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Metabolism, Molecular, and Pharmacogenomics (MMP) > Metabolism (Quiz 1) > Flashcards

Metabolism (Quiz 1) Flashcards

TCA, Glycolysis, Oxidative Phosphorylation, Fatty Acids, Ketones, ETC, cellular energetics

1
Q

Why is metabolism important?

A

Without metabolism, life would cease to exist. We need it to maintain life.

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2
Q

Definition of metabolism.

A

Generation and storage of energy and biosynthetic intermediates from ingested nutrients.

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3
Q

What do cell utilize for energy?

A

ATP

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4
Q

How is ATP obtained?

A

ATP is obtained through a process called respiration. This is the oxidation of fuels to CO2 and H20.

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5
Q

What are unused fuels stored as?

A

Triacylglyerides in adipose tissue

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6
Q

Describe the ATP-ADP cycle.

A

This is the generation and utilization of ATP.

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7
Q

What is respiration?

A

Respiration is the oxidation of fuels to generate ATP.

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8
Q

What are the two main processes that oxidize fuels to generate ATP?

A

TCA cycle and oxidative phosphorylation

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9
Q

How many kilojoules is in one calorie?

A

1 kcal= 4.18 kJ

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10
Q

What form is glucose stored in the body?

A

Glucose is stored as glycogen

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11
Q

Where is glycogen primarily stored?

A

Glycogen is primarily stored in the liver and muscle.

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12
Q

What is the basic structure of proteins?

A

Proteins are amino acids linked together via peptide bonds.

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13
Q

What happens to proteins in metabolism?

A

Proteins are broken down into amino acids during metabolism.

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14
Q

How are triacylglycerols transported in the body?

A

Triacylglycerols are transported via lipoproteins.

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15
Q

What is the basic structure of a triacylglycerol?

A

Triacylglycerols are long chains of carbons linked together.

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16
Q

How is the bulk of our reserved energy stored?

A

Bulk of energy stored as triacylglycerides in adipose tissue (85%). Around 15% is stored as protein in our muscle.

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17
Q

What is the resting metabolic rate (RMR)?

A

This is the amount of energy needed to maintain basic life functions.

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18
Q

What is the daily energy expenditure (DEE)?

A

This is the RMR + physical activity + food digestion and processing

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19
Q

What is the goal of the DEE?

A

The goal of DEE is to maintain caloric needs for physiologic processes to generate needed ATP.

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20
Q

What are the 3 basic fates of glucose?

A

A. Oxidized for energy
B. Stored as glycogen or triacylglycerols
C. Synthesis of compounds

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21
Q

What are the 3 basic fats of amino acids?

A

A. Oxidized for energy
B. Protein synthesis
C. Synthesis of nitrogen containing compounds

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22
Q

What are the 3 basic fates of triacylglycerides?

A

A. Oxidized for energy
B. Storage as triacylglycerides
C. Synthesis of membrane lipids

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23
Q

What are the 3 metabolic states?

A

A. Basal (fasting) state
B. Postprandial (fed) state
C. Starved state

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24
Q

What is considered the basal (fasting) state?

A

This is when you wake up in the morning after eating dinner the night before. Blood glucose levels are lower but still in the normal range.

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25
Q

How are blood glucose levels still within the normal range after sleeping?

A

The liver regulates blood glucose levels at all times in order to fuel the brain and RBCs.

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26
Q

What organ is the main regulator of gluconeogenesis and glycogenolysis?

A

Liver

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27
Q

What is gluconeogenesis?

A

This is the production of glucose from non-carbohydrate sources including lactate, glycerol, and glucogenic amino acids.

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28
Q

What is glycogenolysis?

A

This is the breakdown of glycogen to glucose.

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29
Q

Why does the liver induce glycogenolysis?

A

Liver does this to make glucose to release into blood to supply rest of the body.

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30
Q

Why does skeletal muscle induce glycogenolysis?

A

Skeletal muscle breaks down glycogen into glucose in order to supply itself.

