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PHRM 836 > Sjogren - Exam 3 > Flashcards

Sjogren - Exam 3 Flashcards

1
Q

What is the purpose of metabolism?

A

The purpose of metabolism it to convert exogenous sources of energy (such as food) to usable energy.

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2
Q

What are the principles of redox reactions?

A
  • many redox reactions have both an electron and a proton transferred
  • conversion of pyruvate and NADH to lactate and NAD+ is under anaerobic conditions
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3
Q

What is true about the substrate that accepts electrons in redox reactions?

A

It also gains protons.

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4
Q

What is the Gibbs free energy for ATP hydrolysis?

A

Hydrolysis of ATP has a largely negative delta G.

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5
Q

Why are the steps that require ATP irreversible?

A
  • The negative delta G of the hydrolysis of ATP indicates that reversing the ATP hydrolysis would have a highly positive delta G. This indicates that it would require an input of energy to complete.
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6
Q

Where does metabolic regulation frequently occur at?

A

the rate-limiting or commitment steps

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7
Q

Rate-limiting step

A

the slowest step in the pathway

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8
Q

commitment step

A

the first irreversible step unique to the pathway

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9
Q

Which steps usually involve high-energy substrates?

A

irreversible

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10
Q

Allosteric regulation

A
  • fast
  • activators and inhibitors
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11
Q

Transcriptional/translational regulation

A
  • slow
  • induction of genes for enzymes involved in metabolism
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12
Q

Protein degradation

A
  • slowest
  • ubiquitin-proteasome pathway
  • lysosomal proteolysis
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13
Q

Post-translational modification

A
  • fast
  • phosphorylation
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14
Q

Compartmentation

A
  • fast
  • shuttling substrates to a compartment for biochemical reactions
  • Ex: fatty acid biosynthesis in the cytosol and oxidation in the mitochondria
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15
Q

How is hexokinase (glucose –> G6P) regulated?

A
  • feedback (product inhibition)
  • concentrations of glucose-6-phosphate inhibits hexokinase
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16
Q

What regulates pyruvate kinase (PEP –> pyruvate) via feedforward?

A
  • fructose-1,6-bisphosphate
  • positive allosteric regulation
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17
Q

What is a futile cycle?

A
  • futile cycles are formed by the activation of two irreversible reactions that occur in opposite directions
  • wastes cellular energy
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18
Q

What is one physiological example of a futile cycle?

A

The liver uses a futile cycle between glucose and glucose-1-phosphate as a buffer to maintain blood glucose levels.

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19
Q

What is the Gibbs free energy of fructose-6-phosphate to fructose-1,6-bisphosphate?

A
  • largely negative (indicating that its irreversible)
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20
Q

What is the commitment step for glycolysis?

A

Fructose-6-phosphate –> fructose-1,6-bisphosphate mediated by PFK-1

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21
Q

Where does the glucose come from?

A

digestion and absorption of carbohydrates

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22
Q

What must happen to dietary carbohydrates in order for absorption to occur?

A

Di, oligo, and polysaccharides must be hydrolyzed to monosaccharides to be absorbed.

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23
Q

What is GLUT-1 responsible for?

A

basal non-insulin-stimulated glucose uptake into many cells

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24
Q

What is GLUT-2 responsible for?

A
  • glucose sensing for pancreatic B-cells
  • Together with glucokinase, it forms the B-cell’s glucose sensor and allows glucose to enter the B-cell at a rate proportional to the extracellular glucose level
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25
Q

What is GLUT-3 responsible for?

A

non-insulin mediated glucose uptake into brain neurons

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26
Q

What is GLUT-4 responsible for?

A

insulin-stimulated glucose uptake in muscle and adipose tissue, and thus the classic hypoglycemic action of insulin

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27
Q

Which tissues can increase glucose uptake in response to insulin?

A

muscle and adipose tissue

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28
Q

Which organ can complete gluconeogenesis?

A

liver

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29
Q

How does insulin resistance occur?

A
  • defects in intracellular signlaing
  • downregulation of insulin receptors
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30
Q

What is a consequence of insulin resistance?

A

Type II Diabetes

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31
Q

Where is glucose-6-phosphate used outside of glycolysis?

A
  • glycogen synthesis
  • pentose phosphate pathway
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32
Q

What do liver and pacreatic B-cells use in place of hexokinase?

A

glucokinase

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33
Q

When does glucokinase utilize glucose?

A

Glucokinase only utilizes glucose when the concentration is sufficiently high
- after meals

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34
Q

Where does the switchover from Hexokinase I-III to glucokinase occur?

A

glucose = 5mM (90 mg/dL)

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35
Q

What inhibits PFK-1 (F6P –> Fructose 1,6 -bisphosphate)

A
  • negative regulation by ATP, citrate, and H+
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36
Q

What promotes PFK-1 (F6P –> Fructose 1,6-bisphosphate) (commitment step)

A
  • AMP
  • fructose-2,6-bisphosphate
  • hormonal regulation in liver
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37
Q

How can cells use AMP to sense energy status?

A

A very small % decrease in ATP will be indicated by a very large % increase of AMP. This indicates glycolysis is needed.

