Lecture 13 Information Flashcards

1
Q

Glycolysis overall reaction

A

Glucose + 2ATP + 2 NAD+ => 2 Pyruvic acid + 2 NADH + 2ATP + 2H2O

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2
Q

How many phases and steps are in glycolysis?

A

2 phases and 10 total steps

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3
Q

Where does glycolysis take place?

A

in the cytoplasm

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4
Q

Step 1 of glycolysis

A

convert glucose to glucose 6-phosphate

hexokinase accomplishes this

requires ATP

highly irrevisible

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5
Q

Step 2 of glycolysis

A

isomerize glucose 6-phosphate to fructose 6-phosphate

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6
Q

Step 3 of glycolysis

A

convert fructose-6 phosphate to fructose 1,6 bisphosphate

phosphofructokinase-1 accomplishes this

requires ATP

highly irreversible

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7
Q

Which step guarentees that glucose will go through glycolysis?

A

step 3

can no longer use fructose-6 phosphate / glucose for anything else

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8
Q

Step 4 and 5 of glycolysis

A

produce glyceraldehyde 3-phosphate and dihydroxyacetone phosphate (3 carbons with phosphate)

triosephosphate isomerase converts dihydroxyacetone phosphate to glyceraldehyde 3-phosphate

happens very fast

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9
Q

Step 6 of glycolysis

A

glyceraldehyde 3-phosphate gets 2 phosphates added (oxidized) to convert to 1,3-bisphosphate

in this step, NAD+ is reduced to NADH

glyceradehyde 3-phosphate dehydrogenase accomplishes this

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10
Q

Step 7 glycolysis

A

remove a phosphate from 1,3-bisphosphate to make 3-phosphoglycerate

2 ADP is converted to 2 ATP

phosphoglycerate kinase accomplishes this

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11
Q

Step 10 of glycolysis

A

phosphoenolpyruvate (PEP) is converted to pyrvuate

converts 2 ADP to 2 ATP

pyruvate kinase accomplishes this

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12
Q

What happens to pyruvate?

A

has energy contained in 3 carbons that can still be used for energy

pryuvate moves to the Krebs/Citric Acid Cycle

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13
Q

Which steps drive glycolysis forward?

A

Steps 1, 3, and 10

all steps have large negative ∆Gs

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14
Q

How do more unfavorable steps of glycolysis take place?

A

Change the concentrations of intermediates and substrates to make ∆G favorable

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15
Q

Hypoxic

A

low oxygen in cell

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16
Q

What does hypoxia trigger?

A

an increase in glycolytic enzymes which increases the rate of glycolysis

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17
Q

Warburg effect

A

even after cancer cells develop blood flow and have O2 they still use just glycolysis as an energy source

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18
Q

Why would cancer cells want to keep running glycolysis?

A

glycolysis releases hexokinase which moves to the mitochondria to stop apoptosis inducing factors from being released

factors such as cytochrome c

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19
Q

What molecule might be helpful in treating cancer cells?

A

DCA

DCA makes it more likely that a cell will run glycolysis and then run the Krebs Cycle/ETC

activates pyruvate dehydrogenase

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20
Q

Type I diabetes

A

inability of pancreas to produce enough insulin to trigger the decrease of blood-glucose concentration levels

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21
Q

Type II diabetes

A

inability of target cells to pick up insulin signals

receptors are not as sensitive to insulin

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22
Q

What does insulin trigger?

A

a pathway to place more GLU4 receptors on the cell surface

GLU4 receptors can take glucose out of the blood and into the cell

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23
Q

What do high blood glucose levels do?

A

increase blood pressure

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24
Q

What do low blood glucose levels do?

A

cause hypoglycemia and passing out since brain is not getting glucose

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25
Q

What is glucose metabolism limited by?

A

how much glucose we can take into our cells

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26
Q

What happens when the cell does not have enough glucose?

A

cell relies on other sources of energy like lipids/fatty acids through beta-oxidation

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27
Q

What is a negative side effect of using lipids/fatty acids instead of glucose as energy source?

A

Beta-oxidation produces ketone-bodies as a result

too many ketone-bodies in the blood can lower the pH of blood and trigger keto-acidosis

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28
Q

Where does glucose come from?

A

break off monomers from starch / glycogen chains

break down sucrose into fructose/glucose

gluconeogenesis

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29
Q

How can fructose be used in glycolysis?

A

hexokinase can convert it to fructose 6-phosphate to be used

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30
Q

What happens to carbons from glucose?

A

they are greatly oxidized to CO2

the energy from this oxidation goes to the ETC

31
Q

What is a problem of too much glycolysis in anaerobic conditions?

A

produce a lot of NADH and deplete our NAD+ reservoirs

32
Q

How do we replace our NAD+ reservoirs?

A

through fermentation

33
Q

Different types of fermentation

A

lactic acid and yeast (ethanol)

34
Q

Lactic acid fermentation

A

pyruvate is reduced to lactate

NADH is oxidized to NAD+

lactose dehydrogenase accomplishes this (substrates are NADH and pyruvate)

35
Q

Difference between lactic acid and Alcoholic fermentation?

A

lactic acid is one step and Alcoholic is 2 steps

36
Q

Alcoholic fermentation

A

first, pyruvate is converted to acetaldehyde by pryuvate decarboxylase

second, acetaldehyde is reduced to ethanol through alcohol dehydrogenase

in second step, NADH is oxidized to NAD+

37
Q

What happens when glucose levels are low?

A

have to produce glucose through gluconeogenesis

38
Q

Where does gluconeogenesis take place?

A

the liver

39
Q

Types of substrates for gluconeogenesis?