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31
Q

What has happened to glycogen storage in the liver once the starved state is entered?

A

Glycogen storage is empty and the liver must pull from outside sources.
Liver takes triacylglycerides from adipose tissue to fuel itself and make ketone bodies for the brain. Fatty acids from triacylglycerides can be used in muscle to limit protein breakdown.

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31
Q

What happens to glucose in the postprandial (fed) state?

A

Travels to liver and fuels hepatocytes and replenishes glycogen storage there. Excess glucose is converted to triacylglycerides and transported out to be stored in adipose tissue.

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32
Q

What is characterized by the starved state?

A

This is when the body has not received fuel for 4 or more days. Blood glucose is in the very bottom of normal range.

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33
Q

What are the major essential minerals?

A

Sodium
Potassium
Chlorine
Calcium
Phosphorus
Magnesium
Sulfur (not as important lol)

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34
Q

What are the essential fatty acids?

A

alpha-linoleic and alpha-linolenic acid. Essential as they are used to make EPA and DHA which make eicosanoids.

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35
Q

ATP production occurs via the ______________ of carbohydrates, fats, and proteins.

A

oxidation

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36
Q

Glycogenolysis is ___________.

A

Breakdown of glycogen to glucose

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37
Q

In the starved state, alternative fuels are utilized. These include _________.

A

Ketone bodies. Fatty acids can be used.

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38
Q

What is the process in which ATP becomes ADP and Pi?

A

Hydrolysis (water used to break a bond)

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39
Q

How much energy is released when ATP is cleaved into ADP and Pi?

A

-7.3 kcal/mol

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40
Q

Why is the gamma phosphate cleaved off ATP and not the beta phosphate?

A

The gamma phosphate releases more energy when cleaved while the beta phosphate releases less energy (-3.4 kcal/mol)

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41
Q

What is Gibbs Free Energy?

A

This is the energy change for a reaction given 1M of the substrate under standard conditions.

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42
Q

Why do metabolic pathways have an overall negative Gibbs Free Energy?

A

Negative free energy makes the reaction favorable and favors the production of ATP.

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43
Q

Why does the synthesis of ATP sometimes have positive Gibbs Free Energy?

A

Some energy is required to produce the ATP further into the process.

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44
Q

Overall, negative Gibbs Free Energy signifies a ____________ reaction.

A

Favorable

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45
Q

What are the 1st and 2nd laws of thermodynamics?

A
  1. Energy is conserved
  2. Universe tends towards disorder
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46
Q

What are the 3 ways in which cells utilize ATP to do work?

A
  1. Mechanical work
  2. Transport work (maintain conc. gradients, membrane states, etc)
  3. Biochemical work (anabolic pathways)
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47
Q

What organ system uses the most ATP?

A

Kidneys. This is due to the constant filtering of blood done with concentration gradients.

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47
Q

What is the phosphoglucomutase reaction?

A

Phosphoglucomutase is the enzyme that converts glucose-6-phosphate (G6P) to glucose-1-phosphate (G1P) and vice versa.

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47
Q

Why is the G6P important in the cell?

A

G6P cannot leave the cell therefor it sequesters an energy source inside the cell.

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48
Q

What is the free energy change when phosphoglucomutase converts G6P to G1P?

A

+1.6 kcal/mol

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48
Q

At cell equilibrium, what is the ratio of G1P to G6P?

A

6:94
This makes sense as the phosphoglucomutase reaction converting G6P to G1P is not favorable.

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48
Q

Through the process of cellular respiration, chemical bonds are converted to what key thing?

A

Reduced forms of electron-accepting coenzymes (NAD+ and FAD)

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49
Q

When energy in needed in the cell, G6P goes into __________. However, if there is enough energy already, G6P replenishes glycogen storage via _____________.

A

Glycolysis
Glycogenesis

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49
Q

What type of gradient is created in the inner mitochondrial membrane in order to push forward oxidative phosphorylation?

