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DMD 5242 > Glycolysis/Gluconeogenesis (complete) > Flashcards

Glycolysis/Gluconeogenesis (complete) Flashcards

1
Q

What transports glucose from the lumen of the intestines and kidney into the epithelial cells

A

SGLT

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2
Q

what kind of transport do SGLTs do

A

active transport

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3
Q

what is is required for SGLTs to be able to transport glucose against its concentration gradient

A

sodium in the lumen (it goes with its concentration gradient, and brings glucose with it against glucoses own concentration gradient)

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4
Q

What happens if you have a completely sodium free diet

A

you will eventually lose the ability to absorb glucose into the epithelial cells of the kidney and intestines.

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5
Q

What types of transporters transport glucose from inside the epithelial cells into the blood

A

GLUT transporters

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6
Q

what kind of transport do GLUTs do

A

they do passive transport

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7
Q

Where are GLUTs located

A

in all cells of the body, on the side of the cell bordering the capillaries

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8
Q

Which GLUT is regulated by insulin

A

GLUT 4

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9
Q

Where is GLUT 4 located

A
  1. skeletal muscle cells (myocytes)
  2. Cardiac muscle cells (cardiomyocytes)
  3. Fat cells (adipocytes)
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10
Q

Which GLUTs aren’t regulated by insulin

A

1-3 and 5-13

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11
Q

Where is insulin synthesized

A

pancreatic beta cells

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12
Q

what is insulin

A

a small peptide hormone

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13
Q

What happens to glucose immediately after it leaves the blood and enters into a cell

A

it is phosphorylated into glucose-6-phosphate

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14
Q

why is glucose immediately phosphorylated upon entrance into a cell

A
  1. so that it is “trapped” in that cell and won’t leave
  2. so that it won’t affect the concentration gradient of glucose and glucose will still be able to passively enter the cell
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15
Q

When insulin is synthesized, what is the other byproduct of it’s synthesis that can be used to test the production of insulin

A

C peptide

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16
Q

What are the normal levels of blood glucose

A

75-100 mg/dL

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17
Q

What are the three ways to increase blood glucose

A
  1. glucose absorption in the gut
  2. Glucose recovery from the kidneys
  3. glucose release from the liver
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18
Q

How does insulin allow GLUT-4 to transport glucose from the blood into muscle, fat, and cardiac muscle cells

A

insulin binding to its receptor causes the translocation of GLUT from inside the cell to the cell membrane

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19
Q

What is glucose clearance

A

glucose being taken out of the blood and transported into the tissues

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20
Q

What is the primary action of insulin

A

to cause glucose clearance (uptake of glucose from the blood and into the cells)

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21
Q

What does the enzyme phosphatase do

A

it dephosphorylates Glucose-6-Phosphate to glucose in the liver

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22
Q

where is phosphatase found

A

in the liver only

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23
Q

the lack of what enzyme in skeletal muscle is the reason why skeletal muscle doesn’t release glucose back into the blood

A

the lack of phosphatase

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24
Q

Through what transporter does glucose leave the liver and enter the bood

A

GLUT-2

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25
Q

Can muscle cells uptake glucose even when insulin is not present

A

yes

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26
Q

what stimulates glucose uptake in muscles when insulin is not present

A

muscle contaction

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27
Q

what is the process by which muscle contraction in skeletal muscle causes the uptake of glucose.

A
  1. Contraction uses ATP, and gives off ADP
  2. ADP is used to make more ATP and AMP
  3. High levels of AMP in the cell stimulates AMPK
  4. AMPK stimulates GLUT-4 to move to the cell membrane of muscle cells
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28
Q

When is insulin high, acutely

A
  1. after a meal
  2. in anticipation of a meal
  3. in the morning
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29
Q

When is insulin high chronically

A

insulin resistance (pre-diabetes) or diabetes

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30
Q

What is the effect of the sympathetic nervous system on insulin and glucagon

A

decreases insulin and increases glucagon

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31
Q

what is the effect of the parasympathetic nervous system on insulin and glucagon

A

increases insulin and decreases glucagon

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32
Q

What does insulin do in muscle tissue

A
  1. increases glucose uptake

2. helps in anabolism (building up of muscle)

