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Fundamentals of Molecular Medicine > Glycolysis > Flashcards

Glycolysis Flashcards

1
Q

To lose one pound of weight, ones caloric intake should decrease by approximately how many calories?

1500

2000

2500

3000

3500

A

3500

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2
Q

In order to maintain his/her current weight, hw many calories will a 70 kg sedentary individual require daily?

1550

1850

2150

2450

2750

A

2150

(70 x 24 x 1.3 = 2150)

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3
Q

Under fasting conditions, which of the following is true?

Muscle glycolysis is inhibited

Liver glycolysis is inhibited

Muscle glycogen degradation is inhibited (it can be turned on

Liver glycogen degradation is inhibited

A

Liver glycolysis is inhibited (Muscle glycolysis won’t be inhibited under fasting conditions)

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4
Q

Still under initial fasting conditions which statement is correct (initial fasting conditions)?

Muscle glycogen synthesis increases

Adipocyte fate content increases

Urea synthesis increases

Lactate utilization by RBC increases

A

Urea synthesis increases (AA are now used as energy source and their waste is in urea)

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5
Q

What is diabetes?

Type 1?

Type 2?

A
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6
Q

What are you looking for?

A
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7
Q

A type 1 diabetic has just eaten, but forgot to take insulin. Which of the following will occur as a result?

Fatty acid degradation in the liver will increase

Glycogen degradation in the liver will decrease

Gluconeogenesis in the liver will continue

RBC’s will increase their oxidation of fatty acids

A

Gluconeogenesis in the liver will continue (In absence of insulin gluconeogenesis will continue. But glucose levels will actually continue to rise because insulin is required for glucose uptake by the muscle and the adipose tissue and liver still pumps out glucose via gluconeogenesis. Insulin is required to stimulate glycogen synthesis.)

(RBC’s have no mitochondria and therefore cannot oxidize FA)

(RBC’s have no mitochondria and therefore cannot oxidize FA)

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8
Q

Overview of Glycolysis

A

Two pathways of Glycolysis — Anaerobic and Aerobic

In order to generate Triglyceride we need to go through glycolysis.

Excess glucose goes through glycogen biosynthesis.

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9
Q

Glycolysis in Muscle vs. Liver

A
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10
Q

What type of metabolism is used when sprinting

A

Sprinting — Anaerobic Metabolism

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11
Q

Glucokinase is found…

A

Glucokinase — liver and pancreas.

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12
Q

Hexokinase is found…

A

In every other tissue but the liver and the pancreas

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13
Q

Glucose-1-Phosphate is Isomerized into…

A

Glucose 1 phosphate is isomerated into Glucose-6-P

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14
Q

What is the first committed step in glycolysis?

A

Phosphofructokinase 1 (PFK1) — Irreversible. Committed Step. Regulated Step.

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15
Q

How many ATP’s are used to get to the point of having two triose’s?

A

2 ATP

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16
Q

How does NAD become NADH?

Is this oxidization or reduction?

A

NAD+ accepts two electrons and a proton to become NADH

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17
Q

What is a mutase?

A

Whenever we move a phosphate from one functional group to another.

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18
Q

What is the function of dehydration?

A

Dehydration creates very high energy bond — about twice the energy of a high energy bond in ATP — ATP is 7kcal/mol where as the enolated phosphate is about 14 kcal/mol (which is doubled).

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19
Q

Which enzyme regenerates NAD so it can be reused?

A

Lactate Dehydrogenase regenerates NAD by converting NADH so it can be reused.

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20
Q

The Hexokinase Reaction

A
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21
Q

The Phosphohexose Isomerase Step

A
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22
Q

The Phosphofructokinase-1 Reaction (PFK-1)

A
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23
Q

Difference between Bisphosphate vs. Diphosphate

A
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24
Q

The Aldolase Reaciton

A
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25
Q

The triose phosphate isomerase reaction most closely resembles which other reaction?