A

Electrochemical gradient. This is created through the transfer of electrons to O2 in the ETC.

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49
Q

What drives the phosphoglucomutase reaction?

A

Changes in equilibrium between G1P and G6P. (loss of product, G1P, converts this reaction to a favorable one)

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49
Q

When NAD+ is reduced (GER), how many electrons does it accept?

A

NAD+ accepts 1 H+

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50
Q

What FAD is reduced (GER), how many electrons does it accept?

A

FAD accepts 2 H+

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51
Q

NAD and FAD donate electrons to _______ during the ETC.

A

O2

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52
Q

How much energy is available for ATP synthesis from NADH?

A

-53 kcal

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53
Q

How much energy is available for ATP synthesis from FADH2?

A

-41 kcal

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54
Q

Why is oxygen the main electron acceptor in this whole process?

A

Oxygen has the greatest reduction potential meaning is it the most willing molecule to accept electrons and be reduced (GER). Basically, the transfer of electrons from NADH and FADH2 to O2 is energetically favorable.

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55
Q

What is anaerobic glycolysis?

A

Anaerobic glycolysis is the degradation of glucose without electron transfer to O2.

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56
Q

Why would cells need to be able to produce glucose when no O2 is available?

A

Exercise, heart attack, and stroke, the body still needs to have ATP without proper oxygen levels.

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57
Q

How is ATP created in anaerobic glycolysis?

A

ATP is created via substrate level phosphorylation during anaerobic glycolysis.

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58
Q

What is the main substrate for the TCA cycle?

A

Acetyl-CoA

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59
Q

How many NADH and FADH2 are produced in one TCA cycle?

A

3 NADH
1 FADH2

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60
Q

What is the net energy yield from one turn of the TCA cycle?

A

10 ATP

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61
Q

How many CO2 are produced in one turn of the TCA cycle?

A

2 CO2

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62
Q

What are the 3 fuel groups that can be directly converted to Acetyl-CoA?

A

Fatty acid palmitate
Ketone body acetoacetate
Ethanol

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63
Q

What are the 2 fuel groups that are converted to pyruvate before becoming Acetyl-CoA?

A

Glucose
Animo acid alanine

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64
Q

What is the pyruvate dehydrogenase complex (PDC)?

A

This is the conversion of pyruvate to Acetyl-CoA. It is a main regulatory point in the entire process.

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65
Q

What are the positive allosteric activators of the kinase that phosphorylates the PDC to make it inactive?

A

Acetyl Coa and NADH.
Acetyl CoA and NADH turn on the kinase that turns off the PDC because too much Acetyl-CoA and NADH means the cycle does not need to continue at the moment to make more of those molecules.

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66
Q

What are the compounds that inhibit the kinase the phosphylates the PDC to make it inactive?

A

ADP and Pyruvate
ADP and pyruvate inhibit the kinase and let the PDC be active because ADP signals low energy and more ATP is needed while more pyruvate means that more Acetyl-CoA needs to be made.

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67
Q

What is the 1st step of the TCA cycle?

A

Acetyl-CoA + Oxaloacetate ——-> Citrate

Via citrate synthase

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68
Q

What is the 2nd step of TCA cycle?

A

Citrate ———-> Isocitrate

Via aconitase

69
Q

What is the function of dehydrogenase enzymes?

A

They convert NADH or FADH2 through oxidation and decarboxylation

70
Q

What is the 3rd step of the TCA cycle?

A

Isocitrate ——–> a-ketoglutarate

via Isocitrate dehydrogenase

Produces a NADH and CO2

71
Q

What is the 4th step of the TCA cycle?P

A

a-ketoglutarate ——-> succinyl-CoA

via a-ketoglutarate dehydrogenase

Produces a NADH and CO2

72
Q

What is the 5th step of the TCA cycle?

A

Succinyl-CoA ——> succinate

via succinate thiokinase

Produces a GTP

73
Q

The creation of GTP from GDP and Pi in the conversion of succinyl-CoA to succinate is an example of what?