A

lactate, triacylglycerol and CO2

40
Q

Gluconeogenesis step 1

A

use bisphosphate and pyruvate to produce oxaloacetate

41
Q

First chokepoint of gluconeogenesis

A

convert oxaloacetate to PEP by using GTP

PEP carboxykinase and pyruvate caroxylase accomplish this

weird trip through the cytosol to mitochondria back to the cytosol

42
Q

Second chokepoint of gluconeogenesis

A

convert fructose 1,6 bisphophate to fructose 6-phosphate

use fructose 1,6-bisphosphatase

this is reversing the highly irreversible step 2 in glycolysis

43
Q

Third chokepoint of gluconeogenesis

A

convert glucose 6-phosphate to glucose

glucose 6-phosphatase does the opposite of hexokinase

we do not use or produce ATP here, just remove the phosphate

44
Q

Cori Cycle

A

fermentation meets gluconeogenesis

lactic acid from fermentation can be moved from the muscle into the liver cells

in the liver, the lactate can be converted into pyruvate and go through the process of gluconeogenesis

45
Q

The Pentose Phosphate Pathway (PPP) overview

A

creating pentose sugars from glucose to be used in DNA and RNA

takes place in the cytosol

46
Q

Steps of PPP

A

start with glucose 6-phosphate and use 2 NADP+ to oxidize twice to produce ribose 5-phosphate

NADP+ is reduced to NADPH

47
Q

NADPH

A

produced in the PPP

can reduce the reactivity of free radicals and oxygen species

48
Q

Ribose 5-phosphate

A

produced by PPP

plant cells use it in chloroplasts

other cells use it as an intermediate to produce nucleotides, coenzymes, DNA and RNA (expect to find in cells that are rapidly dividing)

49
Q

Favism

A

people with glucose 6-phosphate dehydrogenase deficiencies can get very sick when they eat fava beans since they do not produce enough NADPH

50
Q

Fava beans

A

contain an oxidizing molecule that NADPH normally reduces

51
Q

Why does favism prevail?

A

individuals with this disease are protected from malaria

paraise does not grow well in glucose 6-phosphate dehydrogenase deficient cells

52
Q

What are 3 levels of control to regulate glucose and gluconeogenesis?

A

enzyme control, hormones, and transcription

53
Q

What are the types of hormone control to regulate glucose / gluconeogenesis?

A

hexokinase bypass, PFK1 bypass, pyruvate kinase bypass

54
Q

Hexokinases in muscle cells versus liver cells

A

in muscle cells, hexokinase 4 has a LOW Km so glucose will be used even without large concentrations

in liver cells, hexokinase 1 has a HIGH Km so glucose will only be used at high concentrations

additionally, muscle cells hexokinases are inhibited by the product G6P and liver cells are not so they can work longer

55
Q

How is glucokinase regulated in the liver?

A

regulated through glucose concentrations

with high concentrations, will go through glycolysis

might not go through glycolysis with low concentrations

56
Q

GKRP

A

“bear hug” protein

takes glucokinase out of commission and places glucokinase in the nucleus

stimulated by the intermediate fructose 6-phosphate

signals that we have low glucose levels and don’t want to go through glycolysis

57
Q

Phosphofructokinase 1 (PFK1) regulation

A

allosterically inhibited by ATP and citrate

ATP is both a substrate and an end product

citrate is a component of the Krebs Cycle and signals that you do not need to keep going through glycolysis

58
Q

Gluconeogenesis enzyme FBPase-1

A

inhibited by AMP which signals that there is not much energy in the cell (AMP > ATP)

prevents gluconeogenesis from taking place

need to use glucose to make fuel

59
Q

Insulin

A

inactivates FBPase-2 and activates PFK-2

stimulates glycolysis and inhibits gluconeogenesis

take sugar to use for ATP

60
Q

Glucagon

A

activates FBPas-2 and inactivates PFK-2

inhibits glycolysis and stimulates gluconeogenesis

61
Q

FBPase-2

A

when activated, stimulates gluconeogenesis

62
Q

PFK-2

A

when activated, stimulates glycolysis

63
Q

What type of receptors does insulin bind to?

A

tyrosine kinase receptors

64
Q

For every one glucose molecule how many pyruvate molecules do we have?

A

2 pyruvate for every 1 glucose

65
Q

What happens to glucose’s carbons at the end of glycolysis?

A

they are oxidized to Co2

The extra energy goes into the ETC by placing placing electrons on NADH

66
Q

2 examples of ketoacids

A

acetoacetate and B-hydroxybutyrate

67
Q

How are ketone bodies used at low concentrations?

A

low concentrations can be used by the brain

when concentrations are too high like in diabetes, trigger ketoacidosis and can have trouble transporting on hemoglobin

68
Q

Active site versus allosteric site in PFK-1

A

Active site has a high affinity for ATP in order to run glycolysis

Allosteric site has a low affinity for ATP because only in high concentrations of ATP do we want to inhibit PFK-1

69
Q

What turns on PFK-1?

A

ADP and AMP since they indicate that there is not a lot of ATP in the cell

70
Q

Fructose 2,6-bisphosphate

A

Activates PFK-1 but inactivates FBPase-1 (which is used in gluconeogensis)

Turns on glycolysis and turns off gluconeogensis

71
Q

What produces fructose 2,6-bisphosphate?

A

PFK-2

72
Q

Insulin and regulating glycolysis

A

Insulin activates PFK-2 which produces fructose 2,6 bisphosphate which will turn on glycolysis through activating PFK-1

73
Q

Glucagon and regulating glycolysis

A

Glucagon inactivates PFK-2 so fructose 2,6 bisphosphate will not be produced and gluconeogenesis can take place

74
Q

Transcription factors

A

regulate the amount of enzymes we produce and therefore can regulate the amount of glycolysis that can take place