Glucose to G6P

G6P to F6P

F6P to F1,6BP

F1,6BP to G3P and Dhap

A

G6P to F6P

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26
Q

When a compound is oxidized, it:

Loses water

Loses electrons

Gains electrons

Gains water

A

Loses electrons

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27
Q

Generation of a High Energy Bond

A
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28
Q

What is NAD+

A
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29
Q

Pellagra

A
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30
Q

The phosphoglycerate kinase reaction

A
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31
Q

What makes a reaction freely reversible vs. Irreversible?

A

Energy in high energy bond in the reactants is the same energy level as ATP in the product so overall energy is the same on both sides of the reactions which makes it reversible.

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32
Q

Substrate Level Phosphorylation

A

Substrate Level Phosphorylation — In the absence of Oxygen

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33
Q

Oxidative Phosphorylation

A

Oxidative Phosphorylation — Requires Oxygen.

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34
Q

Phosphoglycerate Mutase Step

A
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35
Q

Formation of ATP by Pyruvate Kinase

A
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36
Q

What are the 3 Irreversible Steps of Glycolysis?

A
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37
Q

PFK-1

A
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38
Q

Inhibitors of PFK1

A
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39
Q

Activators of PFK-1

A
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40
Q

ATP’s role in PFK-1

A

ATP = Key Inhibitor — Indicates high energy levels.

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41
Q

Where does glycolysis occur?

A

Glycolysis — Occurs in the Cytoplasm

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42
Q

Where is Citrate Made?

A

Citrate is made in the Mitochondria

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43
Q

Explain Citrate’s Role in Glycolysis

A

When Energy levels are high in the Mitochondria citrate accumulates and leaves mitochondria. When it leaves and goes into the cytoplasm it tells Glycolysis to slow down because we have lots of energy.

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44
Q

What’s AMP Role’s in Glycolysis

A

AMP tells glycolysis to speed up

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45
Q

Storing Energy

A

Can’t store ATP because if we stored energy as ATP it would feedback inhibit ATP production. That’s why we store as creatine phosphate in muscle.

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46
Q

F-2,6-BisPhosphate’s role in Glycolysis?

A

Fructose 2,6 Bisphosphate is a major activator of PFK-1 which activates glycolysis.

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47
Q

Where does F2,6BP come from?

A
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48
Q

What is velocity?

A

The rate at which the product of the reactoin is formed.

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49
Q

How does F-2,6-BP Effect the Activity Profile of

PFK-1?

A

F-2,6-BP reduces substrate concentration required for enzyme to reach 1/2 maximal velocity.

The Maximum velocity does not change but the amount of substrate required to reach that velocity is decreased.

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50
Q

Which curve is more active and which is more inhibited?

A

More active curve is to the left — enzyme is active at lower substrate concentrations.

More inhibited curve to the right

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51
Q

What are ATP’s two roles with PFK-1?

A

ATP has two roles in this enzyme — at low ATP conc. it allows it to proceed because its a substrate. But as we increase the ATP it starts to be an inhibitor. That’s why we see the curve go up then down.

Mixed allosteric function. First as a substrate then once too it becomes too much it becomes inhibited.

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52
Q

The glycolytic rate can be increased by which one of the following?

Increasing G6P levels

Increasing ATP levels

Increasing citrate levels

Increasing pyruvate levels

Increasing NAD+ levels

A

Increasing G6P levels (We increase g6p we’ll make more F6P which will increase substrate and increase the rate)

Increasing NAD+ levels — won’t allow glycolysis to increase rate unless we also increase the substrate in that specific enzyme.

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53
Q

A key difference between liver and muscle glycolysis is which one of the following?

F2,6 bp is not Important in muscle

Lactate formation Is exclusive to liver

Glucokinase vx. Hexokinase

Amp only actives in muscle

Muscle will not slow down glycolysis in presence of ATP

A

Lactate formation Is exclusive to liver

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54
Q

What hormone is released when blood glucose levels drop?

Insulin

Glucagon

Vitamin D

Acetylcholine

A

Glucagon

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55
Q

Hormonal Regulation of PFK-2 in Liver

A

R is regulatory subunit

C is catalytic subunit

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56
Q

Why don’t muscle cells respond to low blood sugar?

A

Muscle cells do not have glucagon receptors. Muscle cells don’t respond to low blood glucose.