A

Substrate level phosphorylation

74
Q

What is the 6th step of the TCA cycle?

A

Succinate —–> Fumarate

via succinate dehydrogenase

Produces FADH2

75
Q

What is the 7th step of the TCA cycle?

A

Fumarate ——–> malate

via fumerase

76
Q

What is the 8th step of the TCA cycle?

A

Malate ——-> Oxaloacetate

via malate dehydrogenase

Produces a NADH

77
Q

What is the total energy available from the acetyl group that initiates the TCA cycle?

A

228 kcal/mole

78
Q

Is the TCA efficient?

A

Yes. The TCA cycle conserves 90% of the energy is generates. Only a small amount of of energy is lost as heat (13 kcals)

79
Q

What are the 3 most favorable reactions in the TCA cycle?

A
  1. Oxaloacetate and acetyl CoA to citrate via citrate synthase (-7.7kcal)
  2. Isocitrate to alpha-ketoglutarate via isocitrate dehydrogenase (-5.3kcal)
  3. alpha-ketoglutarate to succinyl-CoA via alpha-ketoglutarate dehydrogenase (-8kcal)
80
Q

Why is the accumulation of malate a favored reaction while fasting
(OAA to malate)?

A

Malate to OAA is favored because the liver uses it during fasting. Malate is used by the liver for gluconeogenesis.

81
Q

During what state is malate accumulation favored?

A

During the fasting state as the liver uses malate in gluconeogenesis.

82
Q

What is the malate-aspartate shuttle?

A

This is the shuttle that pull malate in and out of the mitochondria for gluconeogenesis and the shuttle of reducing equivalents made in glycolysis.

83
Q

What are the two main regulators of the TCA cycle?

A

ATP/ADP ratio and NADH/NAD+ ratio

84
Q

What is the main regulator of the conversion of OAA and acetyl CoA to citrate via citrate synthase?

A

Citrate; Increased levels of citrate negatively feedbacks on citrate synthase to inhibit the production of more citrate.

85
Q

What are the main regulators of the conversion of isocitrate to alpha-ketoglutarate by isocitrate dehydrogenase?

A

ADP and Ca2+ activate isocitrate dehydrogenase to make more alpha-ketoglutarate. This make sense as ADP signals low energy levels and Ca2+ indicates increased cell signaling showing that work is being done.

NADH inhibits isocitrate dehydrogenase as it indicates that there is enough energy already present.

86
Q

What are the main regulators of the conversion of alpha-ketoglutarate to succinyl-CoA via alpha-ketoglutarate dehydrogenase?

A

Ca2+ activates alpha-ketoglutarate dehydrogenase

NADH inhibits the activity of alpha-ketoglutarate dehydrogenase

87
Q

What is the main regulator of the conversion of malate to oxaloacetate via malate dehydrogenase?

A

NADH inhibits the activation of malate dehydrogenase due to NADH signifying high energy levels and no more OAA is needed to continue to TCA cycle.

88
Q

What is the rate-limiting enzyme of the TCA cycle?

A

Isocitrate dehydrogenase

89
Q

The TCA is an open cycle. What does being an open cycle mean?

A

An open cycle means that several intermediates are pulled out based on the needs of the cell.

(Examples of this include malate for gluconeogenesis and a-ketoglutarate to make glutamate in the brain)

90
Q

What are anaplerotic reactions in the TCA cycle?

A

Anaplerotic reactions are pathways that replenish intermediates in the TCA cycle.

91
Q

How can pyruvate be used in an anaplerotic reaction in the TCA cycle?

A

Malate pulled out of TCA cycle for gluconeogenesis. Food is consumed and acetyl-CoA is formed, but no OAA is formed since there is no malate. Pyruvate makes oxaloacetate via pyruvate carboxylase in order for the TCA cycle to continue.

92
Q

What enzyme converts pyruvate to oxaloacetate?

A

Pyruvate carboxylase

93
Q

What is the chemiosmotic hypothesis?

