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MCG > METABOLISM SYLLABUS 2: Glycolysis: functions, pathway, energetics, regulation > Flashcards

METABOLISM SYLLABUS 2: Glycolysis: functions, pathway, energetics, regulation Flashcards

1
Q

function of glycolysis?

A

**1) provide energy for cells **

2) provide intermediates for other metabolic reactions - like a-glycerophosphate for triglyceride and phoshpolipid synthesis; 2,3 bis-phophoglycerate in RBC; acetyl CoA from pyruvate; amino acids such as serine, alanine, glycine

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2
Q

how do RBC get energy?

A

ONLY via glycolysis

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3
Q

to what organs is glycolysis the *major *source of energy (not the only)?

A

embryonic tissue, retina, adrenals, immune cells, exercising muscle

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4
Q

name the steps of glycolysis

A

* denotes irreversible step *

*1: GLUCOSE to G6P via hexokinase

2: G6P to F6P via phosphoglucose isomerase

*3: F6P to F1,6BP via PFK-1

4: F1,6BP to DAP + G3P via aldolase
5: DHAP to G3P via isomerase
* (everything hereforeward is x2)*
5: G3P to 1,3BPG + NADH via G3PDH
6: G3P to 1,3BPG via G3PDH
7: 1,3BPG to 3PG via PG kinase
8: 3PG to 2PG via PG mutase
9: 2PG to PEP via enolase

*10: PEP to Pyruvate via Pyruvate Kinase

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5
Q

what are hexokinases

A

constituitive enzymes w/ a low Km for glucose

subject to product inhibition by G6P and ADP

not specific for glucose

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6
Q

what is glucokinase?

what are its unique properties?

A

the hexokinase isoform in the liver and pancreas

  • has a high Km for glucose, is specific for glucose
  • is not subject to inhibition by G6P and ADP, so will keep working when these products are produced
  • its levels are increased at transcriptional level by high carb diet and insulin
  • is repressed at transcription level by glucagon/epi
  • increases mRNA levels
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7
Q

why is glucokinase > hexokinase for liver function?

A

because glucokinase has a high Km for glucose, so it only works when glucose levels are high, i.e. after meals

thus liver only will respond to high glucose levels

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8
Q

what kind of reaction is the phosphoglucoisomerase (step 2) reaction?

A

G6P -> F6P is acid:bases catalysis by an enzyme

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9
Q

what is the rate limiting step of glycolysis?

A

step 3, by PFK; it is irreversible

involves input of ATP

F6P + ATP -> F1,6 bis P + ADP

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10
Q

what inhibits/stimulates PFK?

A

INHIBITORS: ATP, citrate, glucagon

ACTIVATORS: AMP, Pi, NH4+ , F1,6 bis P, insulin

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11
Q

is PF-1-K highly regulated?

A

yes, because it’s the rate-limiting step of glycolysis

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12
Q

what is F2,6 bis P ? how is it synthesized/broken down?

A

powerful activator of PFK

produced from F6P + ATP -> ADP + F2,6bisP -> F6P + Pi

it is created by action of F2,6 bis phosphokinase

it is broken down by F2,6 bis phosphofructophosphatase to F6P + Pi

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13
Q

what is the active/inactive state of the F2,6 bis P kinase/phosphatase?

what is its effect on PFK?

what controls these states?

A

when F 2,6 bis P kinase is dephoshporylated it is **active; **when it is phosphorylated and **inactive **

when F 2,6 bis P phosphatase is dephoshporylated it is inactive; when it is phosphorylated and active

thus PFK is active when F2,6 bis P kinase is dephosphorylated, thus ALLOWING STEP 3 of glycolysis to proceed

this is controlled by insulin, glucagon/epi:

**INSULIN **promotes the DEPHOSPHORYLATED, ACTIVE state of the kinase, F 2,6 bis P

GLUCAGON/EPI promote the **PHOSPHORYLATED, INACTIVE **state of the kinase

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14
Q

what are the outcomes of the ALDOLASE reaction?

A

F 1,6 Bis P -> G3P + DHAP

1) DHAP can -> alpha glycero P, which is needed for **triglyceride and phospholipid synthesis **
2) or DHAP is converted to G3P by **triose phosphate isomerase **to continue glycolysis

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15
Q

what is the G3PDH rxn?

what inhibits the G3PDH reaction? why?

A

STEP 6 of glycolysis

thiol-reacting compounds and heavy metals such as lead, mercury, cadmium

they thus inhibit glycolysis

b/c G3PDH has thiol groups necessary for its activity, it is reactive w/ these compounds

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16
Q

what is the first ATP-producing step of glycolysis?

A

STEP 7: phosphoglycerate kinase reaction

produces 2 ATPs (1 for each G3P made from the 1 glucose undergoing glycolysis)

1,3 bis PGA + ADP <-> 3 PGA + ATP

occurs b/c 1,3 bis PGA is a high-energy compound

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17
Q

what is substrate level phosphorylation? when in glycolysis does it occur?