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57
Q

When PFK2 is NOT phosphorylated

A

When PFK2 is not phosphorylated it acts as a kinase

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58
Q

When PFK2 is phosphorylated…

A

When PFK2 is phosphorylated it acts as a phosphatase

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59
Q

By phosphorylating PFK2

A

By phosphorylating PFK2 we are destroying F 2,6 BP.

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60
Q

Skeletal Muscle Isozyme of PFK-2…

A

Skeletal Muscle Isozyme of PFK2 never gets phosphorylated. PFK2 in skeletal muscle is only regulated allosterically.

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61
Q

More on PFK-2

A
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62
Q

Skeletal muscle does have protein kinase A but…

A

Skeletal muscle does have protein kinase A but it does not phosphorylate PFK2 because in the skeletal muscle it’s not a substrate for that enzyme.

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63
Q

PFK-2 Regulation in the Liver vs. Muscle

A
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64
Q

Heart PFK-2

A
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65
Q

Regulation of Hexokinase vs. Glucokinase

A
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66
Q

G6P’s effect on Glucokinase vs. Hexokinase

A

G6p is an allosteric inhibitor of Hexokinase. G6p is not however a regulator of Glucokinase.

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67
Q

3 Forms of Pyruvate Kinase

A
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68
Q

L-Form of Pyruvate Kinase

A
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69
Q

M-Form of Pyruvate Kinase

A
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70
Q

Explain the Role of cAMP dependent protein kinase in the liver

A
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71
Q

Which one of these correctly describes the activity state of key glycolytic enzymes if you go for a run after waking up without eating breakfast.

Muscle and liver pfk1 are active

Only liver pfk1 is active

Muscle and liver pfk2 are active (kinase activity)

Only liver Pfk2 is active (kinase activity)

Only muscle PFK-1 and PFK2 kinase activities are active

A

Only muscle PFK-1 and PFK2 kinase activities are active

Muscle and liver pfk2 are active (kinase activity) — no in the liver its the phosphatase activity

Only liver Pfk2 is active (kinase activity) — no again it’s phosphatase activity is active

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72
Q

Allosteric Regulation vs. Covalent Modification

A
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73
Q

Regulation of Liver vs. Skeletal Muscle

A
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74
Q

Where does the liver get its energy for its own function when blood glucose is low?

A

Liver gets its own energy from the Fatty Acids which are released when glucagon is present.

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75
Q

Arsenic poisoning is due to the presence of arsenate and arsenite in the toxin arsenal was as a phosphate analog but arseon-anhydride bonds are unstable and rapidly hydrolyzed in water which glycolytic enzyme catalyzers a reaction that would be most affected by the presence of arsenate:

Glucokinase

PFK -1

PFK-2

Glyceraldehyde 3-phosphate dehydrogenase

Pyruvate Kinase

Lactate dehydrogenase

A

Glyceraldehyde 3-phosphate dehydrogenase (only enzyme that uses a free inorganic phosphate so it will be affected)

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76
Q

Fluoride inhibits enolase, and is used in water and toothpaste to keep oral bacteria from growing and creating dental caries. Red blood cell pyruvate kinase deficiency can lead to mild anemia. which of the following glycolytic intermediates would accumulate in common in both of these conditions?

Pyruvate only

Glucose only

Pep only

3-phosphoglycerate only

2-phosphoglycerate only

Glyceraldehyde 3-phosphate only

1, 2, 3

4, 5, 6

1, 3, 5

2, 4, 6

A

Pyruvate only

Glucose only

Pep only

3-phosphoglycerate only

2-phosphoglycerate only

Glyceraldehyde 3-phosphate only

1, e, 3

4, 5, 6

1, 3, 5

2, 4, 6

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77
Q

Differential Regulation

A
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78
Q

Describe the Cori Cycle

A
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79
Q

Why Enzyme Kinetics?

A
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80
Q

Enzyme Kinetics

A
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81
Q

What are the two Major Assumptions in Enzyme Kinetics

A
82
Q

K1

A

Rate constant for ES complex Formation

83
Q

K2

A

Rate constant for ES complex Breakdown

84
Q

K3

A

Rate consent for Product formation

85
Q

Derive the Michaelis-Menton Equation based on the assumptions made.