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33
Q

What does insulin do in the liver

A
  1. inhibits ketogenesis
  2. activates lipogenesis
  3. activates glycogenesis
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34
Q

What does insulin do in adipose tissue

A
  1. causes glucose uptake
  2. activates lipogenesis
  3. activates adipogenesis
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35
Q

What levels in the blood are decreased with the release of insulin

A
  1. glucose
  2. fats
  3. Ketones
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36
Q

Along with insulin, what are the other major hormones that promote fat storage and inhibits fat usage

A

None, insulin is the only major hormone that promotes fat storage and inhibits the use of fats

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37
Q

how easy is it to gain fat without insulin

A

nearly impossible

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38
Q

What hormones counter the affect of insulin on fats (Which ones cause the breakdown and usage of fats?)

A
  1. glucagon
  2. catecholectamines
  3. cortisol
  4. Growth Hormone (GH)
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39
Q

What is the affect of glucagon, cortisol, catecholectamines, and growth hormone on blood glucose levels

A

they increase blood glucose levels

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40
Q

Are glucagon, cortisol, catecholectamines, and GH catabolic or anabolic

A

catabolic

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41
Q

what is the effect of insulin on blood glucose levels

A

it decreases blood glucose levels

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42
Q

is insulin catabolic or anabolic

A

anabolic

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43
Q

What is the primary regulator of insulin and glucagon

A

plasma glucose concentration

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44
Q

plasma glucose concentration is the primary regulator of insulin and glucagon. what happens when it’s high, what happens when it’s low

A

When it is high, insulin is secreted and glucagon isn’t

When it is low glucagon is secreted and insulin isn’t

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45
Q

What is the effect of glucagon on muscle tissue

A

there is no effect

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46
Q

why doesn’t glucagon have an effect on muscle tissue

A

because there are no glucagon receptors in muscle tissue

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47
Q

What is the effect of glucagon on the liver

A
  1. glycogenolysis
  2. gluconeogenesis
  3. ketogenesis
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48
Q

What is the effect of glucagon on adipose tissue

A

Lipolysis

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49
Q

Which types of cells don’t have glucagon receptors?

  • adipocytes
  • myocytes
  • hepatocytes
A

myocytes - muscle cells

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50
Q

Which types of cells don’t have insulin receptors

  • adipocytes
  • myocytes
  • hepatocytes
A

All cells have insulin receptors

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51
Q

What are the molecules and enzymes (E:) of glycolysis

A 
1  Glucose
      E: Hexokinase (glucokinase)
2 Glucose-6-Phosphate
      E: Phosphohexose Isomerase
3 Fructose-6-phosphate
      E: Phosphofructokinase-1 (PFK-1)
4 Fructose-1,6-Bisphosphate
      E: Aldolase (cuts the 6-C molecule into 2 3-C molecules)
5 Glyceraldehyde - 3 phosphate (2)
      E: Glyceraldehyde-3-phosphate dehydrogenase
6 1,3-bisphosphoglycerate (2)
      E: phosphoglycerate kinase
7 3-phosphoglycerate (2)
      E: phosphoglycerate mutase
8 2-phosphoglycerate (2)
      E: Enolase
9 Phosphoenolpyruvate (PEP) (2)
      E: Pyruvate kinase
10 Pyruvate (2)
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52
Q

What portion of glycolysis is referred to as the preparatory phase

A

From the start, up until the 6 carbon molecule splits into two 3 carbon molecules

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53
Q

Why are the first few steps (up until the splitting point) called the preparatory phase

A

because up until this point, energy has only been used, no energy has been given off

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54
Q

What is the payoff phase of glycolysis

A

the second half of glycolysis, after the 6 carbon molecule splits, up to the creation of pyruvate

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55
Q

why is the second half of glycolysis referred to as the payoff phase

A

because it is in the second half of glycolysis that NADH and ATP are created

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56
Q

how many ATP are created for each glucose molecule that goes through glycolysis, how do you get this number?

