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DMD 5242 > Glucose Metabolism (complete) > Flashcards

Glucose Metabolism (complete) Flashcards

1
Q

What is the primary source of glucose between meals

A

glycogenolysis of the hepatic glycogen

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2
Q

What are the three sources of glucose that increase blood glucose

A
  1. dietary carbohydrates
  2. glycogen
  3. Lactate, amino acids, Glycerol
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3
Q

What is the process of turning glycogen into glucose calles

A

glycogenolylsis

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4
Q

what is the process of turning glucose in to glycogen called

A

glycogenesis

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5
Q

what is the process of turning lactate, amino acids, and glycerol into glucose called

A

gluconeogenesis

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6
Q

What are the two processes of glucose storage (these decrease blood glucose)

A
  1. glycogenesis

2. lipogenesis

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7
Q

what is lipogenesis

A

the formation of triacylglycerols in the liver

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8
Q

Where are the two most significant tissues that store glycogen

A
  1. the liver

2. skeletal muscle

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9
Q

For what purpose does skeletal muscle do glycogenolysis

A

it does glycogenolysis to have glucose for its OWN energy

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10
Q

for what purpose does the liver do glycogenolysis

A

the liver does glycogenolysis, then ships out the glucose for the rest of the body

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11
Q

What kind of transporter carries glucose in and out of hepatic cells

A

GLUT-2

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12
Q

is GLUT-2 an insulin dependent transporter

A

nope

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13
Q

Where do glucose go first after it gets absorbed in the intestines

A

it goes to the liver

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14
Q

What happens to glucose that is not absorbed in the liver

A

it goes out to the rest of the tissues

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15
Q

What does the peak in blood glucose cause to happen

A

secretion of insulin

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16
Q

where does insulin come from

A

pancreatic beta cells

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17
Q

Which type of cells aren’t insulin dependent

A 
red blood cells 
white blood cells
lens and cornea of the eye
liver
brain
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18
Q

what is the main function of insulin

A

causes the absorption of blood glucose into cells

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19
Q

what is the transporter of glucose in the liver

A

GLUT-2

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20
Q

Which types of cells are insulin dependent

A

Most tissues, particularly adipose and muscle tissue

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21
Q

Which glucose transmitter is found in muscle and adipose cells

A

GLUT-4

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22
Q

Which transporter is insulin dependent

A

GLUT-4

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23
Q

What is the process of glucose uptake in cells that are insulin dependant after a carbohydrate meal

A
  1. a spike in blood glucose occurs
  2. spike in blood glucose causes secretion of insulin
  3. insulin binds its receptor
  4. this causes vesicles with GLUT-4 to move to, and fuse with the membrane
  5. the GLUT 4 now in the membrane transports glucose into the cell
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24
Q

what is the process of glucose uptake in cells that are insulin dependent while fasting

A
  1. no spike in blood glucose
  2. this means no insulin secretion
  3. vesicles with GLUT-4 move away from the membrane
  4. less GLUT-4 in the membrane leads to less glucose absorption.
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25
Q

What is PKB and how does it affect the insulin/GLUT-4 process

A
  1. insulin activates its receptor
  2. its receptor sends a substrate of some sort to PKB
  3. substrate activates PKB
  4. PKB phosphorylates contractile elements to bring the vesicles with GLUT-4 to the membrane
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26
Q

What is diabetes mellitus

A

a group of disorders that have absolute or relative deficiencies of insulin

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27
Q

What do all types and disorders of diabetes exhibit

A

hyperglycemia (high blood sugar)

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28
Q

What is the process by which muscles get glucose while you are fasting

A
  1. Muscle contraction uses ATP and gives off ADP and Pi
  2. 2 ADP’s are used by adenylate kinase to produce ATP and AMP
  3. ATP is used up in contractions, but AMP levels in the cell rise
  4. High AMP levels stimulate AMPK
  5. AMPK causes the translocation of GLUT-4 vesicles to the membrane
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29
Q

What enzyme uses two ADPs to create ATP and AMP

A

adenylate kinase

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30
Q

what happens in muscle cells when AMP levels get high

A

AMPK is activated

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31
Q

What does AMPK do in muscles cells

A

it causes translocation of the GLUT-4 vesicles to the membrane

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32
Q

what is another way for muscle cells to bring the vesicles with GLUT-4 into the membrane besides insulin

A

muscular contractions (ATP–> ADP–>AMP–>AMPK–>translocation of GLUT-4 vesicles)

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33
Q

What is the first step of glucose metabolism regardless of the path that it will take

A

Reaction with glucokinase, or hexokinase into

GLUCOSE-6-Phospate

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34
Q

What do kinases do

A

they phosphorylate things

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35
Q

Why is the phosphorylation of glucose into glucose-6-phosphate so important

A
  1. glucose-6-phosphate it highly charged and polar. This makes it so it can’t leave the cell
  2. changing it from glucose maintains a concentration gradient or high glucose on the outside and low glucose on the inside so that the GLUTs can continue to bring glucose into the cell
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36
Q

Are GLUT transporters active or passive transporters

A

they are passive meaning that they work with a concentration gradient

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37
Q

What is hexokinase

A

a phosphorylating enzyme that converts glucose into glucose-6-phosphate.

