Chapter 16: Regulation of Glycogen Metabolism Flashcards

1
Q

Insulin produced in the fed state leads to

A
  • Anabolism
  • Glycolytic flux/glycogen synthesis
  • Works by dephosphorylation
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2
Q

Glucagon produced in the fasting state leads to

A
  • Catabolism

- Glycogen break down

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3
Q

Glycogen

A
  • The storage form of glucose
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4
Q

Glucose residues linked by

A
  • Alpha-1,4-glycosidic bonds

- Alpha-1,6-glycosidic bond every 10 residues

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5
Q

In muscle, glycogen serves as

A
  • An energy store for the synthesis of ATP
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6
Q

In the liver, glycogen functions as

A
  • A glucose reserve to maintain blood sugar levels
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7
Q

Glycogen stores are depleted after

A
  • After 2 days when when gluconeogenesis is the major source of blood glucose
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8
Q

GLUT 4

A
  • Glucose transporter present on muscle cell
  • Sensitive to insulin
  • In the cytoplasm > insulin stimulation gets it to membrane
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9
Q

Glycogen phosphorylase cleaves

A
  • Only alpha-1,4-glycosidic bonds in glycogen
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10
Q

Two interconvertible forms of glycogen phosphorylase

A
  • Glycogen phosphorylase A

- Glycogen phosphorylase B

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11
Q

Glycogen phosphorylase A is the

A
  • More active form
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12
Q

Glycogen phosphorylase B is the

A
  • Less active form

- Requires AMP

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13
Q

Glycogen phosphorylase B is converted to A by

A
  • Phosphorylation

- Glycogen phosphorylase kinase (Ca+ dependent)

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14
Q

Glycogen phosphorylase A is converted to B by

A
  • Protein phosphatase I
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15
Q

3 components involved with regulation of glycogen degradation in muscle

A
  • AMP
  • ATP
  • G-6-P
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16
Q

Cleavage of alpha-1,4-glycosidic bonds in glycogen requires

A
  • Pyridoxical phosphate prosthetic group
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17
Q

Glycogen phosphorylase is controlled by

A
  • Reversible phosphorylation
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18
Q

Glucose shifts T to R equilibrium toward

A
  • T state
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19
Q

Epinephrine promotes

A
  • Glycogen degradation in muscle
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20
Q

Hormones regulation mechanism

A
  • Covalent modification
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21
Q

Main source of epinephrine in glycogen degradation in muscle

A
  • Adrenal medulla
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22
Q

Epinephrine binding site

A
  • B-adrenergic receptor on muscle cells
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23
Q

Binding of epinephrine to B-adrenergic receptors on muscle cells activates

A
  • Adenylate cyclase
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24
Q

cAMP stimulates

A
  • Pr K A
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25
Q

Phosphorylation stimulates glycogen phosphorylase kinase that …

A
  • Phosphorylates glycogen phosphorylase b > a activation
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26
Q

Glycogen degradation process

A
  • Glycogen degradation > G-1-P > ATP formation (3)
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27
Q

Regulation of glycogen synthesis in muscle occurs via

A
  • Covalent modification
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28
Q

Glycogen synthase is inactivated by

A
  • Phosphorylation
29
Q

Inactivation of glycogen synthase causes

A
  • cAMP/Pr K A

- Turning off glycogenesis

30
Q

Less active glycogen synthase b requires

A
  • Glucose-6-Phosphate
31
Q

Glycogen synthase is activated by

A
  • Dephosphorylation
32
Q

Insulin activates a protein phosphatase I, favoring

A
  • Dephosphorylation of glycogen synthase
33
Q

Activation of glycogen synthase turns on

A
  • Glycogenesis

- Adds glucose units to non-reducing end of polymer

34
Q

Coordinate control of glycogen metabolism occurs via

A
  • Hormone-mediated cascade
35
Q

Protein Kinase A phosphorylates BOTH

A
  • Glycogen synthase

- Glycogen phosphorylase

36
Q

PP1 removes phosphate groups, favoring

A
  • Glycogen synthesis
37
Q

Pr K A phosphorylates and activates an inhibitor of PP1, making

A
  • Making PP1 less active

- Favoring Glycogenolysis

38
Q

Glycogen in the liver exists as

A
  • Granules
39
Q

Glycogen stores increase after

A
  • Eating (insulin)
40
Q

Liver glycogen metabolism maintains

A
  • Blood sugar level

- Liver glucose-6-phosphatase also important

41
Q

Primary hormone involved in liver glycogen metabolism

A
  • Glucagon

- Similar mechanism to epinephrine

42
Q

Liver glycogen phosphorylase B is NOT activated by

A
  • AMP (muscle enzyme is)
43
Q

Glycogen phosphorylase A is inactivated by

A
  • Glucose
44
Q

Insulin favors

A
  • Glycogen synthesis in the liver
45
Q

Glucose favors

A
  • Glycogen synthesis
46
Q

Glycogen provides blood glucose for

A
  • The first hours in post absorptive phase
47
Q

Glycogen stores are depleted after

A
  • 2 days when gluconeogenesis is the major source of blood glucose
48
Q

Nibbler’s Disease

A
  • Will require 24 hour period of feeding
  • Can’t use glucose
  • Can’t cope with periods of starvation
49
Q

Glycogen synthase and glycogen phosphorylase is controlled via

A
  • Coordinate control
50
Q

Glycogen metabolism is generally regulated/determined by

A
  • Levels of cellular metabolites

- Hormone-mediated mechanisms

51
Q

Glucagon and epinephrine hormones mediate phosphorylation of key regulatory enzymes via

A
  • cAMP-dependent mechanisms
52
Q

Glycogen phosphorylase is activated by

A
  • Phosphorylation
53
Q

Glycogen synthase is inhibited by

A
  • Phosphorylation
54
Q

Von Gierke’s Disease is caused by a lack of

A
  • Liver glucose-6-phosphatase
55
Q

Von Gierke’s Disease consequences

A
  • Patients are unable to produce free glucose from glycogen

- Glucose-6-phosphate accumulates

56
Q

McArdle’s Disease is caused by

A
  • A defective muscle glycogen phosphorylase

- Makes prolonged exercise painful

57
Q

Insulin favors biosynthesis in both

A
  • Both liver and muscle tissues
58
Q

Epinephrine works on the

A
  • Muscle cell
59
Q

Glucagon works on the

A
  • Hepatocyte
60
Q

Glycogen synthase in the active (a) form is

A
  • Dephosphorylated
61
Q

Glycogen synthase in the inactive (b) form is

A
  • Phosphorylated
62
Q

Glycogen phosphorylase in the active (a) form is

A
  • Phosphorylated
63
Q

Glycogen phosphorylase in the inactive (b) form is

A
  • Dephosphorylated
64
Q

Phosphorylase b active form

A
  • R form
65
Q

Phosphorylase b inactive form

A
  • T form
66
Q

Phosphorylase a inactive form

A
  • T form
67
Q

Phosphorylase a active form

A
  • R form
68
Q

Control of glycogen phosphorylase activity by reversible phosphorylation is catalyzed by

A
  • Glycogen phosphorylase kinase