A
86
Q

What happens when V = 1/2 Vmax

A
87
Q

Km for glucokinase vs. Hexokinase

A

Km for Glucokinase is about 7mmolar which is much higher than km for hexokinase

88
Q

Is Km a true measure for affinity?

A

Km for Glucokinase is about 7mmolar which is much higher than km for hexokinase

This is is not a true measurement for affinity

89
Q

Graphical Representation of the Michaelis Menton Equation

A
90
Q

Lineweaver Burk Derivation

A
91
Q

Lineweaver Burk Plot

A
92
Q

Km and Vmax

A
93
Q

Competitive Inhibitors

A
94
Q

Non-Competitive Inhibitors

A
95
Q

Explain the concept of Apparent Km

A

When an inhibitor is present you need more substrate to kickoff inhibitor and get to the necessary km that is half Vmax. That’s why we call it the apparent km because the concentration is much more not because the actual km has changed but because you also have to take into account additional substrate amount to kick off the inhibitor.

96
Q

How do most drugs effect enzyme activity?

A

Most drugs inhibit enzyme activity.

97
Q

Lineweaver Burk of Competitive Inhibition

A
98
Q

Lineweaver Burk Plot for Non-Competitive Inhibition

A
99
Q

If the Vmax of enzyme 1 is 20 units per sec and the Vmax of enzyme 2 is 10 units/sec then the Km”s of the enzymes can be related by which of the following?

The km of enzyme 1 is one half that of enzyme 2

We cannot determine it from the data we have.

A

We cannot determine it from the data we have.

100
Q

Summary of Enzyme Kinetics

A
101
Q

Summary of Inhibitors in Enzyme Kinetics

A
102
Q
A

Hyperglycemia

103
Q

An individual has inherertided a mutation in the regulatory subunit of pea which has greatly reduced affinity for camp during fasting this mutation lead to which one of the following?

Hypoglycemia

Hyperglycemia

Hyperactive muscle glycolysis

Hyperactive liver glycolysis

A

Hypoglycemia

104
Q

A classification of pre-obese refers to a BMI of

15-18.4

18.5 -24.9

25-29.9

30-39.9

> 40

A

25-29.9

105
Q

What is the velocity of an enzyme catalyses reaction when [S] is 0.5 k

Vmax

  1. 25 vmax
  2. 33 vmax
  3. 5 vmax
  4. 67 vmax
  5. 75 vmax
A

0.33 vmax

106
Q

Dietary fructose is obtained primarily from which one of the following?

Starch

Milk

Apples

French Fries

Pizza

A

Apples

107
Q

Fructose Metabolism

A
108
Q

Fructose and Galactose come from…

A

Fructose and Galactose come from dishaccarides.

They enter glycolysis but in different ways.

109
Q

Where does all of our fructose get metabolised?

A

Liver metabolizes all of our Fructose

110
Q

Features of Fructokinase

A

This enzyme has a low Km and High Vmax* — Low substrate concentration and works very fast.

111
Q

Aldolase B

A

Aldolase B — Found in Liver— Only in liver— F1,6BP

112
Q

Which key regulatory step is skipped when fructose enters glycolysis?

Hexokinase

Glucokinase

Gructokinase

PFK-1

PFK-2

Pyruvate

A

PFK-1 — Which means it’s hard to regulate

113
Q

IV Fructose Loading

A
115
Q

Is IV Fructose loading the same as eating excess fructose?

A

No, Direct injection of fructose into the veins not through eating

116
Q

Fructokinase Velocity and Substrate Concentration

A

High Vmax but low Km

117
Q

Essential Fructosuria

A
118
Q

Explain what happens when you give someone IV Glucose

A

If you give someone IV fructose you get lots of lactic acid which overcomes the buffering capacity of the blood and blood pH begins to drop — not good

Individuals given IV fructose almost died so we use IV glucose instead.

119
Q

Hereditary Fructose Intolerance

A
121
Q

Is Essential Fructosuria Worrysome?