A

4, ,
one is created during the phophoglycerate reaction of 1,3 bisphosphoglycerate into 3 phosphoglycerate.
the second is created during the pyruvate kinase reaction of PEP into pyruvate
So two for each 3 carbon molecule that goes through the second half of glycolysis, and each glucose molecule ends up sending two 3 Carbon molecules through the second half of glycolysis

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57
Q

How many NADH are created for each glucose molecule that goes through glycolysis. How do you get this number

A

2.
one is created during the glyceraldehyde-3-phosphate dehydrogenase reaction of glyceraldehyde-3-phosphate into 1,3-bisphosphoglycerate
(but because this reaction occurs twice per glucose molecule, you get two total NADH from one glucose molecule)

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58
Q

What is the Actual net ATP gain from glycolysis

A

2 ATP, the 4 created in the second half of glycolysis minus the two reactions that use ATP in the first half of glycolysis

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59
Q

What are the reactions in glycolysis that use ATP

A
  1. The Hexokinase/Glucokinase reaction of glucose into glucose-6-phosphate
  2. The PFK-1 reaction of fructose-6-phosphate into fructose-1,6-bisphosphate
60
Q

Which two steps in the preparatory phase of glycolysis add a phosphate to the molecule

A
  1. the hexokinase/glucokinase reaction

2. the PFK-1 reaction

61
Q

what is significant about the location of the phosphate that is added in the PFK-1 reaction

A

it is added to the #1 carbon (which is opposite to the phosphate added by glucokinase/hexokinase to the #6 carbon) this allows the glucose molecule to split into two identical molecules

62
Q

Which steps in glycolysis are irreversable

A

Step 1. Glucokinase/hexokinase
Step 3. phosphofructokinase-1 (PFK-1)
Step 9. Pyruvate kinase

63
Q

How many pyruvate are formed in glycolysis from each molecule of glucose

A

2

64
Q

Where does pyruvate go after it is formed in glycolysis

A

to the mitochondra

65
Q

How does pyruvate enter the inner membrane of the mitochondria

A

through a pyruvate carrier

66
Q

Pyruvate gets converted to what molecule in the mitochondria

A

Acetyl-CoA

67
Q

What is the enzyme that converts pyruvate into Acetyl-CoA

A

the pyruvate dehydrogenase complex

68
Q

What are all of the products created in the pyruvate dehydrogenase complex reaction

A
  1. Acetyl-CoA
  2. NADH
  3. CO2
69
Q

High Levels of what lead to deactivation of the pyruvate dehydrogenase complex

A
  1. ATP
  2. NADH
  3. Acetyl-CoA
70
Q

What are the 5 cofactors that are needed for the pyruvate dehydrogenase complex to work

A
  1. Coenzyme A
  2. NAD+
    3, TPP
  3. Lipoic Acid
  4. FAD
71
Q

Besides the high levels of ATP, NADH, and Acetyl-CoA what inhibits the pyruvate dehydrogenase complex

A

Phosphorylation by pyruvate dehydrogenase kinase

72
Q

What dephosphorylates the Pyruvate dehydrogenase complex, and does that activate it, or inactivate it

A

pyruvate dehydrogenase phosphatase, and this activates it

73
Q

What is the primary reason that the liver runs glycolysis

A

to convert glucose into glycogen and fat

74
Q

What are the regulators of glycolysis

A
  1. Glucose
  2. ATP
  3. AMP
  4. Fructose, 2-6-bisphosphate
  5. PK phosphorylation
  6. Fructose-1,6-bisphosphate
75
Q

How does ATP regulate glycolysis

A

High levels of ATP indicate that the cell has plenty of energy, and so it inhibits glycolysis. It does this at PFK-1
and at the PK

76
Q

What are the two places that ATP acts on in inhibiting glycolysis

A
  1. PFK-1

2. PK

77
Q

How does glucose regulate glycolysis

A

glucose is the initial substrate of glycolysis, and at least in the liver glucokinase is the first enzyme to act on glucose. it has a high Km, or low affinity for glucose, so if glucose levels are low, then glycolysis activity is low. is glucose is high, glycolysis levels are high

78
Q

How does AMP regulate glycolysis

A

AMP is made by breaking down ATP. so it is high when energy is being used, and it is low when energy isn’t being used. So if AMP is low, then it will inhibit glycolysis.