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38
Q

What does high ATP regulate?

A
  • inhibits hexokinase, PFK-1, and pyruvate kinase
39
Q

What does high AMP regulate?

A
  • activates PFK-1 and pyruvate kinase
40
Q

What has a critical role in cellular energy homeostasis?

A

AMP-activated protein kinase (AMPK)

41
Q

Which stage (and steps) of glycolysis consumes ATP?

A

Priming stage

  • Hexokinase converting Glucose–> G6P
  • PFK converting F6P –> F1,6bisphosphate
42
Q

Which stage (and steps) of glycolysis generates ATP?

A

Energy extraction

  • Phosphoglycerate kinase converting glycerate-1,3-bisphosphate to Glycerate-3-phosphate
  • Pyruvate kinase converting PEP to pyruvate
43
Q

Are the reversible steps of glycolysis regulated?

A
  • Not really
  • The enzymes keep the reactions near equilibrium
44
Q

What is the role of pyruvate kinase?

A

Pyruvate kinase converts phosphoenolpyruvate (PEP) into pyruvate

45
Q

How is pyruvate kinase regulated?

A
  • activated by Fructose-1,6bisphosphate
  • inhibited by ATP and alanine
46
Q

What are the fates of pyruvate in anaerobic conditions?

A
  • transamination to form alanine
  • reduction to form lactate
47
Q

What happens to pyruvate when oxygen is available?

A
  • it undergoes oxidative phosphorylation and forms Acetyl CoA
48
Q

How is ATP generated in red blood cells?

A
  • RBCs don’t have mitochondria and use anaerobic fermentation to generate ATP
49
Q

Where does one carbon source for gluconeogenesis come from?

A
  • Lactate can be transported to the liver via the Cori cycle to serve as a substrate for gluconeogenesis.
50
Q

Regulation of PFK-1 by citrate is an example of:

A

feedback inhibition

51
Q

Describe the metabolic problem of a fructose-only diet?

A

Fructose metabolism bypasses the highly regulated PFK-1 step in glycolysis. This means that glycolysis continues to happen – leading to the overproduction of pyruvate and glycerol-3-phosphate which are both precursors to triglycerides.

52
Q

What are all of the carbon sources for gluconeogenesis?

A

lactate, amino acids, glycerol, fructose

53
Q

What is the rate-limiting step of gluconeogensis?

A

PEP carboxykinase converting oxaloacetate to phosphoenolpyruvate (PEP) is the rate limiting step.

54
Q

Identify the regulation mechanism to suppress glycolysis and to promote gluconeogenesis:

A
  • G6P accumulates only during gluconeogenesis – this inhibits hexokinase
  • allosteric
55
Q

How does alcohol interfere with gluconeogenesis?

A
  • oxidation of ethanal depletes NAD+
  • NAD+ is used to convert lactate into pyruvate
  • Because there’s an excess of NADH, pyruvate is depleted at is it converted to lactate
  • no pyruvate = no gluconeogenesis
56
Q

What are the fates of glucose-6-phosphate in cells?

A
  • gluconeogenesis (liver)
  • glycogen synthesis
  • glycolysis
  • pentose phosphate pathway
57
Q

What does the liver use glycogen for?

A

The liver uses glycogen to maintain blood glucose levels. (The liver generates glucose from glycogen)

58
Q

What do muscles use glycogen for?

A

The muscles use glycogen as a storage molecule as more G6P is regenerated.

59
Q

How is glycogenesis regulated?

A
  • allosterically
  • glycogen synthase
  • G6P promotes glycogen synthase
60
Q

How is glycogenolysis regulated?

A
  • phosphorylase
  • phosphorylase is allosterically promoted by AMP
  • phosphorylase is allosterically inhibited by G6P and ATP
61
Q

True statements for gluconeogenesis:

A
  • It should be off when glycolysis is on
  • It can use several different carbon sources
  • Most of the enzymes used are the same as glycolysis
  • It is activated in the liver during fasting
  • It is negatively regulated by ADP
62
Q

What is the function of the pyruvate dehydrogenase complex?

A

It catalyzes the conversion of pyruvate to acetyl CoA

63
Q

What are the 3 reactants of the pyruvate dehydrogenase complex?

A
  • pyruvate
  • CoA
  • NAD+
64
Q

What are the 3 products of the PDH enzyme complex?

A
  • CO2
  • Acetyl-CoA
  • NADH + H+
65
Q

What is the function of Coenzyme A (CoA) in the PDH enzyme complex?

A
  • acts as an acetyl group carrier
66
Q

What are the different sources of Acetyl CoA?

A
  • produced from glucose (glucose –> pyruvate –>)
  • produced from fatty acids
  • produced from ketogenic amino acids
67
Q

What are the different fates of Acetyl CoA?

A
  • Used in the TCA cycle –> CO2
  • –> ketone bodies
  • –> fatty acids
  • –> cholesterol
68
Q

Under what conditions are ketone bodies produced?

A
  • during prolonged fasting
  • during ketogenic (low carb - high fat) diet
69
Q

How are ketone bodies utilized to produce energy?