A

No ill effects from this disorder. But because there’s fructose in the urine it gives a positive test for a reducing sugar test. Glucose also tests positive which is used to test for diabetes so fructosuria can misleadingly tell you someone has diabetes

123
Q

Explain how Hereditary Fructose Intolerance is Managed

A

Self-limiting disease — if born with mutation — they would throw up after apple sauce and you’d then stop giving it to them. The treatment is an appropriate diet that doesn’t have fructose.

124
Q

Aldolase A and C vs. Aldose B

A

Aldolase A and C cannot split F-1,6-BP but B can split either F1P or F16BP

125
Q

What happens when F1P is high

A

When F1P is high you have a problem with glycogen degradation

126
Q

How Does Uric Acid Effect the Kidney?

A

Uric acid blocks ability of the kidney to remove lactate from the blood making acidosis worse.

127
Q

The net yield of ATP when fructose is converted to 2 Molecules of Pyruvate is:

No ATP

1 ATP

2 ATP

3 ATP

4 ATP

A

2 ATP

128
Q

How Much Net Yeild of ATP does Fructose use compared to Glucose

A

Fructose has the same net yield of ATP as Glucose

129
Q

Galactose Metabolism

A
130
Q

What is Galactosemia?

A
131
Q

Galactosemia Classic Type

A
132
Q

Non-Classical Galactosemia

A
133
Q

What foods have Galactose?

A

Galactose is from anything derived from milk. E.g. Cheese

134
Q

Galactose vs. Glucose

A

Galactose is an epimer of Glucose — Hydroxyl is on opposite side at carbon 4 of glucose.

135
Q

UDP-Glucose

A

UDP-Glucose is an Activated Glucose

UDP-Glucose is always regenerate so you only need small amount

138
Q

The Polyol Pathway

A
140
Q

How do you treat Galactosemia?

A

By removing Galactose from Diet.

141
Q

Phosphoglucomutase

A

Phosphoglucomutase is necessary to get glucose from Glycogen.

142
Q

Digestion and Absorbtion of Carbohydrates

A
143
Q

Starch

A
144
Q

Dietary Carbohydrates

A
145
Q

Digestion of Starch

A
146
Q

Galactitol

A

Galactitol creates an osmotic Imbalance in the eye.

147
Q

Cataract Formation in Galactosemia

A

Rapid formation of cataracts in both classical and non-classical

148
Q

Starch Digestion Continued

A
149
Q

The net yield when one mole of galactose is converted to 2 moles of pyruvate is:

0 Moles of ATP

1 Mole of ATP

2 Moles of ATP

3 Moles of ATP

4 Moles of ATP

A

2 Moles of ATP

Just like glucose it only takes one ATP to get from Galactose to G6P just like one Glucose takes one ATP to Get to G-6P

150
Q

Brush Border Membrane of Intestinal Epithelial Cells

A
151
Q

Sucrase Iso-Multase Complex

A
152
Q

Glucoamalyse Complex

A
153
Q

More Brush Border Enzymes

A
154
Q

Isomaltase Enzyme Activity

A
155
Q

Sucrase, Isomaltase, and glucoamylase enzyme activities

A
156
Q

Lactase Activity

A
157
Q

Lactose Intolerance

A
158
Q

Transport of Monosaccharides

A

Transporter allows glucose to be concentrated inside the lumen.

Fructose only transported via a Facilitated transporter.

Glucose transport is coupled to sodium transport

Sodium potassium ATP-ase Na is primary transported and Glucosed is secondarily transported.

Sodium gradient drives Glucose active transport

Sodium Potassium ATP-ase uses ATP and 3 Na in to drive movement of glucose and galactose in.

160
Q

Glucose Accumulation and Diabetes

A

Glucose accumulation, from diabetes, will be reduced to sorbitol which will get trapped in the eye and forms cataracts.

161
Q

High Glucose levels and HbA1C levels?

A

High glucose leads to non-enzymatic glycosylation— hbA1C is elevated because it is a glycosylated protein. HbAIC is used as a measure of glycemic control, how well you can control your blood sugar. Is it greater than the normal 5%?

162
Q

What happens to Nervous System when Glucose levels are high?

A

Nervous system proteins also gets glycosylated which leads to neuropathy.

165
Q

Glut -1

A

GLut1 is a low km transporter

166
Q

Glut 2

A
167
Q

Glut 3

A

Glut 3— two glucose transporters are needed to get glucose into the neurons.