79
Q

At which places does a low level of AMP regulate glycolysis

A

PFK-1

80
Q

How does Fructose-2,6-bisphosphate regulate glycolysis

A

Fructose-2,6-bisphosphate is a product of PFK-2, which runs side by side of PFK-1. Fructose-2,6-bisphosphate activates PFK-1.

81
Q

What enzyme leads to creation of fructose-2,6-bisphosphate. and what is the initial substrate this enzyme uses

A

PFK-2 is the enzyme that converts fructose-6-phosphate into fructose-2,6-phosphate.

82
Q

We know that the product of PFK-2 (fructose-2,6-bisphosphate) activates PFK-1. but what are the regulators of PFK-2

A

insulin

glucagon

83
Q

What are the three locations of glycolysis that are regualted by insulin and glucagon

A

Glucokinase
PFK-1
Pyruvate Kinase

84
Q

What is the effect of insulin on glucokinase, PFK-1 and pyruvate kinase

A

insulin activate glucokinase, PFK-1, and Pyruvate kinase

85
Q

When is insulin present, and able to activate glycolysis

A

in a fed state

86
Q

what is the effect of glucagon on glucokinase, PFK-1, and pyruvate kinase

A

glucagon represses activity of glucokinase, PFK-1, and pyruvate kinase

87
Q

When is glucagon present, and able to repress glycolysis

A

in a fasting state

88
Q

How does insulin affect Glucokinase

A

it helps to stimulate its creation, and release from the nucleus

89
Q

how does glucagon affect glucokinase

A

it represses its activity

90
Q

how does insulin affect PFK-1

A
  1. PFK-2 creates and increases fructose-2,6-bisphosphate levels
  2. fructose-2,6-bisphosphate activates PFK-1
  3. fructose-2,6-bisphosphatase takes fructose-2,6-bisphosphate and turns it back into fructose-6-phosphate
  4. insulin inactivates fructose-2,6-bisphosphatase, keeping fructose-2,6-bisphosphate levels high, which increases PFK-1

so insulin activates PFK-1

91
Q

how does glucagon affect PFK-1

A
  1. glucagon activates adenylate cyclase
  2. adenylate cyclase creates cAMP
  3. cAMP activates PKA
  4. PKA phosphorylates and activates fructose-2,6-bisphosphatase
  5. fructose-2,6-bisphosphatase turns fructose-2,6-bisphosphate into fructose-6-Phosphate
  6. decreased levels of fructosr-2,6-bisphosphate leads to deactivation of PFK-1

Glucagon decreases PFK-1 activity

92
Q

How does insulin affect Pyruvate kinase

A

insulin dephosphorylates pyruvate kinase (PK), which activates it

93
Q

How does glucagon affect pyruvate kinase (PK)

A
  1. glucagon binding activates adenylate cyclase
  2. adenylate cyclase turns ATP into cAMP
  3. cAMP activates PKA
  4. PKA phosphorylates and inactivates PK
94
Q

What are the non-hormonal regulators of glucokinase

A

high Km

95
Q

What are the non hormonal regulators of PFK-1

A

activators
AMP
fructose-2,6-bisphosphate

Deactivators
ATP

96
Q

What are the non hormonal regulators of PK

A

activators
fructose-1,6-bisphosphate
dephosphorylation

inactivators
phosphorylation
ATP
Alanine

97
Q

What are the three enzymes of glycolysis that need to be bypassed in gluconeogenesis (only in liver)

A
  1. Glucokinase
  2. PFK-1
  3. PK
98
Q

How is the bypass of glucokinase in the liver done

A

by glucose-6-phosphatase

99
Q

how is the bypass of PFK-1 in gluconeogenesis done

A

by Fructose-1,6-bisphosphatase. But this enzyme is regulated too.