A

production of energy in the form of ATP without mito or oxygen

occurs when 1,3 bis PGA + ADP -> 3PGA + ATP

18
Q

what does 1,3 bis PGA do for energy of the glycolysis rxn?

A

it traps energy, allows its release as ATP

if not for 1,3 bis PGA, this energy would ahve been released as heat:

G3P + NAD+ <-> 3PGA + NADH + heat

instead of:

G3P + Pi + NAD+ <-> NADH + 1,3 bis PGA [add ADP] <-> 3PGA + ATP

19
Q

why is arsenic toxic?

A

it competes w/ Pi for G3P, forming 1-arseno-3-phophoglyceric acid which is **not a high energy compound **like 1,3 bis PGA

this immediately decays to 3PGA + heat, w/o ATP production

20
Q

what does the RBC mutase do?

A

moves Pi, converts small amounts of 1,3 bis PGA to 2,3 bis PGA

this is an important allosteric effector of hemoglobin:oxygen affinity

21
Q

what in glycolysis can produce serine?

A

3PGA

22
Q

what is fluoride’s effect on glycolysis?

A

inhibits enolase, STEP 9

this blocks glycolysis

23
Q

what is yielded from the final step of glycolysis?

A

pyruvate kinase catalyzes the high energy PEP to yield 2 ATP

IRREVERSIBLE REACTION

24
Q

how many ATP are produced from each glucose -> 2 pyruates of glycolysis?

A

2 ATP used at the beginning in hexokinase, PFK steps

4 ATPs produced, 2 at G3P and 2 at pyruvate kinase step

NET: 2 ATP

25
Q

what inhibits or activates pyruvate kinase activity?

A

INHIBITORS: ATP, NADH, acetyl CoA: indicate high energy

STIMULATORS: F1,6 BIS P, the PFK reaction’s product

INSULIN stimulates

26
Q

is pyruvate kinase active or inactive when phoshporylated? what causes phosphorylated or dephosphorylated state?

A

PK is INACTIVE when PHOSPHORYLATED, via GLUCAGON -> CAMP-PKA PHOSPHORYLATION

PK is ACTIVE when DEPHOSPHORYLATED, via INSULIN

27
Q

how does K+ regulate Pyruvate Kinase activity?

A

PK needs high intracellular levels of K+ for its activity

this is mediated by the Na+/K+ ATPase

28
Q

what amino acid can pyruvate produce?

A

alanine

29
Q

3 irreversible steps of glycolysis?

A

hexokinase, PFK, PK reactions

30
Q

how does insulin regulate glycolysis

A

STIMULATES it by:

1) INCREASING GLUCOKINASE LEVELS
2) ACTIVATING the PFK and PK reactions via DEPHOSPHRYLATIONS

31
Q

how does glucagon regulate glycolysis

A

INHIBITS it by

1) DECREASING GLUCOKINASE levels
2) INHIBITING PFK and PK via cAMP-PKA-dependent PHOSHPORYLATIONS

32
Q

what high energy signals impact PK activity?

A

INHIBIT it

ATP, citrate

33
Q

what inhibits PK

A

high energy signals like ATP, NADH, acetyl CoA

34
Q

how does fructose interact w/ glycolysis?

A

LIVER acts on F1P via liver aldolase B, producing DHAP + glyceraldehyde

DHAP enters glycolysis

glyceraldehyde is phoshporylated to G3P by triosephosphokinase, enters glycolysis

thus DHAP and G3P from F1P can enter glycolysis and become pyruvate or go opposite way and become glucose

35
Q

what are liver aldolase B’s actions?

A

1) can cleave F1P in the liver
2) can leave F1,6 bis P in other tissues, thus contribute to glycolysis

36
Q

what is the cause of hereditary fructose intolerance? what happens?

A

aldolast B deficiency

these individuals cannot metabolize F1P

F1P accumulates in the liver; a high level of accumulation depletes ATP and is toxic to the liver

37
Q

how do you treat hereditary fructose intolerance?

A

limit fructose and sucrose in the diet

38
Q

what causes lactose intolerance?

A

deficiency in lactase, the enzyme that hydrolyzes lactose into glucose and galactose

39
Q

what occurs in galactosemia?

A

deficiency of galactose-1-phosphate uridylyltransferase

thus cannot convert Galactose-1-P -> Glucose-1-P

Galactose-1-P accumulates, and this is toxic to the liver

treat by: eliminating lactose from diet, which comes from lactose

this is a problem for nursing mothers!

40
Q

do tumors have rapid or slow rate of glycolysis?

A

rapid

because glycolysis is a rapid way to produce ATP in absence of oxygen and mitochondria which often are poorly coupled or functional in tumors

MCG (77 decks)

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