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38
Q

where is hexokinase found

A

in all cells, including the liver

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39
Q

what is glucokinase

A

a phosphorylating enzyme that converts glucose into glucose-6-phosphate.

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40
Q

Where is glucokinase found

A

only in the liver

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41
Q

What is the Km of hexokinase

A

.2 mM

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42
Q

What is the Km of glucokinase

A

10mM

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43
Q

how is the high Km of glucokinase in comparison to the low Km of hexokinase significant

A
  1. This means that Hexokinase has a much greater affinity to glucose than Glucokinase.
  2. It also means that the speed at which hexokinase converts glucose into glucose-6-phosphate will be much less affected by decreases in blood glucose than Glucokinase.
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44
Q

What does the Km of a substance refer to

A

it refers to the amount of substrate that is needed to have the reaction at half of it’s maximum speed (1/2 Vmax)

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45
Q

What is the normal range for blood glucose concentration

A

70-100 mg/dL

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46
Q

What is the concentration of blood glucose needed for hexokinase to be at it’s half of it’s maximum reaction speed (1/2 Vmax)

A

3.6 mg/dL

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47
Q

What does it mean that hexokinase will be at half of its maximum reaction speed when blood glucose is at 3.6 mg/dL

A

that hexokinase will be completely saturated, even when blood glucose is well below it’s normal range, and an increase in blood glucose won’t cause it to be more saturated.
(even when blood glucose is low or high, hexokinase will still be converting glucose into glucose-6-phosphate at a high rate)

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48
Q

What is the concentration of blood glucose needed for glucokinase to be at its half of maximum reaction speed (1/2 Vmax)

A

180 mg/dL

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49
Q

what does it mean that glucokinase will be at half of its maximum reaction speed when blood pressure is at 180mg/dL

A

that glucokinase will be well below saturation at normal blood glucose levels, and that a change in blood glucose levels will highly affect the saturation of, and the speed of reaction of glucokinase.
(when blood glucose is low, glucokinase activity is low. when blood glucose is high, glucokinase activity is high)

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50
Q

What does it mean that hexokinase is a constitutive enzyme

A

that it is always at optimal levels all of the time

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51
Q

What does it mean that glucokinase is an induced enzyme

A

that it is only at optimal levels in the presence of the inducer

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52
Q

what is the inducer of glucokinase

A

insulin

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53
Q

how does insulin induce glucokinase

A

by phosphorylation

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54
Q

Is hexokinase inhibited by glucose-6-phosphate

A

yes

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55
Q

is glucokinase inhibited by glucose-6-phosphate

A

no

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56
Q

In people with type 1 diabetes how would the activity of glucokinase be

A

it would be low because the synthesis of glucokinase is induced by insulin

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57
Q

When is glucokinase activity high

A

shortly after a carbohydrate meal

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58
Q

When is glucokinase activity low

A

between meals/when fasting

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59
Q

when is hexokinase activity high

A

it’s always constant (except in very severe cases of hypoglycemia)

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60
Q

How active do we want glucokinase while we are fasting

A

we want it inactive while we are fasting, so that more glucose can be sent out to the body

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61
Q

What keeps glucokinase inactive while we are fasting

A

glucokinase regulatory protein binds to glucokinase inactivating it

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62
Q

Where is glucokinase located when bound to the glucokinase regulatory protein

A

in the nucleus

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63
Q

what causes glucokinase to be released from the glucokinase regulatory in the protein

A

a rise in glucose levels in the cell, due to a rise in blood glucose levels after a meal

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64
Q

What causes glucokinase to be sent back into the nucleus and to be bound and inactivated by glucokinase regualtory protein

A

an increase in concentration of fructose-6-phosphate in the cell (an intermediate in glycogenesis)

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65
Q

What besides glucose in the cell can cause glucokinase to be released by glucokinase regulatory protein

A

an increase in concentration of fructose-1-phosphate in the cell (from fructose)

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66
Q

What begins to occur when we are fasting that causes glucokinase to be bound by glucokinase regulatory protein

A

gluconeogenesis

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67
Q

what about gluconeogenesis causes glucokinase to be bound by glucokinase regulatory protein

A

in gluconeogenesis, Amino Acids, lactate, glycerol, and pyruvate are converted into fructose-6-phosphate (on their way to becoming glucose) this is what causes glucokinase regulatory protein to bind glucokinase

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68
Q

What affect does insulin have on glucokinase

A

Insulin induces glucokinase by upregulating the production of it

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69
Q

How does insulin influence the absorption of blood glucose into the liver

A

it doesn’t directly assist in bringing in glucose. But it does induce glucokinase, which converts glucose into glucose-6-phosphate when it enters the cell. this keeps the glucose concentration low in the cell and the glucose gradient pushes glucose into the cell

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70
Q

Which enzyme would be better for the brain, glucokinase or hexokinase

A

hexokinase, because it has a higher affinity for glucose and is always active, even in low blood glucose levels. Glucokinase would be bad because it is only active in high blood glucose levels

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71
Q

is someone with defective glucokinase, with low activity, considered diabetic, Why?