100
Q

What is the process by which fructose-1,6-bisphosphatase is regulated so that it can bypass the PFK-1 reaction

A

fructose-1,6-bisphosphatase is inhibited by fructose-2,6-bisphosphate.
this is created by PFK-2, and it is eliminated (back into fructose-6-phosphate) by fructose-2,6-bisphosphatase
when fructose-2,6-bisphosphatase is active, converts the fructose-2,6-bisphosphate into fructose-6-phosphate.
this means lower levels of fructose-2,6-bisphosphate, which means the fructose-1,6-bisphosphatase is active, and bypasses the PFK-1 reaction

101
Q

How is the bypass of the pyruvate kinase reaction done

A
  1. pyruvate that is normally converted into Acetyl-CoA and run through the Krebs cycle is instead converted into Oxaloacetate by Pyruvate carboxylase.
  2. Oxaloacetate is converted into Malate by MDH (malate dehydrogenase)
  3. Malate is shipped out of the mitochondria
  4. Malate is converted back into Oxaloacetate by MDH
  5. Oxaloacetate in converted back into PEP by PEPCK
102
Q

Where does the bypass reaction of PK happen

A

first portion is in the mitochondria, then the second portion is in the cytosol

103
Q

What are the enzymes that play in the PK bypass reaction

A
  1. Pyruvate carboxylase
  2. MDH
  3. MDH
  4. PEPCK (phosphoenolpyruvate carboxykinase)
104
Q

What is the effect of insulin on gluconeogenesis, and how does it do that

A

it inhibits gluconeogenesis

  1. by dephosphorylating PK (activating PK)
  2. by deactivating fructose-2,6-bisphosphatase, increasing fructose-2,6-bisphosphate, which activates PFK-1, and inhibits fructose-1,6-phosphatase
105
Q

What is the effect of glucagon on gluconeogenesis, and how does it do that

A

it activates gluconeogenesis

  1. by phosphorylating and deactivating PK
  2. by activating adenylate cyclase, which increases cAMP, which activate PKA, which phosphorylates fructose-2,6-bisphosphatase, which activates it, which lowers fructose-2,6-bisphosphate, which inhibits PFK-1 and activates fructose1,6-bisphosphatase
106
Q

What is the effect on pyruvate carboxylase by insulin and glucagon (pyruvate carboxylase is used in the pyruvate kinase bypass reaction)

A

insulin and glucagon have no effect on pyruvate carboxylase

107
Q

What is the effect on PEPCK (PEPcarboxykinase) by insulin and glucagon (PEPCK is used in the pyruvate kinase bypass reaction)

A

Insulin inhibits PEPCK

glucagon activates PEPCK

108
Q

What is the affect of high levels of alanine on glycolysis/gluconeogenesis

A

high levels of alanine inhibit pyruvate kinase (increasing gluconeogenesis)

109
Q

If no hormones regulate pyruvate carboxylase, then what does

A

Acetyl-CoA

110
Q

how does Acetyl-CoA regulate pyruvate carboxylase

A

high levels of Acetyl-CoA activate pyruvate carboxylase (shows that there is enough energy in the liiver, so it can be used in a different way, glycogenesis, lipogenesis, or glucose shipped out to the body)

111
Q

Why is it significant that the pathways of glycolysis and gluconeogenesis are reciprocally regulated (What activates one pathway deactivates the other)

A

to avoid a futile cycle

112
Q

We know how to do gluconeogenesis from pyruvate right, what different things can be converted into pyruvate

A
  1. Lactate
  2. alanine
  3. cysteine
  4. glycine
  5. serine
  6. tryptophan
113
Q

What happens once Lactate, alanine, cystein, glycine, serine, and tryptophan have been converted into pyruvate (in gluconeogenesis)

A

the pyruvate is converted into Oxaloacetate, then into malate, then shipped out of the _____, converted back into Oxaloacetate, then back into PEP

114
Q

Some Amino acids aren’t converted into pyruvate, but into Oxaloacetate, which ones are they

A

Aspargine

Aspartate

115
Q

Is glycerol a gluconeogenic substrate

A

yes

116
Q

how does glycerol enter the gluconeogenic pathway

A

glycerol is converted into Glyceraldehyde-3-phosphate by glycerol kinase, then from glyceraldehyde-3-phosphate into dihydroxyacetone phosphate, and then from dihydrosyacetone into fructose-1,6-bisphosphate. and then up through gluconeogenesis

