Glycogenesis and Glycogenolysis Flashcards

1
Q

Glycogen breakdown in muscle

A

Will only breakdown to make ATP, for its own benefit

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2
Q

Glycogen breakdown in liver

A

Via glut2, the glucose will be sent to other tissues through the blood

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3
Q

Amount of glycogen in muscle and liver

A

400 g muscle

100 g liver

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4
Q

Insulin independent tissues

A
Must tissues (adipose, muscle...)
Use glut4
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5
Q

Insulin dependent tissues

A

Erythro/leukocytes, lens, cornea, liver (uses glut2), brain

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6
Q

Insulin stimulated translocation of glut4 to membrane

A
  1. Insulin binds to tyrosine kinase (PKB)
  2. Activated receptor promotes glucose transporters to membrane
  3. Glucose transporters allow glucose uptake into cell
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7
Q

Amp stimulated protein kinase translocation of glut4

A

In low insulin levels, muscles need glucose for energy. So high AMP and low ATP (from adenylate kinase reaction) will stimulate AMPK which will promote the translocation of glut4 transporters to the membrane during muscle contraction.

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8
Q

Hexokinase

A

Km=.2mM
Constitutive enzyme (always have optimum levels)
In all tissues
Inhibited by product

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9
Q

Glucokinase

A

Km=10mM
Induced enzyme (only optimum levels with inducer insulin)
In liver
Not inhibited by product

Increase glucose = increase activity

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10
Q

Where is GK when you’re fasting?

A

Bound to GKRP (in hepatocyte nucleus)

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11
Q

How does GK release from GKRP to cytosol?

A

High glucose and high F1P

Low F6P

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12
Q

Glycogenesis overview

A
  1. Glucose to G6P using hexokinase or GK (ATP hydrolysis)
  2. G6P to G1P
  3. G1P and UTP react making UDPGlucose and PPi
  4. UDPGlucose is added to NR end of glycogen primer via glycogen synthase, liberated UDP
  5. UDP and ATP will regenerate UTP
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13
Q

Without a pre existing glycogen fragment, how is glycogen made?

A

Glycogenin will serve as a receptor of glucose residues. It is a protein dimer with RTKs are arranged head to toe.

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14
Q

Glycogen synthetase

A

Forms alpha 1-4 bonds

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15
Q

Branching enzyme

A

Glucosyl-4:6 transferase attaches alpha 1-6 bonds

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16
Q

Glycogenolysis overview

A

Glycogen phosphorylase will phosphorylate a glucose at the NR end and will cause glycogen breakdown

17
Q

Glycogen phosphorylase specificity

A

Will cleave glycogen up to glucose molecule away from a branch, so a debranching enzyme will do the rest: a transferase will transfer the last 3 of the branch to the existing glycogen chain, and an alpha16 glucosidase will cleave off the branched glucose

18
Q

Regular levels of blood glucose

A

70 - 100 mg/dL

19
Q

When glycogen phosphorylase and glycogen synthase are phosphorylated, what happens?

A

Phosphorylated glycogen phosphorylase = active = glycogen breakdown
Phosphorylated glycogen synthase = inactive = no glycogen synthesis

20
Q

Active protein kinase a =

A

Phosphorylated phosphorylase kinase which will phosphorylate glycogen phosphorylase (= glycogenolysis), glycogen synthase (= no glycogenesis), and inhibitor 1 (= inhibit inhibitor (phosphoprotein phosphotase) = glycogenolysis).

21
Q

Glycogen synthase kinase 3

A

Phosphorylates glycogen synthase making it inactive

22
Q

What happens when epinephrine binds to alpha antagonist receptor?

A

Epi binds, activating specific G proteins to activate PLC. PLC turns PIP2 into IP3 and DAG. IP3 will then release Ca2+ from the ER. Calmodulin is then formed and PKC is also activated. Calmodulin will phosphorylate phosphorylase kinase and will phosphorylate glycogen phosphorylase and synthase. The calmodulin dependent protein kinase and PKC will also phosphorylate glycogen synthase.

23
Q

Regarding glycogen metabolism, insulin will

A

Limit cAMP production
Activate hepatic protein phosphotases
Activate phosphodiesterase that converts cAMP to AMP
Inactivate glycogen synthase kinase 3

24
Q

A high insulin/glucagon ratio means

A

More insulin, less glucagon, favoring glycogen synthesis

25
Q

Difference between glycogen metabolism regulation in muscle and liver

A
  1. Glucagon has no effect on muscle
  2. AMP and Ca2+ are activators of glycogen phosphorylase in muscle, not liver
  3. Glucose is not an inhibitor of muscle glycogen phosphorylase
26
Q

Von gierkes disease

A

G6p problem
Severe hypoglycemia, ketosis, hyperuricemia, hyperlipemia
Liver and kidney

27
Q

Coris disease

A

Debranching enzyme problem
Like type 1 but milder
Muscle and liver

28
Q

Andersons disease

A

Branching enzyme
Liver failure
Liver

29
Q

Mcardles disease

A

Phosphorylase problem
Can’t preform strenuous exercise, normal life
Muscle

30
Q

Hers disease

A

Phosphorylase problem
Like type 1 but milder
Liver

31
Q

3 ways muscle glycogen can be phosphorylated

A

High amp after muscle contraction using ATP
Nerve impulses that release Ca2+
Epinephrine cascade resulting in high camp