A

Hypothesis that proposes the energy for ATP synthesis is provided by the electrochemical gradient across the inner mitochondrial membrane.

94
Q

What are the 5 requirements for oxidative phosphorlyation?

A
  1. electron donors (NADH and FADH2)
  2. Electron acceptor (O2)
  3. Intact mitochondrial membrane
  4. Components of the ETC
  5. ATP synthase
95
Q

What are the steps of oxidative phosphorylation?

A
  1. Complex I
  2. Coenzyme Q
  3. Complex III
  4. Cytochrome C
  5. Complex IV
96
Q

What are the two important characteristics of ATP synthase?

A

A. It takes 12 protons to make a full turn
B. One turn generates 3 ATPs

97
Q

Why are the 3 protein complexes in the ETC filled with iron or copper centers?

A

Iron and copper centers are good electron acceptors.

98
Q

What are the characteristics of complex I in the ETC?

A

In this complex, FMN (just a cofactor that can accept and carry electrons) accepts 2 electrons from NADH. FMN transfers the electrons to the iron center which transfers the electrons to coenzyme Q.

99
Q

Complex II is not involved in the ETC, but it involved in electron transfer. Why can it not donate electrons to the ETC?

A

Complex II cannot donate electrons to the ETC because it does not span the mitochondrial membrane.

100
Q

What type of protein is complex III of the ETC?

A

Complex III is a cytochrome meaning it is a protein that contains a bound heme.

101
Q

Where is energy released in the ETC?

A

Between complexes III and IV.

102
Q

What is the main purpose of complex IV in the ETC?

A

Complex IV uses bound copper to facilitate the collection of 4 electrons and the reduction of O2 to form H2O.

103
Q

How many protons are pumped across the membrane during the entire ETC?

A

10 protons

104
Q

How much energy is available from NADH and FADH2 in the ETC?

A

30%. The ETC is not very efficient. The ETC is a major source of heat.

105
Q

Will the transfer of electrons to oxygen from all compounds have a negative Gibbs free energy?

A

Yes.

106
Q

What is the main regulator of ATP synthase?

A

Increased ADP. More ADP is binding to ATP synthase to form ATP.

107
Q

T or F: Oxygen is used in complex I and III of the ETC, but not in IV.

A

False. Oxygen is only used in complex IV. A whole O2 accepts 4 electrons to be reduced to 2 molecules of H20.

108
Q

T or F: Without oxygen, the ETC cannot produce ATP.

A

True

108
Q

T or F: Similar to the TCA cycle, the ETC is reversible and dependent on ATP/ADP ratio within the cell.

A

False. The ETC is not reversible.

109
Q

T or F: The ETC utilizes a large portion of our body heat.

A

False. The ETC produces a large amount of body heat.

109
Q

T or F: Uncoupling reduces O2 consumption and heat production.

A

False. Uncoupling results in increased O2 consumption and heat production in order to maintain electrochemical gradient.

110
Q

What is uncoupling?

A

Uncoupling is proton leakage into the matrix of the mitochondria without going through ATP synthase.

111
Q

What are uncoupling proteins?

A

UCPs are proteins that form proton conductance channels in the inner mitochondrial membrane that move protons from the inner mitochondrial space to the matrix. The big one to know is UCP1.

112
Q

What is UCP1?

A

UCP1 is thermogenin. It is found in brown fat and function in heat production via nonshivering thermogenesis.

113
Q

More than __________ of RMR is due to maintaining the electrochemical gradient.

A

20%

114
Q

What are the two chemical uncouplers discussed in class?

A

Chemical uncouplers are lipid soluble compounds that transport protons from the cytosol to the matrix.

The two discussed were 2,4- Dinitrophenol and salicylate (degradation product of aspirin)

115
Q

How does the chemical uncoupler 2,4-Dinitrophenol work?