117
Q

Can we get glucose from fatty acids

A

nope

118
Q

Why can’t we get glucose from fatty acids

A

Beta-oxidation (breaking down of fatty acids) leads to Acetyl-CoA, when Acetyl-CoA goes through the citric cycle, 2 CO2’s leave, so you can’t use them to create more glucose. (no net gain of C)

119
Q

Why can lipolysis increase glucose production if beta-oxidation doesn’t

A

becuase lipolysis is the breakdown of a triglyceride. triglycerides have glucogenic parts

120
Q

what are the parts of a triglyceride

A

glyceride

fatty acids

121
Q

which pars of a triglyceride are glucogenic

A

glyceride

122
Q

If fatty acids can’t be turned into glucose, what do they become in lipolysis

A

Acetyl-CoA

123
Q

What is the NET gain of ATP in glycolysis

A

2 ATP (2 Used, 4 made)

124
Q

What is the NET gain of NADH in glycolysis

A

2 NADH

125
Q

When using glycerol to make glucose, how many glycerol molecules are needed to make one glucose molecules

A

2

126
Q

when using glycerol to make glucose, how many ATP are required to make a molecule of Glucose

A

2 (1 per glycerol molecule)

127
Q

When using glycerol to make glucose, how many NADH are required to make a molecule of glucose

A

2 (1 per glycerol molecule)

128
Q

Where does gluconeogenesis from glycerol occur

A

only in the liver

129
Q

In starvation what is the first source of glucose

A

Amino Acids from the muscle

130
Q

If Fatty acids can’t produce glucose, what good are they in starvation when we need energy

A

They can be a source of ketone bodies,

131
Q

What is the initial substrate in the formation of ketone bodies

A

Acetyl-CoA

132
Q

What is the good that comes from ketone bodies

A

they can be used like glucose (for energy)

133
Q

When do we get anaerobic glycolysis

A

Anaerobic glycolysis occurs in the absence of oxygen, or when energy demand is high and immediate

134
Q

What is the difference between aerobic and anaerobic glycolysis

A

aerobic glycolysis allows the NADH’s made in glycolysis to be used in the ETS-Ox Phos system to make more ATP.
Anaerobic glycolysis can’t use the NADH’s made in glycolysis, so the 2 ATP from glycolysis are the only ATP’s made

135
Q

How many ATPs are made from aerobic glycolysis (not including the Aceyl-CoA going through the crebs cycle)

A

7
2 from glycoglysis
5 from the two NADHs made (2.5 ATP per NADH that goes through the ETC-Ox-phos system)

136
Q

how many ATP are made from anaerobic glycolysis

A

2

137
Q

if the NADH made in glycolysis can’t go to the ETS-Ox Phos system becuase of anaerobic conditions what happens to it

A

The NADH is used by lactate dehydrogenase to create lactate from pyruvate. and NAD+ results

138
Q

What is the enzyme that makes lactate,

A

lactate dehydrogenase

139
Q

When do we make lactate

A

in anaerobic conditions

140
Q

What is the significance of Lactate dehydrogenase using NADH and leaving NAD+

A

the NAD+ can be used to continue glycolysis, so more ATP can be made

141
Q

When do we have anaerobic glycolysis

A
  1. in RBCs (because they don’t have mitochondria)
  2. in vigorously working muscle (inadequate oxygen delivery)
  3. Blockage of blood flow
  4. in many tumors
142
Q

What happens to the lactate that is created by lactate dehydrogenase in anaerobic conditions (usually from RBC’s and working muscle)

A
  1. it can be taken to resting skeletal muscle or the heart
  2. it can be taken to the liver
  3. it can be used by the very muscle that created it
143
Q

What happens to the lactate that has been taken to resting skeletal muscle or heart

A

it is converted into pyruvate, then it goes through the krebs cycle and ETS-Ox phos

144
Q

what happens to the lactate that has been taken to the liver

A

it is converted into pyruvate, then it goes through gluconeogenesis to produce glucose

145
Q

what is the Cori cycle

A

the catabolism of glucose carbons to lactate in the peripheral tissue, then the anabolism of lactate back into glucose in the liver

DMD 5242 (10 decks)

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