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Chem > Gluconeogensis > Flashcards

Gluconeogensis Flashcards

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1
Q

Under what metabolic conditions does gluconeogenesis occur?

A

Starvation, exercise and diabetes

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2
Q

What is gluconeogenesis

A

The prediction of glucose from non carbohydrate sources

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3
Q

What are the different precursors that can produce glucose

A

Pyruvate, amino acids (alanine and glutamine) —> CAC intermediates

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4
Q

Is gluconeogenesis the direct reversal of glycolysis

A

No

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5
Q

How is pyruvate converted to PEP

A

There are 2 steps:
Both being exergonic reactions

  1. Pyruvate is converted to oxaloacetate via pryruvate carboxalate (irreversible)
    2 Oxaloacetate + GTP is converted to phosphoenolpyruvate via PEPCK (PEP, reversible)
    - decarboxylation and phosphate transfer
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6
Q

What organs express glucose-6-phosphatase?

A

Kidney, liver , GI

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7
Q

Why doesn’t muscle express glucose-6-phosphatase ?

A

Because the muscle doesn’t want to release glucose, therefor will not express the enzyme

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8
Q

How is F1,6BP converted to F6P

A

Hydrolysis if C1 of the phosphate ester bond by F1,6 Bisphosphatase

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9
Q

What enzyme does F1,6 Bisphosphatase oppose?

A

PFK-1

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10
Q

How is glucose-6-phosphate converted to glucose?

A

Hydrolysis of C6 to form glucose via glucose 6 phosphotase, irreversible

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11
Q

Where does gluconeogenesis predominately occur

A

In the liver and kidneys

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12
Q

What enzyme does G6phosphatse oppose

A

Glucokinase

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13
Q

What are the difference in the alternative pathways to forming PEP from pyruvate?

A

PEPCK-C
- activated by glucagon therefore is inducible
- happens in the cytosol of the cell

PEPCK-M
- is constitutive
- occurs in the mitochondria

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14
Q

Describe the pathway of PEPCK-C

A

Pathway is used during starvation, when glucagon is released
Alanine ->(Pyruvate -> oxaloacetate -NADH TO NAD+-> malate) -> malate -NAD+ TO NADH-> oxaloacetate -**> PEP (+CO2)
**increase in glucagon means INC PEPCK, pulling the pathway

(With in the cell )

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15
Q

Describe the pathway with PEPCK-M

A

Lactate -> pyruvate -> (pyruvate -> oxaloacetate **-> PEP) ->PEP
** PEPCK-M

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16
Q

What is are the inhibitors of fructose bisphosphate?

A

Fructose 2,6 Bisphosphate and AMP

17
Q

What are the activators of PFK-1?

A

AMP and F2,6BP

18
Q

Why is F2,6BP an important regulator in glycolysis and gluconeogenesis?

A

It tells us blood glucose levels, high amounts of it mean glycolysis and low amounts mean gluconeogenesis

19
Q

What happens in the hepatocyte in responses to low blood glucose (use enzymes)

A
  1. Glucagon is released
  2. Increases activity of Protein Kinase A
  3. Phosphorylates FBPase-2 to decrease amount of F26BP and increase F6P
  4. Increase in F6P singals to PFK-1 to decrease activity, increase activity of FBPase-1
  5. Increase in gluconeogensis
20
Q

what happens in the hepatocyte when there is an increase in blood sugar?

A
  1. Increase in blood suagr
  2. Increase in insulin production
  3. Protein phosphatase-1 which dephophorylated regulatory domain of PFK-2 (inactivates FBPase-2)
  4. PFK-2 converts F6P to F26BP (increase in F26BP)
  5. Increase in F26BP means increase in PFK-1 activity, inhibiting FBPase-1
  6. Increases glycolysis
21
Q

What happens with the regulation of PFK-2 in the skeletal muscle?

A
  • controlled by allosterics (PFK-2)
  • High levels of F6P increases glucose uptake muscles
22
Q

What regulates the activity of glucokinase in the liver

A
  • Glucose and F1P increase the activity
  • F6P decreases the activity
23
Q

How is glucokinase regulated by GKRP?

A
  • F6P enhances the binding of GK by GKRP
  • Increased F6P = gluconeohgensis is active
  • F1P reduces the binding of GKRP
  • singals well fed state = glycolysis
24
Q

What are the competivite binders of glucokinase

A
  • glucose and GKRP
25
Q

How is the binding of GKRP regulated

A
  • Phosphorylation of GKRP by AMPK reduces the binding of glucokinase by GKRP
  • AMPK is active in the presence of increased AMP (signal low energy levels therefore enhanced glycolysis)

Chem (9 decks)

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