A

It is lipid soluble and contains a proton with a pKa near 7.2. It crosses the inner mitochondrial membrane to the outside where H+ is high (very acidic too) and picks up a proton and carries it back across the membrane. At the lower concentration of H+ ions within the mitochondrial matrix, the H+ dissociates.

116
Q

What are reactive oxygen species?

A

These are generated during the course of metabolism due to oxygen not getting 4e-.

117
Q

Where is the major site of superoxide formation?

A

Coenzyme Q in the ETC. Coenzyme Q can add just 1 electron to oxygen forming superoxide.

118
Q

What is one drug metabolizing enzyme that makes many free radicals?

A

CYP450

119
Q

What are the 5 amino acids most susceptible to free radical damage?

A

Histidine
Cysteine
Arginine
Methionine
Proline

Protein damage can cause it to fragment and cross-link leading to protein degradation.

119
Q

What types of cellular damage can occur due to free radicals?

A

Protein and DNA damage

120
Q

What are the forms of protection from free radicals?

A

Cellular compartmentation
Antioxidant defense enzymes
Antioxidants
Metal

121
Q

What are the two enzymes that break down reactive oxygen species during cell compartmentation?

A
  1. Superoxide Dismutase- converts superoxide (O2-) to H2O2 and O2
    (primary defense against oxidative stress)
  2. Catalase- reduces H2O2 to H2O
122
Q

What is glutathione regulation of oxidative damage? (Glutathione redox cycle)

A

Glutathione peroxidase reduce H2O2 to 2 molecules of water. In that process, two molecules of glutathione form glutathione disulfide. Glutathione disulfide is converted back to glutathione with input from NADPH and glutathione reductase.

123
Q

What are the 5 nonenzymatic free radical scavengers?

A
  1. Vitamin E
  2. Vitamin C
  3. B-carotene
  4. Uric Acid
  5. Melatonin
124
Q

What is the goal of mitochondrial membrane transport?

A

The goal is to get ATP out of the mitochondrial matrix and bring ADP in. Other goals include bringing in phosphate groups, pyruvate, and H+.

125
Q

What is the function of the ATP-ADP translocase in mitochondrial membrane transport?

A

The ATP-ADP translocase is an antiporter that brings in ADP to the mitochondrial matrix and kicks ATP out.

126
Q

How do phosphate groups and pyruvate get into the mitochondrial matrix?

A

Phosphate groups and pyruvate get into the mitochondrial matrix along with H+ using symporters that are driven by the electrochemical gradient.

127
Q

What are the structural components of ATP synthase?

A

F1 headpiece of alpha and beta dimers and an F0 pore of C subunits.

128
Q

T or F: Electron transport in the ETC is random and generates ATP.

A

False. Electron transport is done to get keep the electrochemical gradient and ATP is generated by ATP synthase.

129
Q

Where does the cellular process of glycolysis occur?

A

The cytosol

130
Q

What is the net yield of energy from glycolysis?

A

2 ATP (4 are made IN TOTAL but 2 are used in the preparative phase), 2 NADH, and 2 Pyruvate all from 1 glucose molecule

(glucose is 6 carbons and pyruvate is 3 so makes sense why 2 pyruvate are made)

131
Q

What are the two general phases of glycolysis?

A

Preparative phase- 2 ATPs used
ATP-generating phase- 4 ATP and 2 NADH created

132
Q

What is the 1st step of glycolysis?

A

Glucose ———> glucose-6-phosphate via hexokinase (glucokinase in the liver).

This step uses ATP

133
Q

What is the 2nd step of glycolysis?

A

Glucose-6-phosphate ———> fructose-6-phosphate via phosphoglucose isomerase

134
Q

What is the 3rd step of glycolysis?

A

Fructose-6-phosphate ——-> fructose-1,6-bisphosphate via phosphofructokinase-1

This step uses ATP, is irreversible, and commits glucose to glycolysis

135
Q

What is the 4th step of glycolysis?

