

A

NADH

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12
Q

what does phosphoglycerate kinase result in the formation of?

A

the first ATP (substrate level phosphorylation)

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13
Q

why are 1,3 BPG and phosphpenolpyruvate special?

A

they are both high energy intermediates and compounds, respectively. they can form ATP within the involvement of the ETC in mitochondira

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14
Q

what does pyruvate kinase result in?

A

formation of the 2nd ATP

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15
Q

what are the fates of pyruvate?

A

aerobic –acetyl coA(pyruvate dehydrogenase)–enters TCA cycle
anaerobic –lactate(lactate dehydrogenase)–goes to liver via Cori cycle

also in liver–gluconeogenesis(pyruvate carboxylase) –oxaloacetate

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16
Q

what are the 3 irreversible reactions in glycolysis?

A

glucokinase/hexokinase
phosphofructokinase 1
pyruvate kinase

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17
Q

what were the two substrate level phosphorylation reactions in glycolysis?

A

phosphoglycerate kinase

pyruvate kinase

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18
Q

what is the overall reaction of aerobic glycolysis?

A

aerobic

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19
Q

how many ATP are formed in aerobic glycolysis?

A

8 ATP

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20
Q

how many ATP are formed in anaerobic glycolysis?

A

2 ATP

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21
Q

what are inhibitors of glycolysis?

A

arsenate and fluoride

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22
Q

why does fluoride have to be added to blood collection tube in clinical labs?

A

if fluoride wasn’t added - there would be a reduction in the glucose due to its utilization by RBC and WBC, resulting in an erroneously low value for blood glucose

23
Q

what is the significance of glycolysis in tissues which complete oxidation takes place

A

brain, skeletal muscles - glucose is converted to pyruvate, that is later converted to acetyl coA that enters the TCA cycle for complete oxidation of glucose

24
Q

why is glycolysis significant in adipose tissue?

A

glyceraldehyde-3-phosphate (provides glycerol component) that is used for TAG formation

25
Q

why is glycolysis significant for RBC?

A

anaerobic glycolysis is the major source of energy - forms 2,3 BPG

glycolysis also important in retina, lens and
tumor cells

26
Q

when does 2,3 BPG increase?

A

when a person moves to a high altitude - facilitates unloading - right shift

27
Q

what is hemolytic anemia?

A

RBC PK deficiency

second most common form of hemolytic anemia

28
Q

what is the most common form of hemolytic anemia?

A

G6PD definicieny

29
Q

what is lactic acid an example of?

A

metabolic acidosis - commonly seen

30
Q

when is lactic acid observed?

A

increase conversion of pyruvate to lactate (increase NADH/NAD+ ratio)
strenuous muscle activity
inherited deficiency of pyruvate dehydrogenase (leigh disease)
thiamine deficiency = lowered activity of pyruvate dehydrogenase
defect in gluconeogensis (decrease conversion of lactate to glucose)
decreased blood supply results in anaerobic metabolism in the peripheral tissues

31
Q

what do cancer cells used as the main source of ATP?

A

glycolysis - ‘Warburg effect’

32
Q

what do tumor cells utilize in PET scans?

A

fluorodeoxyglucose (FDG)

pharmacological inhibitor of glycolysis are explored for use as therapeutic agents in variety of cancers

33
Q

what is galactose deficiency

A

galactosemia/galactosuria, cataracts in childhood (excess galactose is converted to galatitol via aldose reductase)
Treatment: no galactose in diet

34
Q

what is Gal-1-P uridyl transferase deficiency?

A

same as galactokinase deficiency but more severe with vomiting/diarrhea after milk ingestion, liver disease, lethargy mental retardation,
Tx=no galactose in diet

35
Q

what is fructoinase deficiency?

A

fructosuria - benign

36
Q

what is aldolase B deficiency?

A

fructosuria - liver and prominal renal tubule disorder

tx = no fructose in diet

37
Q

pyruvate kinase deficiency?

A

chronic hemolysis, you increase 2,3 BPG and other intermediates in the RBX - autosomal recessive

38
Q

what inhibits HK?

A

g-6-p = product inhibition

39
Q

what stimulates GK?

A

insulin in the liver

40
Q

what activates PFK-1?

A

AMP

F-2,6-bisP

41
Q

what inhibits PFK-1?

A

ATP

Citrate

42
Q

what activates PFK-2?

A

insulin

43
Q

what inhibits PFK-2?

A

glucogon

44
Q

what activates PK?

A

F-1,6-bisP

insulin

45
Q

what inhibits PK?

A

ATP
Acetyl Co A
Alanine
Glucagon

46
Q

what does GLUT 1 + 3 transporters do?

A

basal uptake - neurons and brain

47
Q

What does GLUT 2 transporters do?

A

liver

48
Q

what does Glut 4 transporters do?

A

adipose and muscle

49
Q

why is glucokinase needed in the liver?

A

to reduce high BGL after a large meal

50
Q

what does glucokinase do in the pancreas?

A

recognition of high BGL and –> insulin release

51
Q

genetic deficieicny of GK can lead to what?

A

DM in the young type 2 (MODY 2)

52
Q

where is GK stored at high fructose 6-P levels?

A

nucleus

53
Q

what is important to remember about exercising muscle and AMP levels

A

high levels of AMP overcome inhibition by ATP