A

Yes, because they would have a decreased ability to phosphorylate Glucose and thus less glucose would enter the liver, and more would stay in the blood

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72
Q

in the final step of glycogenolysis and gluconeogenesis what is the benefit of controlling glucokinase by it binding to GKRP

A

glycogenolysis and gluconeogenesis are attempting to make glucose, if glucokinase weren’t controlled it would be working in oppposition to these, turning glucose back into glucose-6-phosphate

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73
Q

Which has a higher Km glucokinase, or hexokinase

A

glucokinase

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74
Q

Is hexokinase or glucokinase inhibited by glucose-6-phosphate

A

hexokinase

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75
Q

Which tissue uses the GLUT-2 transporter, liver or muscle

A

liver

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76
Q

which tissue has glucokinase, liver or muscle

A

liver

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77
Q

What are the steps of glycogenesis

A
  1. glucokinase/hexokinase convert glucose into glucose-6-phosphate
  2. glucose-6-phosphate is isomerized into glucose-1-phosphate by phosphoglucomutase
  3. glucose-1-phosphate and UTP are combined to form UDP-glucose and PPi
  4. PPi is hydrolized to form two molecules of inorganic phosphate Pi
  5. The Glucose end of UDP-glucose is transferred to a glycogen primer at the non-reducing end by glycogen synthase
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78
Q

What is a glycogen primer

A

it is a protein molecule on the reducing end, with a few glucose molecules bound by alpha 1-4 bonds.

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79
Q

When we use up glycogen in fasting, do we use all of our glycogen that we have stored

A

no, we leave a little bit as a primer

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80
Q

To which end of a glycogen chain or glycogen primer do we add new glucose molecules (from UDP-glucose via glycogen synthase)

A

the non-reducing end

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81
Q

What kind of bond is created between the glucoses of glycogen

A

Alpha 1-4

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82
Q

What happens to the UDP-portion of UDP-glucose after glucose is added to the existing glycogen chain

A

nucleoside diphosphokinase transfers the terminal phosphoryl from ATP to UDP regenerating the UTP we need to create UDP-Glucose

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83
Q

What happens if there are no glycogen primers upon which to add more molecules of glucose (from UDP glucose)

A

the protein Glycogenin can serve as an acceptor of the glucose molecules

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84
Q

What is the structure of glycogenin

A

it is a dimer, in which there are receptor tyrosine residues on each end (head and toe), these tyrosine residues bind a few glucose molecules from UDP glucose, then glycogen synthase adds more to it

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85
Q

what happens to glycogenin after a long glycogen chain has been added

A

it remains attached to the glycogen strand

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86
Q

is ATP used in glycogenesis

A

Yes

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87
Q

how many ATPs are used in each round (addition of one glucose) of glycogenesis

A

2 ATP are used

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88
Q

in which steps of glycogenesis is ATP used

A
  1. glucose to glucose-6-phosphate by glucokinase or hexokinase
  2. UDP to UTP
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89
Q

Is glycogen branched or not

A

it is branched

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90
Q

What enzyme is used in the branching of glycogen

A

the branching enzyme (glucosyl 4:6 transferase)

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91
Q

What kind of bond is used between the branches of glycogen

A

alpha 1-6 bond

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92
Q

How does branching of glycogen happen

A

the branching enzyme cleaves off 5-8 of the glucoses on the non reducing end of a glycogen strand and transfers it to an interior portion of the glycogen

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93
Q

What type of end does the branching of glycogen create more of? reducing or non reducing

A

non reducing

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94
Q

why is it significant that many non reducing ends are created in the branching of glycogen

A

because that means that there are many more non-reducing ends to which more glucose can be attached

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95
Q

How many more non-reducing ends are made per each new branch of glycogen made

A

1 non-reducing end per branch of glycogen formed

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96
Q

How close can a new branch of glycogen be added to an existing branch point of glycogen

A

the new branch of glycogen needs to be at least 4 units away from the existing branch point

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97
Q

Why does the cell store glycogen instead of glucose

A

because glucose is osmotically active and if there were too high of concentrations in the cell, then the cell would lyse (tear/blow up and die)

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98
Q

What is glycogenolysis

A

the breakdown of glycogen into glucose

99
Q

What are the three enzymes used in glycogenolysis

A
  1. glycogen phosphorylase
  2. Debranching enzyme
  3. phosphoglucomutase
100
Q

What enzyme is both found in glycogenolysis and glycogenesis

A

phosphoglucomutase

101
Q

What is the first step of glycogenolysis

A

glycogen phosphorylase acts on the non-reducing ends of glycogen and breaks the most terminal alpha 1-4 bond and phoshorylates the C1 of glucose to make glucose-1-phosphate

102
Q

What is the first enzyme used in glycogenolysis

A

glycogen phosphorylase

103
Q

what bonds does the glycogen phosphorylase break

A

the terminal most alpha 1-4 bond on the non-reducing end

104
Q

what bonds aren’t broken by glycogen phosphorylase

A

the alpha 1-6 bonds between branches, and any alpha 1-4 bond that is 4 units away or closer to a branch point

105
Q

What is left after glycogen phosphorylase has worked on glycogen

A

Glucose-1-phosphate and a branched glycogen with branches that are 4 units long

106
Q

What enzyme comes in and works on the branched glycogen after glycogen phosphorylase