A

Fructose-1,6-bisphosphate ——> glyceraldehyde-3-phosphate (OR Dihydroxyacetone phosphate) via aldolase

136
Q

What enzyme interconverts glyceraldehyde-3-phosphate and Dihydroxyacetone phosphate?

A

Triose phosphate isomerase

137
Q

What is the 5th step of glycolysis?

A

Glyceraldehyde-3-phosphate ——————>1,3-bisphosphoglycerate via glyceraldehyde-3-phosphate dehydrogenase

This step produces an NADH

138
Q

What is the 6th step of glycolysis?

A

1,3-bisphosphoglycerate ——> 3-phosphoglycerate via phosphoglycerate kinase

This step produces an ATP

139
Q

What is the 7th step of glycolysis?

A

3-phosphoglycerate ——> 2-phosphoglycerate via phosphoglyceromutase

140
Q

What is the 8th step of glycolysis?

A

2-phosphoglycerate ——> phosphoenolpyruvate via enolase

141
Q

What is the 9th and final step of glycolysis?

A

Phosphoenolpyruvate ——> pyruvate via pyruvate kinase

This step produces an ATP

142
Q

What is the overall negative energy of glycolysis?

A

-22kcal/mol

143
Q

What is the glycerol-3-phosphate shuttle?

A

This is a shuttle used in glycolysis to bring in reducing equivalent NADH to the mitochondria. DHAP is converted to glyercol-3-phosphate via cytosolic glycerol-3-phosphate dehydrogenase (takes H+ from NADH and gives to DHAP). Glycerol-3-phosphate can cross into mitochondria where is it converted back to DHAP via mitochondrial glycerol-3-phosphate dehydrogenase by donating H+ from it to FAD. The whole goal is to bring in the H+ to mitochondria for ETC.

144
Q

What is the malate-aspartate shuttle?

A

This shuttle is an antiporter focused on getting NaDH from glycolysis into mitochondria. Oxaloacetate (OAA) receives the electrons from NaDH via malate dehydrogenase to form malate. Malate passes through membrane into mitochondria. Malate then donates the H+ to NAD to form NADH via malate dehydrogenase and that reform oxaloacetate. OAA is then tranamininated to aspartate and that can cross the membrane back into the cytosol. When transaminated, glutamate becomes alpha-ketogluterate and that can cross the membrane and reenter to cytosol.

145
Q

What is the goal of anaerobic glycolysis?

A

It uses pyruvate to form lactate without oxygen via lactate dehydrogenase.

146
Q

What happens to lactate once it is created?

A

It is taken up by the liver, heart, and skeletal muscle and can be oxidized back to pyruvate for gluconeogenesis. (cori cycle)

147
Q

What regulates enzymes involved in glycolysis?

A

Energy

148
Q

What molecule regulates hexokinase in glycolysis?

A

Glucose-6-phosphate inhibits hexokinase in glycolysis.

149
Q

What molecules regulate phosphofructokinase-1 (PFK1) in glycolysis?

A

AMP and Fructose-2,6-bisphosphate activate PFK1. ATP and citrate inhibit PFK1.

150
Q

What molecules regulate pyruvate kinase in glycolysis?

A

Fructose-1,6-bisphosphate activates pyruvate kinase. ATP inhibits pyruvate kinase.

151
Q

Why is glucokinase not inhibited by high levels of glucose-6-phosphate but hexokinase is?

A

In the liver, where glucokinase is present, it wants to keep converting glucose to glucose-6-phosphate so it can store it as glycogen. Glucokinase also has a high Km and Vmax

152
Q

What is the rate-limiting enzyme of glycolysis?

A

Phosphofructokinase-1 (PFK1)

153
Q

What is the major inhibitor of PFK1?

A

ATP!

154
Q

What is the name of the process that creates ATP from fatty acids?

A

Beta-oxidation

155
Q

How do fatty acids travel in the blood?

A

They travel in the hydrophobic binding pocket of albumin

156
Q

How are fatty acids activated?

A

FAs are activated by Acyl CoA Synthetase. It activates FAs by attaching a phosphate group donated by ATP. FAs are then named fatty acyl CoA.

