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MFM > Glycolysis and Regulation > Flashcards

Glycolysis and Regulation Flashcards

1
Q

what is the final product of glycolysis in the absence of O2 or mitochondria in a fed state?

A

lactate

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2
Q

how is lactate removed from RBC and an exercising muscle ?

A

the Cori cycle in the liver

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3
Q

process of Cori Cycle

A
  1. lactate produced in glycolysis is transferred to liver via blood
  2. lactate reconverted to pyruvate by LDH and then glucose via gluconeogenesis
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4
Q

what is pyruvate converted to in aerobic, fed conditions?

A

acetyl coa or alanine

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5
Q

what is pyruvate converted to in aerobic, fasting condition?

A

oxaloacetate (to go to gluconeogenesis)

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6
Q

what is pyruvate converted to in anaerobic, fed conditions?

A

lactate

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7
Q

what is metabolic acidosis or lactic acidosis?

A

excess lactic acid in blood of above 5mM, or a pH of less than 7.2

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8
Q

pathology of metabolic acidosis

A

increased NADH/NAD+ ratio prevents pyruvate from getting into TCA cycle, and shunts pyruvate to lactate

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9
Q

cause of lactic acidosis

A
  1. excess alcohol
  2. hypoxia or respiratory failure
  3. interferences with ETC or TCA cycle
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10
Q

what are examples of interferences with ETC or TCA cycle?

A
  1. genetic deficiencies of proteins encoded by mtDNA
  2. ischemia
  3. cyanide poisoning
  4. CO2 poisoning
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11
Q

how does excess alcohol increase NADH?

A

ethanol is broken down by alcohol dehydrogenase and NAD to make acetylaldehyde and NADH and then by acetylaldehyde dehydrogenase and NAD to make NADH and acetate (increased NADH)

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12
Q

how does inhibition of ETC cause increased NADH

A

the normal function converts NADH to NAD, so if there is no conversion, NADH builds up in the cell

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13
Q

functions of glycolysis

A
  1. ATP production
  2. major pathway for oxidizing glucose into intermediates that we use and metabolizing dietary sugars/fructose/galactose
  3. substrate for further oxidation
  4. intermediates and products can provide substrates for other pathways
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14
Q

example of intermediates used

A
  1. RBC use 1,3BPG to make 2,3BPG, which is a strong negative allosteric regulator for O2 binding to Hb
  2. 5 carbon sugars of dNTPs
  3. dihydroxyacetone phosphate is precursor for glycerol 3 phosphate used for TG and phospholipid synthesis
  4. acetyl coa precursor for FA and cholesterol synthesis
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15
Q

what can pyruvate convert to? (aerobic, fed condition)

A

alanine, acetyl coa

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16
Q

what is the main regulator of glycolysis?

A

energy charge - when ATP/ADP ratio high, glycolysis is inhibited, when ATP low and AMP/ADP high, glycolysis rate increases

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17
Q

3 sites of regulation for glycolysis

A
  1. hexokinase
  2. PFK-1
  3. pyruvate kinase
18
Q

where is hexokinase found?

A

muscle, brain, lots of tissues

19
Q

where is glucokinase found?

A

pancreatic beta cells and liver

20
Q

Km and affinity of glucokinase, and its implications

A

high Km and low affinity for glucose, so is active after a meal

21
Q

glucokinase during fasting

A

inactive during fasting and when glucose levels are low, so the liver doesnt compete with other tissues for available glucose

22
Q

Km and affinity of hexokinase

A

low Km, high affinity for glucose, so is used to provide G6-P for ATP production even when glucose is low

23
Q

when is hexokinase most active

A

when G6-P is being rapidly used

24
Q

inhibitor of PFK-1

A

ATP, citrate

25
Q

activators PFK-1

A

AMP, fructose 2,6 bisphosphate

26
Q

PFK-1’s binding sites and shape

A

tetramer, 6 binding sites, 2 for substrates ATP and fructose 6-P and 4 allosteric modulators (inhibitors and activators)

27
Q

explain PFK1 regulation in muscle

A

during exercise, AMP is high, ATP is low. AMP activates PFK-1 and glycolysis is promoted. (ATP and citrate inhibit)

28
Q

regulation of PFK1 in liver

A

insulin activates PFK2, which generates F2,6BP, which activates PFK1

29
Q

how are PFK2 and FBPase-2 regulated?

A

they are encoded by a single gene but have 2 catalytic enzymes so they are a double headed enzyme.
when PFK2 is active, FBPase-2 is inactive; when FBPas-2 is active, PFK2 is inactive

30
Q

what does FBPase do

A

generates F6P

31
Q

what does PFK2 do

A

generate F2,6BP, positive allosteric modulator for PFK1

32
Q

explain concentration of F2,6BP and PFK1 after a meal?

A

insulin is high, and PFK-2 is active, which makes F2,6BP, which activates PFK1, and glycolysis is stimulated

33
Q

explain concentration of F2,6BP in fasting state

A

glucagon is high, FBPase-2 is active, and F2,6BP levels fall, PFK-1 is inactive, glycolysis inhibited

34
Q

what regulates pyruvate kinase?

A

F1,6BP is allosteric activator, ATP is allosteric inhibitor, and glucagon

35
Q

how does glucagon regulate PK?

A

when glucose is low, glucagon is high, so PKA is active, which phosphorylates liver PK and TURNS IT OFF, reduced PK, glycolysis is inhibited and phosphoenolpyruvate enters gluconeogenesis pathway

36
Q

what occurs with mercury poisoning?

A

glyceraldehyde 3-P dehydrogenase is inactivated

37
Q

what occurs with arsenic poisoning?

A

arsenite can substitute with Pi in reaction and forms the unstable molecule 1-arseno-3-phosphoglycerate

38
Q

what occurs if there is a genetic deficiency of PK or phosphoglycerate kinase?

A

these are ATP generating steps, so ATP will not be generated, therefore, cell will not export electrolytes, maintain proper osmotic balance and will swell and lyse - hemolytic anemia

39
Q

what is hereditary fructose intolerance?

A

genetic deficiency or aldolase B, found in liver, prevents liver from making sufficient ATP

40
Q

outcome of hereditary fructose intolerance?

A

cellular phosphate accumlates in fructose-1-P form, thus depleting cell of Pi and Pi becomes too glow for G3P dehydrogenase reaction, and rate of glycolysis reduces, and makes insufficient ATP

MFM (39 decks)

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