A

the Debranching enzyme

107
Q

What are the two catalyltic activities of the debranching enzyme

A
  1. Transferase activity

2. alpha 1-6 glucosidase activity

108
Q

How does the debranching enzyme cleave the bonds of the 4-unit branched glycogen

A
  1. it transfers the 3 units linked by alpha 1-4 bonds to the non reducing end of the opposing unit branch, making a 1 unit branch and a 7 unit branch
  2. the glucosidase portion of the debranching enzyme cleaves the alpha 1-6 bond of the branch point (releases a free glucose molecule)
109
Q

What is the first step of the debranching of glycogen

A

the transferase portion of the debranching enzyme transfers the 3 unit portion of a glycogen strand (leaves the one glucose bound to the other branch by an alpha 1-6 bond) to the non-reducing end of another 4 unit branch

110
Q

what is left of two 4 unit branches of glycogen after the debranching enzyme has done its transferase portion

A

there is a 7 unit branch, and a 1 unit branch

111
Q

what does the glucosidase portion of the debranching enzyme do

A

it cleaves the alpha 1-6 bond between the single glucose and the longer glycogen branch

112
Q

How many glucoses are freed by the debranching enzyme per branch that the debranching enzyme debranches.

A

one (the glucose that had formed the alpha 1-6 bond as a branch point)

113
Q

which enzyme in glycogenolysis releases more glucose molecules, the glycogen phosphorylase or the debranching enzyme

A

the glycogen phosphorylase

114
Q

what happens after the debranching enzyme gets rid of the branching in glycogen

A

glycogen phosphorylase begins removing a single unit (glucose 1 phosphate) from the non-reducing end of the linear glycogen chain

115
Q

What happens to all of the glucose-1-phosphate in the cell following the glycogen phosphorylase and debranching enzyme actions of glycogenolysis

A

phosphoglucomutase converts glucose-1-phosphate into glucose-6-phosphate

116
Q

Is the phosphoglucomutase step a reversable one

A

yes
Glycogenesis: converts Glucose-6-P into Glucose-1-P
Glycogenolysis: converts glucose-1-P into Glucose-6-P

117
Q

What is the difference between glycogenolysis in the liver and the muscle

A

the presence of glucose-6-phosphatase

118
Q

what does glucose-6-phosphatase do

A

it converts glucose-6-phosphate into glucose

119
Q

In which tissue does glucose-6-phosphatase exist? muscle or liver

A

liver

120
Q

what does the presence of glucose-6-phosphatase allow the liver to do that muscle cannot

A

it creates free glucose that can be released in the blood, and travel to other tissues. The liver can do this, the muscle cannot

121
Q

What are the two enzymes that regulate glycogenesis and glycogenolysis

A

Glycogen synthase

Glycogen phosphorylase

122
Q

Why do we need to regulate glycogenesis and glycogenolysis

A

because it would be a futile cycle if they were both running. One creates glucose from glycogen, the other created glycogen from glucose

123
Q

What do we want the activity of glycogen synthase and glycogen phosphorylase to be like during fasting

A

we want high glycogen phosphorylase activity and low glycogen synthase activity

124
Q

What do we want the activity of glycogen synthase and glycogen phosphorylase to be like after a carbohydrate meal

A

we want glycogen synthase to be high and glycogen phosphorylase activity to be low

125
Q

What are the two things that control and regulate the activity of glycogen synthase and glycogen phosphorylase

A

Hormones and allosteric factors

126
Q

How do hormones affect the activity of glycogen synthase and glycogen phosphorylase

A

they either cause phosphorylation or dephosphorylation of the two enzymes, this changes whether they are active or not.

127
Q

What are the two enzymes responsible for phosphorylation and dephosphorylation of glycogen synthase and glycogen phosphorylase

A

phosphatase and kinase

128
Q

does the kinase phosphorylate or dephosphorylate

A

it phosphorylates

129
Q

does the phosphatase phosphorylate or dephosphorylate

A

it dephosphorylates

130
Q

when is glycogen synthase active

A

when it isn’t phosphorylated

131
Q

when is glycogen phosphorylase active

A

when it is phosphorylated

132
Q

What must the activity of the kinase and phosphatase be if we want to glycogen synthase to be active

A

the kinase needs to be inhibited and the phosphatase needs to be activated.

133
Q

What must the activity be of the kinase and the phospatase if we want glycogen phosphorylase to be inactive

A

the kinase needs to be inhibited and the phosphatase needs to be activated

134
Q

what must the activity of the kinase and the phosphatase be if we want glycogen phosphorylase to be active

A

the kinase needs to be active and the phosphatase needs to be inactive

135
Q

what must the activity of the kinase and the phosphatase be if we want glycogen synthase to be inactive

A

the kinase needs to be active and the phosphatase needs to be inactive

136
Q

If we want glycogenesis to occur what must the activity of the kinase and the phosphatase be

A

the kinase needs to be inactive and the phosphatase needs to be active

137
Q

if we want glycogenolysis to occur what must the activity of the kinase and the phosphatase be

A

the phosphatase needs to be inactive and the kinase needs to be active

138
Q

in glycogenesis are glycogen synthase and glycogen phosphorylase phosphorylated or dephosphorylated

