Glucose metabolism and gluconeogenesis Flashcards

1
Q

At which end of glycogen is glc added/removed?

A

at the nonreducing end

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2
Q

Why store glucose as glycogen?

A

reduce osmotic pressure

Concentration gradient

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3
Q

Why glycogen instead of starch?

A

Glycogen has a high branching network which makes more glucose easier to access at one time when needed quickly.

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4
Q

Phospholysis of glycogen yields:

A

(glc)n-1 and glc-1-P by glycogen phosphorylase

G1P is then converted into G6P, which undergoes glycolysis in the muscle or is converted to glc and dumped into the blood in the liver

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5
Q

Can glc-1-P go directly into glycolysis?

A

Noap. Must first be converted to glc-6-P, ya ninny

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6
Q

By what process is the last glucose on a glycogen branch removed? what does it yield?

A

The final glucose is removed by hydrolysis, yielding glc (not G1P)

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7
Q

2 activities of debranching enzyme:

A

1) a(1–>4) transglycosylase (transferring the triglucoside)

2) a(1–>6) glucosidase (hydrolyzing off the glc)

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8
Q

input and output of ATP in glycolysis when starting with G6P (product of phosphorlyisis of glycogen)

A

1 ATP input in the beginning stages of glycolysis.
4 ATPs produced
Net: 3 ATPs yielded

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9
Q

5 basic steps of making glycogen

A
  1. convert glc to G6P (glucokinase)
  2. convert G6P to G1P (phosphoglucomutase)
  3. Further activate G1P by making UDP-glc
  4. Add a glc unit to the nonreducing end of a glycogen chain
  5. make branches
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10
Q

2 forms of phosphorylase

A
phosphorylas a (phosphorylated, more active form) 
phosphorylase b (not phosphorylated, less active)
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11
Q

What enzymes add/remove phosphate from phosphorylase a and b?

A
  • can be attatched or removed by phosphorylase kinase

- removed by phosphorylase phosphotase

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12
Q

Hormone cascade which leads to the activation of Glycogen phosphorylase

(Phosphorylation system)

A
  • [glc] low in blood = hormone GLUCAGON dumped in blood.
  • glucagon binds to liver receptor, activating ADENYLATE KINASE which activates cAMP
  • cAMP activates PKA
  • PKA phospphorylates PHOSPHORYLASE KINASE, activating it.
  • phosphorylase kinase phosphorylates phosphorylase, activating it
  • phosphorylase phospholyses glycogen into G1P which becomes glc and is dumped in blood
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13
Q

signal amplification

A

a small amount of hormone (glucagon) will cause the activation of a large amount of phosphorylase.

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14
Q

Does muscle respond to glucagon?

A

No. That is a huger signal, therefore not the muscle’s problem

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15
Q

In the muscle, does AMP or ATP activate or inhibit phosphorylase?

A

AMP will activate phosphorylase

ATP inhibits it

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16
Q

Does phosphorylation of glycogen synthase turn it on or off?

A

turns it off

17
Q

2 forms of glycogen synthase

A

1) glycogen synthase a (not phosphorylated, active)
2) glycogen synthase b (phosphorylated, inactive)
(opposite of phosphorylase a and b)

18
Q

glycogen synthase is allosterically activated by…

A

glc and G6P

19
Q

What does glycogen synthase (GSK) kinase do?

A

turns off glycogen synthase by phosphorylating it

20
Q

What does insulin do to PKB?

A

insulin activates PKB, which turns off GSK, thus activating glycogen synthesis

21
Q

common gluconeogenesis precursors:

A

lac, some amino acids, glycerol

22
Q

where does the conversion of puryate to oxaloacetate take place?

A

in the mitochondria

23
Q

Can pyr, oxa, NADH or PEP cross the mitochondria?

A

only pyr and pep can. Oxa and NADH cannot

24
Q

How to overcome the problem of not having cytosolic NADH available for gluconeogenesis?

A

Depends on precursor used.
-If using lac–>glc, cytosolic NADH can be produced (no need for mitochondrial NADH):

   NAD+   NADH
        l        l lac                pyr  ----->etc.etc.

-If using ala–>pyr–>–>glc, need a transport NADH from mitochondria.

ala–>pyr (enters mito)–>oxa–>mal (can cross membrane into cytosol)–>oxa–>PEP

25
Q

Where do the following rxns take place in the cell?:

1) pyr–>oxa
2) oxa–>PEP

A

1) mitochondria

2) cytosol and mitochondria

26
Q

Which is the only place where G6P can be converted to glc?

A

liver

27
Q

How many ATP equivalents are used in glucoeogenesis? How many NADH’s consumed?

A

6 ATP equivalents used

2 NADH consumed

28
Q

What does fru-2,6-bP do to PFK-1 and FBP-1?

A
  • activates PFK-1

- inhibits FBP-1

29
Q

What does high or low [fru-2,6-bP] signal?

A

high conc = signal to run glycolysis

low conc = signal to run gluconeogenesis

30
Q

Difference between PFK-2 and FBP-2

A

SAME PROTEINE. BIFUNCTIONAL ENZYME.

PFK-2 produces F6P from F-2,6-P
FBP-2 does the reverse

31
Q

low blood [glucose] leads to…

A

increased glucagon secretion–>increased [cAMP]–>Increased enzyme phosphorylation–>Activation of FBP-2 and inactivation of PFK-2–> deacreased [F-2,6-bP]–>inhibition of PFK-1 and activation of FBP-1–>increase gluconeogenesis