157
Q

What enzyme converts fatty acyl CoA to fatty acylcarnitine so it can cross into the inner mitochondrial membrane?

A

Carnitine Palmitoyl Transferase -1 (CTP1)

158
Q

What transporters brings fatty acylcarnitine through the inner mitochondrial membrane?

A

Carnitine Acylcarnitine translocase

159
Q

Once fatty acylcarnitine enters the inner mitochondrial membrane, what is is converted to and what enzyme does this?

A

Fatty Acylcarnitine is converted back into fatty acyl CoA via CPTII. At this point in the inner mitochondria, it can undergo beta-oxidation.

160
Q

Where does beta-oxidation occur within the cell?

A

Mitochondrial matrix

161
Q

What is the goal of beta-oxidation?

A

The goal is to produce reducing equivalents and acetyl CoA to enter the TCA cycle. Acetyl CoA can also be used to make keton bodies.

162
Q

What is the 1st step of beta-oxidation?

A

Fatty acyl CoA ——-> trans fatty enoyl CoA via acyl CoA dehydrogenase

Acyl CoA dehydrogenase oxidizes the alpha and beta positions

Produces an FADH2 (can make 1.5 ATP)

163
Q

What is the 2nd step of beta-oxidation?

A

Trans fatty enoyl CoA ——-> L-beta-hydroxy Acyl CoA via Enoyl CoA Hydratase

Enoyl CoA Hydratase oxidizes the beta position

Uses H20

164
Q

What is the 3rd step of beta-oxidation?

A

L-beta hydroxy Acyl CoA ——-> Beta-keto acyl CoA via beta-hydroxy Acyl CoA dehydrogenase

Oxidation of beta position

Creates NaDH (makes 2.5 ATP)

165
Q

What is the 4th step of beta-oxidation?

A

Beta-keto acyl CoA ——–> fatty acyl CoA and Acetyl CoA via beta-keto thiolase

cleavage of an acetyl CoA here

uses a CoASH

166
Q

What happens if unsaturated fatty acids are used in beta-oxidation?

A

Beta-oxidation proceeds as normal until the double bonds are encountered.

167
Q

What is the enzyme that converts a cis double bond to a trans double bond in the beta oxidation of unsaturated fatty acids?

A

Enoyl CoA Isomerase

168
Q

What is left is you start with an odd number chain length fatty acid for beta oxidation?

A

3-Carbon fatty acid called propionyl CoA is left. That is converted to succinyl CoA and enters the TCA cycle.

169
Q

Energy is released when fatty acids are converted to _______.

A

Acetyl CoA

170
Q

What is beta oxidation regulated by?

A

The energy needs of the cell

171
Q

What is the most important place that uses ketone bodies as fuel?

A

Brain

172
Q

Can red blood cells use ketone bodies as a fuel source?

A

No, they have no mitochondria which is where ketone bodies are utilized.

173
Q

1 mole of beta-hydroxybutyrate = _______ moles of ATP

A

21.5 moles of ATP

174
Q

What is the 1st step of ketone body production?

A

2 Acetyl CoA ——> Acetoacetyl CoA via Thiolase

175
Q

What is the 2nd step of ketone body production?

A

Acetoacetyl CoA ——> HMG CoA via HMG CoA Synthase

176
Q

What is the 3rd step of ketone body production?

A

HMG CoA ——> Acetoacetate via HMG CoA lyase

177
Q

What is the 4th step of ketone body production?

A

Acetoacetate ——–> D-Beta-hydroxybutyrate via D-B-hydroxybutyrate dehydrogenase (creates an NADH)

Acetoacetate can also be spontaneously converted to Acetone

178
Q

During ketone body production, the body wants to make d-b-hydroxybutyrate from acetoacetate. However, _____________ is made spontaneously from acetoacetate.

A

Acetone

Metabolism, Molecular, and Pharmacogenomics (MMP) (3 decks)

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