A

they are dephosphorylated

139
Q

in glycogenolysis are glycogen synthase and glycogen phosphorylase phosphorylated or dephosphorylated

A

the are phosphorylated

140
Q

When we are fasting are glycogen synthase and glycogen phosphorylase phosphorylated or not

A

they are phosphorylated

141
Q

after a carbohydrate meal are glycogen synthase and glycogen phosphorylase phosphorylated or not

A

they aren’t phosphorylated

142
Q

What is the name of the kinase enzyme that when active keeps glycogen phosphorylase active and phosphorylated,

A

phosphorylase kinase

143
Q

What is the name of the phosphatase that causes dephosphorylation of glycogen synthase and glycogen phosphorylase

A

phosphoprotein phosphatase-1

144
Q

What directly regulates the activity of phosphoprotein phosphatase-1

A

Phosphoprotein phosphatase-1 inhibitor

145
Q

How does phosphoprotein phosphatase-1 inhibitor inhibit phosphoprotein phosphatase-1

A

when phosphoprotein phosphatse-1 inhibitor is activated it binds to phosphoprotein phosphatase-1 and inactivates it.

146
Q

What are the three major hormones that affect the activity of glycogen synthase and glycogen phosphorylase

A

glucagon, insulin, and epinepherin

147
Q

Which hormone(s) cause phosphorylation of glycogen synthase and glycogen phosphorylase

A

epinepherin and glucagon

148
Q

Which hormone causes dephosphorylation of glycogen synthase and glycogen phosphorylase

A

insulin

149
Q

Where is glucagon from

A

pancreatic alpha cells

150
Q

What is the main stimulant of the release of glucagon

A

low blood glucose

151
Q

What tissues does glucagon act on when it comes to glycogenesis and glycogenolysis

A

the liver only

152
Q

What is the end result of glucagon on the liver

A

the breakdown of glycogen into glucose that can be released into the blood

153
Q

Where is epinepherine from

A

the adrenal medulla

154
Q

What causes epinepherine to be released

A

truama, stress, and physical activity

155
Q

What tissues does epinepherine act on when it comes to glycogenesis and glycogenolysis

A

The liver and muscles

156
Q

What does epinepherine cause in the muscles and liver

A

glycogenolysis

157
Q

What are the steps from secretion of epinepherine and glucagon to the end start of glycogenolysis

A
  1. the hormones bind their receptors activating adenyl-cyclase
  2. Adenylate cyclase converts ATP to cAMP
  3. cAMP binds to protein kinase A (PKA) and activates it
  4. PKA phosphorylates and activates phosphorylase kinase (which phosphorylates glycogen phosphorylase to activate it)
  5. PKA phosphorylates and deactivates glycogen synthatse
  6. PKA also phosphorylates and activates phosphoprotein phosphatase inhibitor-1
  7. phosphoprotein phosphatase inhibitor-1 binds phosphoprotein phospatase-1 and inactivates it (keeping both glycogen synthase and glycogen phosphorylase phosphorylated)
158
Q

What are the three main kinases that can phosphorylate and deactivate glycogen synthase

A
  1. PKA
  2. Phosphorylase kinase
  3. Glycogen synthase 3
159
Q

What enzyme is activated by the binding of epinepherine and glucagon

A

adenylate-cyclase

160
Q

What does adenylate cyclase do

A

converts ATP to cAMP

161
Q

what does cAMP do in glycogenolysis

A

activates protein kinase A (PKA)

162
Q

What is the structure of PKA

A

it is a tetramer with two catalytic and two regulatory subunits

163
Q

What causes the subunits of PKA to separate

A

binding of 2 cAMP to each of the regulatory subunits, this causes the four subunits to separate

164
Q

is the tetramer form of PKA active, or is the separated form active

A

when the subunits are separate it is active, when they are together PKA is inactive

165
Q

How many cAMPs must bind to PKA to cause the subunits to separate and become active

A

4, two to each of the regulatory subunits

166
Q

What are the three things that PKA can do once it has become an active monomeric unit

A
  1. phosphorylates glycogen synthase and keeps it inactive
  2. phosphorylates phosphorylase kinase, which then phosphorylates glycogen phosphorylase to keep it active
  3. phosphorylates the inhibitor protein, which binds to and inhibits phosphoprotein phosphatase-1 and inhibits it from dephosphorylating glycogen synthase and glycogen phosphorylase
167
Q

We know that PKA phosphorylates glycogen synthase, what other enzymes can phosphorylate glycogen synthase and inactivate it?