168
Q

Glut 4

A
169
Q

Glut 5

A
170
Q

Glut 1 Deficiency Syndrome

A
171
Q

Glycolysis and Diabetes

A
172
Q

Glycolysis and Diabetes in the Liver

A
175
Q

Where do Proteins Get Digested?

A

Proteins get digested in the stomach.

176
Q

Gluconeogenesis

A
177
Q

Reactions that reverse the Pyruvate Kinase Step of Glycolysis

A
178
Q

Reaction that Reverses the PFK-1 Reaction

A
179
Q

Reaction that Reverses Glucokinase (Liver and Pancrease)/Hexokinase (all other tissues)

A
180
Q

Are fats and carbs digested in the somach?

A

Fats and carbs are not digested in the stomach.

182
Q

Inflammation of the Pancreas

A

Inflammation of Pancreas will lead to pancreatic amylase in the blood which makes it a marker for Pancreatic inflammation.

183
Q

Compartmentation issues in Gluconeogenesis

A
184
Q

Draw out the overview of regulation of Gluconeogenesis

A
185
Q

Regulation of Glycolysis and Gluconeogenesis when levels of blood sugar is high

A
186
Q

Regualtion of Glycolysis and Gluconeogenesis when Glucose levels are low in the blood

A
187
Q

Summary of Gluconeogenesis

A
188
Q

Signal Transduction

A
189
Q

Structure of the Insulin Receptor

A
190
Q

Tyrosine Kinase Activity

A
191
Q

What is IRS-1

A
192
Q

Glucagon Receptor

A
193
Q

G-Proteins

A
194
Q

G - Protein Cycle

A
195
Q

G-Protein Regulation

A
197
Q

Cholera and Pertussis

A
198
Q

Diabetes Revisited

A
199
Q

Summary of Signal Transduction

A
208
Q

Transporters…

A

Transporter allows glucose to be concentrated inside the lumen.

209
Q

Fructose and Transport

A

Fructose only transported via a Facilitated transporter.

210
Q

What is Glucose Transport Coupled With?

A

Glucose transport is coupled to sodium transport

211
Q

Primary vs. Secondary Transport

A

Sodium potassium ATP-ase Na is primary transported and Glucosed is secondarily transported.

212
Q

What drives glucose into serosal side of the intestine?

A

Sodium gradient drives Glucose active transport

213
Q

What does the sodium potassium pump use?

A

Sodium Potassium ATP-ase uses ATP and 3 Na in to drive movement of glucose and galactose in.

222
Q

NASH

A

Non-Alcoholic Steatohepatitis

NASH— Fat accumulation in the liver. — Found in diabetics with poor control of sugar levels.

223
Q

Young girl has been diagnosed with type 1 diabetes. one of her symptoms was blurry vision, which occurred tue to which of the following:

Elevated glucose in the urine

Elevated glucose in the blood

The production of HbA1c

Altered Glut4 Proteins

Reduction of Glucose

Oxidation of glucose

A

Reduction of Glucose — ( Glucose going to sorbitol is a reduction of glucose — sorbitol leads to blurred vision)

224
Q

Which one of the following enzymatic reactions needs to be bypassed in synthesizing glucose from pyruvate.

G3PDH

Enolase

Phosphoglyrcerate kinase

Pyruvate kinase

Aldolase

A

Pyruvate kinase

229
Q

Starting with two molecules of lactate, ho many molecules of ATP/GTP are required to synthesize one glucose molecule?

2

3

4

5

6

7

8

A

6

230
Q

Anabolic vs. Catabolic

A

Always takes more energy to make something than to degrade it.

231
Q

What is a symptom for someone with a defect of FATTY Acid Oxidation

A

Hypoglycemia because a lack of energy to perform gluconeogenesis.

245
Q

If the GTPase activity of a G protein were mutated, and rendered inactive, which one of the following would occur?

Inactivation of a G protein activity

Constant activation of G protein Activity

No effect on G Protein

A

Constant activation of G protein Activity

246
Q

Galactose Metabolismm

A

Fundamentals of Molecular Medicine (77 decks)

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