Quiz 7 Flashcards

1
Q

what is hexokinase inhibited by

A

G6P and ADP (products)

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2
Q

what is glucokinase inhibited by? What is it not inhibited by? What is it induced by?

A

NOT inhibited by G6P and ADP
Repressed by glucagon
Inducible transcriptionally by high carb diet and insulin

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3
Q

what kind of reaction is aldose G6P to ketose F6P

A

acid base catalysis (phosphoglucoisomerase)

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4
Q

What is PFK inhibited by

A

citrate and ATP (high E signals)

Glucagon (hormonal)

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5
Q

what is PFK stimulated by? what is it repressed by?

A

AMP, Pi, NH4, F 1,6 bis P (product, weird!)

Insulin stimulates as well (hormonal)

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6
Q

what are the binding sites on PFK?

A

there are 8
2 for substrates (ATP and F6P)
2 allosteric inhibitory (ATP and citrate)
4 allosteric activation (AMP, Pi, NH4, F 1,6 BP)

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7
Q

how is hormonal of PFK accomplished

A

complex system with fructose 2,6 BP which is a powerful activator. F 2,6 BP formed from F6P + F2,6 bis phosphokinase. Broken down by F2,6bisphosphosphatase.

  • Kinase activated in dephosphorylated form, phosphatases inactivated in dephosphorylated form.
  • insulin promotes dephosphorylated form, glucagon and epinephrine promote phosphorylated form
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8
Q

how are glucagon and epinephrine able to act in glycolysis pathway

A

via cAMP-PKA pathway.

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9
Q

what does Glyceraldehyde 3 Phosphate dehydrogenase (G3PDH) have that is necessary

A

reactive thiol sites to catalyze the transfer of a high energy group phosphate to G3P - this is why thiol reacting compounds like heavy metals are dangerous because they inhibit glycolysis at this step

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10
Q

how is the high energy trapped in the first transfer of P to ADP in glycolysis

A

Oxidation of aldehyde on C1 of G3P to carb acid on C1 of 3PGA was trapped in high energy intermediate 1,3 bis PGA which is what gives off the ATP. If we didn’t trap this energy, it would just get released as heat

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11
Q

what are the three irreversible steps of glycolysis

A

hexokinase (Glucose to G6P)
PFK (F6P to F1,6 BP)
PK (Phosphoenol pyruvate to pyruvate)

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12
Q

what is enolase inhibited by

A

fluoride

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13
Q

how is PK regulated

A

inhibited by ATP, NADH, and Acetyl CoA (signs of high energy)
Stimulated by Fructose 1.6 BP which is its product

*Also regulated by glucagon – cAMP – PKA phosphorylation which inhibits its activity. Insulin stimulates it via dephosphorylation

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14
Q

sucrose is metabolized to

A

glucose and fructose

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15
Q

what does fructose become

A

Fructokinase turns it into Fructose 1-P. Aldolase B can turn this into DHAP or glyceraldehyde. Glyceraldehyde becomes G3P with triose kinase and ATP

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16
Q

why would you have hereditary fructose intolerance

A

because you dont have aldose B which is the only thing that can cleave Fructose 1P to DHAP and glyceraldehyde.

17
Q

what is lactose metabolized to

A

glucose and galactose

18
Q

what does galactose become

A

galactokinase turns it into galactose 1P. Uridyl transferase turns it into Glucose 1P. Phosphoglutamutase turns this into G6P.

19
Q

what is wrong in galactosemia

A

uridyl transferase is deficient so high levels of galactose 1P accumulate

20
Q

will high levels of pyruvate inhibit the H or M isoform

A

H

21
Q

what enzymes are important in the pyruvate to ethanol rection

A

PTT/Vitamin B1 is cofactor for pyruvate decarboxylase, removes CO2
ALcohol Dehydrogenase turns acetaldehyde into ethanol (and oxidizes NADH to NAD)

22
Q

how is PDH regulated

A

E1 inhibited by ATP
E2 inhibit by product inhibition of Acetyl CoA
E3 product inhibition by NADH

Also has hormonal control – PDH kinase phosphorylates E1 and inhibits its activity. NOT mediated by cAMP PKA and not effected by glucagon or epinephrine.

23
Q

what does PDH phosphatase do

A

dephosphorylates E1-P and activates E1. STRONGLY increased by insulin. Insulin stimulates glucose to pyruvate

24
Q

where does insulin stimulate glucose to pyruvate

A

GK, PFK, PK, PDH

25
Q

what can succinyl coA be pulled out to form

A

heme

26
Q

what can OAA be pulled out to form

A

glucose, aspartate, asparagine, pyrimidines

27
Q

what can citrate be pulled out to form

A

fatty acids

28
Q

what can alpha KG be pulled out to form

A

glutamate, glutamine, proline, ornithine

29
Q

what happens if OAA is removed from cycle

A

OAA is not regenerated and the cycle stops as acetyl CoA accumulates - anaplerotic rxns can replenish OAA that is pulled out or deficient

30
Q

what reactions can replenish OAA

A
  1. Pyruvate carboxylase - contains biotin (the vit B used to carry CO2 in enzymatic rxns). ATP is necessary for this carboxylation. VERY stimulated by acetyl CoA
  2. Many AA care catabolized to TCA intermediates
  3. PEP carboxynase converts PEP (glycolysis) to OAA
31
Q

what are there NO carriers for in the mitochondria

A

OAA, alpha GP, DHAP, NADH/NADPH

32
Q

what can malate be exchanged for in the mitochondria

A

Dicarboxylate carrier
Tricarboxylate carrier
Alpha keto glutarate carrier