A

Phosphorylase kinase

Glycogen Synthase Kinase-3 (GSK-3)

168
Q

Which hormones can initiate the cAMP/PKA route to glycogenolysis

A

glucagon and epinepherine

169
Q

Which hormone can initiate the calcium calmodulin route to glycogenolysis

A

epinepherine

170
Q

To what receptor does epinepherine bind to in order to initiate the cAMP/PKA route to glycogenolysis

A

it binds to the Beta-adrenergic receptor

171
Q

to what receptor does epinepherine bind to in order to initiate the calcium calmodulin route to glycogenolysis

A

it binds to the alpha receptors in the liver

172
Q

What are the steps of upregulating glycogenolysis and inhibiting glycogenesis initiated by epinepherine binding to the alpha receptors in the liver

A
  1. epinepherine binds to alpha receptors
  2. this activates phospholipase C (PLC)
  3. Phospholipase C hydrolizes PIP into DAG and IP3
  4. IP3 stimulates the release of calcium from the endoplasic reticulum
    5a. Ca++ and DAG activate Protein kinase C
    5b. Calmodulin also binds Ca++ and Ca-Calmodulin levels increase
  5. Ca-calmodulin activates phosphorylase kinase and calmodulin dependent protein kinase.
  6. Phosphorylase kinase, protein kinase C, and calmodulin dependent protein kinase all phosphorylate and inactivate glycogen synthase
  7. Phosphorylase kinase also phosphorylates (and Activates) glycogen phosphorylase
173
Q

In the process of upregulating glycogenolysis and inhibiting glycogenesis initiated by epinepherine binding to the alpha receptors in the liver. what happens directly after epinepherine binds

A

Phospholipase C is activated and hydrolizes PIP into DAG and IP3

174
Q

What are the products given off of the reaction between phospholipase C and PIP

A

DAG

IP3

175
Q

What does DAG go on to do after it and IP3 came from the hydrolysis of PIP by Phospholipase C

A

DAG goes onto to activate Protein Kinase C

176
Q

What Does IP3 go on to do after it and DAG came from the hydrolysis of PIP by phospholipase C

A

IP3 goes on to stimulate the release of Ca++ from the endoplasmic reticulum

177
Q

What does Ca++ go on to do after it’s release from the endoplasmic reticulum was stimulated by IP3

A
  1. it goes on to activate protein kinase C (along with DAG)

2. It gets bound by calmodulin to make Ca-calmodulin

178
Q

What does protein kinase C do after it is activated by Ca++ and DAG

A

it phosphorylates and inactivates glycogen synthase

179
Q

What does Ca-Calmodulin in the cell

A
  1. it activates calmodulin dependent protein kinase

2. it activates phosphorylase kinase

180
Q

What does calmodulin dependent protein kinase go on to do after it has been activated by ca-calmodulin

A

it phosphorylates and inactivates glycogen synthase

181
Q

What does phosphorylase kinase go on to do after it has been activated by Ca-calmodulin

A
  1. it phosphorylates and inactivates glycogen synthase

2. it phosphorylates and activates glycogen phosphorylase

182
Q

what are the effects of insulin on the hepatic glycogen metabolism in comparison to the effects of glucagon

A

insulin does the opposite. insulin reverses all of the effects of glucagon on hepatic glycogen metabolism

183
Q

In what ways does insulin inhibit glycogenolysis and stimulate glycogenesis

A
  1. Limits the production of cAMP
  2. activates hepatic protein phosphatases
  3. activates the phosphodiesterase that converts cAMP to AMP
  4. inactivates glycogen synthase kinase 3
184
Q

how does the limiting of the production of cAMP by insulin decrease glycogenolysis and increase glycogenesis

A

cAMP goes onto to activate PKA,
PKA inactivates glycogen synthase
PKA activates glycogen phosphorylase (through phosphorylase kinase)
PKA also activates phosphatase inhibitors (those inhibit phosphatases, keeping things phosphorylated)
Without cAMP those things don’t happen

185
Q

How does the activation of protein phosphatases by insulin decrease glycogenolysis and increase glycogenesis

A

protein phosphatases dephosphorylate both glycogen synthase and glycogen phosphorylase
glycogen synthase is now active
glycogen phosphorylase is now inactive

186
Q

how does the inactivation of glycogen synthase kinase 3 by insulin decrease glycogenolysis and increase glycogenesis

A

glycogen synthase kinase 3 phosphorylates and inactivates glycogen synthase, keeping it inactive. So when it is inactive, glycogen synthase becomes more active

187
Q

What are the levels of insuiln and glucagon like after a carbohydrate meals

A

insulin is high and glucagon is low

188
Q

What does the high insulin levels and low glucagon levels after a carbohydrate meal lead to in terms of glycogen metabolism

A

it leads to increased glycogenesis (glycogen synthesis) and decreased glycogenolysis (glycogen degredation)

189
Q

What are the levels of insulin and glucagon like during fasting

A

insulin levels are low, and glucagon levels are high

190
Q

what does the high glucagon levels and low insulin levels during fasting lead to in terms of glycogen metabolism

A

it leads to increased glycogenolysis (glycogen breakdown) and decreased glycogenesis (glycogen synthesis)

191
Q

besides hormonal regulation of the of glycogen metabolism, what is the other type of regulation of glycogen metabolism

A

allosteric regulation

192
Q

what is allosteric regulation of glycogen metabolism

A

the influence of metabolite levels and the energy status of the cell on glycogen synthase and glycogen phosphorylase

193
Q

which type of glycogen metabolism regulation can override the other? hormonal or allosteric

A

allosteric regulation can override hormonal regulation

194
Q

What allosteric factors inhibit glycogenolysis and increase glycogenesis in the liver

A
  1. glucose
  2. glucose-6-P
  3. ATP
195
Q

Why does high levels of glucose in the cell inhibit glycogenolysis and increase glycogenesis in the liver

A

if there is an excess of glucose in the cell, then we don’t want to break down glycogen to make more of it, but store more of it as glycogen

196
Q

Why do high levels of glucose-6-Phosphate in the cell inhibit glycogenolysis and increase glycogenesis in the liver

A

just like glucose, if there is an excess of glucose-6-P in the cell then we will use it to make glycogen, not break glycogen down to create more of it.