A
  • Ketone bodies are converted to acetyl-CoA in nonhepatic tissues
  • Acetyl-CoA is used as a fuel in the TCA cycle
70
Q

What is the rate-limiting step of ketone synthesis from acetyl-CoA?

A

HMG-CoA synthase

  • promoted by glucagon
  • inhibited by insulin
71
Q

Describe the uses of TCA cycle intermediates in biosynthesis:

A
  • critical building blocks for gluconeogenesis and amino acid synthesis (neurotransmitters)
72
Q

What is the purpose of anaplerotic reactions?

A
  • supply TCA cycle intermediates
  • When amino acids are not sufficient, pyruvate is the main source of TCA cycle intermediates.
73
Q

Explain why triheptanoin is used during pyruvate carboxylase deficiency.

A
  • Pyruvate carboxylase is essential in gluconeogenesis. Triheptinoin is used to during deficiency because it can be converted to acetyl-CoA and succinyl-CoA to continue supplying the TCA cycle intermediates.
74
Q

Why isn’t the initial reaction in glycolysis the commitment step?

A

Glucose-6-phosphate can be utilized in other pathways.

75
Q

Why does high intake of sucrose increase the risk of obesity?

A

Fructose metabolism bypasses the highly regulated PFK-1 step in glycolysis.

76
Q

True statements about ketone bodies:

A
  • High levels of ketone bodies in the blood result in exhaling acetone
  • Ketone body production involves HMG-CoA as an intermediate
  • Ketone bodies are mainly produced in the liver
  • Ketone bodies are water-soluble
77
Q

What are the 5 coenzymes involved in the PDH complex?

A
  • Thiamine pyrophosphate (TPP)
  • Lipoamide
  • FAD
  • CoA
  • NAD+
78
Q

True Hexokinase reaction statements:

A
  • The reaction requires energy in the form of ATP
  • It results in trapping glucose inside the cell
  • The reaction has a negative delta G
  • The reaction is negatively regulated by G6P
79
Q

In order for oxaloacetate to cross the mitochondrial membrane, it must first be converted to either ___________ or _________.

A
  • aspartate
  • malate
80
Q

Why can’t the liver utilize ketone bodies as a source for energy?

A

The liver lacks the enzyme thiophorase that converts acetoacetic acid to acetoacetyl-CoA.

81
Q

What is the overall “reaction” of oxidative phosphorylation?

A

carbon fuel + O2 –> CO2 + H2O + Energy

82
Q

How does the flow of electrons in the ETC result in ATP synthesis?

A
  1. Electrons from NADH and FADH2 are transferred to O2
  2. This creates a proton gradient
  3. ATP synthase produces ATP by using the proton gradient
83
Q

True statements regarding coenzymes:

A
  • NADH is the reduced form
  • FAD is the oxidized form
  • Flavin coenzymes function as prosthetic groups
  • Both NADH and FADH2 are produced in the TCA cycle
84
Q

How would cyanide affect the ETC and oxidative phosphorylation?

A
  • cyanide inhibits cytochrome c oxidase (complex IV)
  • this would increase the pH of the intermembrane space
  • It would inhibit ATP synthesis
85
Q

Describe the mechanism of energy loss caused by uncouplers:

A
  • uncouplers (2,4-dinitrophenol) increase the rate of O2 consumption
  • they dissipate the proton gradient which prevents ATP synthesis
  • the energy is lost as heat
86
Q

What is the role of uncouplers in humans?

A
  • Expressed in brown adipose tissue, which play a major role in non-shivering thermogenesis, especially in newborns
87
Q

Identify key enzymes that remove reactive oxygen species:

A
  • superoxide dismutase (SOD) and catalase are the primary defense mechanism
  • glutathione peroxidase uses glutathione as a reductant
88
Q

Identify the organs and tissues especially sensitive to reactive oxygen species in diabetic patients:

A
  • cells that cannot restrict the uptake of glucose are vulnerable
  • retina
  • kidney
  • peripheral nerves
89
Q

Why is brown adipose tissue common in hibernating animals?

A

They need to generate heat while energy need is low

90
Q

True statements regarding nicotinamide coenzymes:

A
  • They are polar and water soluble
  • They act as high energy electron carriers in the TCA cycle (mitochondria)
  • They act as high energy electron carriers in glycolysis (cytosol)
  • They cannot be used to produce ATP in the absence of mitochondria
91
Q

Why does the oxidation of FADH2 generate less ATP than oxidation of NADH in oxidative phosphorylation?

A

Oxidation of FADH2 occurs in complex II, bypassing on proton-pumping step across the inner mitochondrial membrane

92
Q

True statements regarding Flavin coenzymes:

A
  • They can act as high energy electron carriers in the TCA cycle
  • They act as prosthetic groups on enzymes
  • They cannot be used to produce ATP in the absence of mitochondria
  • A vitamin is part of the structure of Flavin coenzymes
93
Q

Which component of ETC is also an enzyme in the TCA cycle?

A

succinate dehydrogenase/ Complex II

PHRM 836 (3 decks)

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