197
Q

Why do high levels of ATP in the cell inhibit glycogenolysis and increase glycogenesis in the liver

A

because high levels of ATP indicate that the cell is at a high energy state. so the breakdown of glycogen to create more ATP isn’t necessary

198
Q

What are the allosteric factors that inhibit glycogenolysis and increase glycogenesis in the muscle

A
  1. ATP

2. Glucose-6-phosphate

199
Q

What are the allosteric factors that inhibit glycogenesis and increase glycogenolysis

A
  1. Ca++

2. AMP

200
Q

In muscle is glucose an inhibitor of glycogen phosphorylase

A

No

201
Q

Why isn’t glucose an inhibitor of glycogen phosphorylase

A

because the amount of glucose in the cell doesn’t get high because once it enters the cell hexokinase converts it into glucose-6-phosphate

202
Q

In muscle, how many different ways are there to increase activation of glycogen phosphorylase

A

3

203
Q

what are the 3 ways in muscle to increase activation of glycogen phosphorylase

A
  1. Increased levels of AMP
  2. Nerve inpulses
  3. Epinepherine
204
Q

How do we get increased levels of AMP in the muscle, anb how does that lead to activation of glycogen phosphorylase

A

During contraction the muscle uses up ATP and gives off AMP. As these AMP levels rise AMP binds to glycogen phosphorylase and activates it without phosphorylating it

205
Q

How do nerve inpulses lead to activation of glycogen phosphorylase in muscle

A

Nerve impulses cause Ca++ to be released from the sacrcoplasmic reticulum. then the Ca++ binds to calmodulin, and then Ca-Calmodulin activates phosphorylase kinase, and phosphorylase kinase activates glycogen phosphorylase

206
Q

How does epinepherine cause increased activation of glycogen phosphorylase in muscle

A

epinepherine binds to its receptor and activates adenylate cyclase, this creates cAMP and cAMP activates PKA. PKA then inactivates glycogen synthase, activates the inhibitor than inhibits the phosphatase from deactivating glycogen phosphorylase, and lastly it activates phosphorylase kinase to activae glycogen phosphorylase.

207
Q

How does glycogen regulate glycogen synthesis

A
  1. it inhibits the formation of glycogen by making the active form of glycogen synthase a better substrate for protein kinase A
  2. it also inhibits the phosphoprotein phosphatase from dephosphorylating glycogen synthase, keeping it inactive, and not letting more glycogen be stored.
208
Q

What are the 5 types of glycogen storage disorders that we need to know

A 
1 - Von Gierke's disease
3 - Cori's disease
4 - Anderson disease
5 - McArdle's disease
6 - Her's disease
209
Q

What is the defective enzyme in Von Gierke’s disease (type 1 glycogen storage disorder)

A

Glucose-6-phosphatase

210
Q

What is the problem with having a defect in glucose-6-phosphatasee like in glycogen storage disorder type 1, Von Gierke’s disease.

A

because glucose-6-phosphatase is defective, the liver can’t go from glucose-6-phosphate back to glucose. so the liver can’t ship glucose out to the rest of the body.

211
Q

What are problems that arise in glycogen storage disorder type 1, Von Gierkes disease

A

Being unable to reproduce glucose from glucose-6-phosphatase leads to:

  • Massive enlargement of the liver
  • Failure to thrive
  • Severe hypoglycemia
  • Ketosis
  • Hyperuricemia
  • Hyperlipemia
212
Q

What organs are most affected by glycogen storage disorder type 1. Von gierke’s disease

A

liver and kidney

213
Q

How is glycogen storage levels affected with type 1 glycogen storage disorder von gierke’s disease

A

the levels of glycogen are increased

214
Q

What is the defective enzyme in type 3 glycogen storage disorders, Cori’s disease

A

The debranching enzyme

215
Q

What is the problem that arises with having a defecting debranching enzyme for glycogen, like in type 3 glycogen storage disorder, Cori’s disease

A

if you can’t debranch the glycogen, then you will be unable to break it down enough. so there will be extra glycogen because we don’t break it down enough

216
Q

What are the problems that arise in Type 3 glycogen storage disorder, Cori’s disease

A

They are all similar to type 1 Von Gierke’s disease, just milder

  • increased liver size
  • hypoglycemia
  • ketosis
  • hyperuricemia
  • hyperlipemia
217
Q

What organs are affected by Type 3 Glycogen storage disorder, Cori’s disease

A

The muscle and liver

218
Q

How are the levels of glycogen affected by type 3 glycogen storage disorder, Cori’s diseas

A

increased amount of glycogen

Shorter outer branches

219
Q

What is the enzyme that is defective in type 4 glycogen storage disorder, Andersen’s disease

A

The Branching enzyme

220
Q

What happens to a person with type 4 glycogen storage disorder, Andersen’s disease

A

they usually have liver failure at age 2 and pass away

221
Q

What tissue is affected by andersen’s disease, type 4 glycogen storage disorder

A

the liver

222
Q

What is the glycogen storage like for someone with andersen’s disease, Type 4 glycogen storage disorder

A

it has very long outer branches

223
Q

What is the enzyme that is defective in type 5 glycogen storage disorder, McArdle’s disease

A

phosphorylase (in the muscle)

224
Q

What happens to a person with McArdle’s disease, type 5 glycogen storage disorder

A

they are unable to do strenuous exercise because of painful muscle cramps, otherwise they are normal

225
Q

What tissue is affected by McArdle’s disease (Type 5)

A

the muscle

226
Q

what is the glycogen like in someone with McArdles disease

A

pretty normal, but slightly increased amounts

227
Q

What is the enzyme that is bad in type 6 glycogen storage disorder, Her’s disease

A

phosphorylase (in the liver)

228
Q

What happens to the person with type 6 glycogen storage disorder, Her’s disease

A

they have the same symptoms as someone with Von Gierke’s disorder, just more mild

  • enlarged liver
  • hypoglycemia
  • ketosis
  • hyperuricemia
  • hyperlipemia
229
Q

What tissues are affected in Her’s disease (type 6 glycogen storage disorder)

A

the liver

230
Q

what is the glycogen storage like in someone with Her’s disease

A

increased amount of glycogen

231
Q
  1. Muscle glycogen cannot contribute directly to blood glucose because:
A

A. Muscle glycogen can’t be converted to glucose-6-P
B. Muscle lacks glucose-6-phosphatase
C. Muscle contains no glycogen phosphorylase
D. Muscle lacks phosphoglucomutase

B

232
Q

Type I glycogen storage disease (Von Gierke’s Disease) is associated with severe fasting hypoglycemia. This is due to:

A

A. the inability of the liver to release the glucose into the blood.
B. the inability of the liver to synthesize glycogen.
C. a deficiency of glycogen phosphorylase in the liver.
D. A and B are correct.
E. A, B, and C are correct.

A

233
Q
  1. Which of the following enzymes involved in glycogen metabolism would be active if the insulin/glucagon ratio is extremely low?
A 
A.	Glycogen phosphorylase
B.	Phosphorylase kinase
C.	Glycogen synthase
D.	A and B are correct
E.	A, B, and C are correct.

D

234
Q

Which of the following enzymes involved in glycogen metabolism will be phosphorylated during fasting (interval between meals)?

A 
A.	Glycogen phosphorylase
B.	Glycogen synthase
C.	Protein kinase A
D.	A and B are correct
E.	A, B, ad C are correct

D

235
Q

McArdle’s Disease (Type V Glycogen Storage Disease) is characterized by a limited ability to perform strenuous exercise because of painful muscle cramps. The cause of this condition is a congenital deficiency of:

A 
A.	glucose-6-phosphatase in the liver
B.	glycogen phosphorylase in the liver
C.	glycogen phosphorylase in the muscle
D.	branching enzyme in the liver
E.	debranching enzyme in the muscle

C

236
Q
  1. An individual is born with a defective protein phosphatase inhibitor. What effect would such a disorder have on glycogen metabolism?
A

Increased glycogen synthesis

237
Q
  1. Caffeine is a phosphodiesterase inhibitor. What effect would the consumption of several cups of coffee have on glycogen metabolism?
A

this gives rise to more cAMP, this activates protein kinase A, which activates glycogen phosphorylase

238
Q
  1. If an individual is born with a GLUT-2 deficiency, would you expect him/her to have fasting hypoglycemia? Explain.
A

Yes, because the liver can’t transport glucose out in to the blood

239
Q
  1. There is a strain of mice that is deficient in muscle phosphorylase kinase. Phosphorylase b in muscle of such mice cannot be converted into phosphorylase a. Nevertheless, heavy exercise results in depletion of muscle glycogen. Explain.
A

Muscle contraction uses ATP and creates ADP, this then goes to AMP, AMP binds directly to glycogen phosphorylase activating it, even though it may not be phosphorylated

240
Q
  1. If glycogen inhibits its own formation, why do you see massive accumulation of glycogen in Von Gierke’s Disease (Type I Glycogen Storage Disease)?
A

Because it can’t turn glucose-6-phosphate into glucose, and glucose-6-phosphate is a positive influence on glycogen synthase and a negative influence on glycogen phosphorylase. This even happens if the glycogen synthase is phosphorylated and in its inactive.

241
Q
  1. Compared to glucokinase, hexokinase:
A 
A.	is a constitutive enzyme.
B.	is found in all tissues.
C.	is inhibited by glucose-6-P.
D.	a and b are correct.
E.	a, b, and c are correct.

E

242
Q
  1. Compared to hexokinase, glucokinase:
A 
A.	is a constitutive enzyme.
B.	is found in all tissues.
C.	is inhibited by glucose-6-P.
D.	is not specific for glucose.
E.	has a higher KM.

E

243
Q

This enzyme is present in all tissue types (hexokinase Vs. glucokinase)

A

Hexokinase

DMD 5242 (10 decks)

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