Glycolysis/Gluconeogenesis (complete) Flashcards
(145 cards)
1
Q
What transports glucose from the lumen of the intestines and kidney into the epithelial cells
A
SGLT
2
Q
what kind of transport do SGLTs do
A
active transport
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)
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.
5
Q
What types of transporters transport glucose from inside the epithelial cells into the blood
A
GLUT transporters
6
Q
what kind of transport do GLUTs do
A
they do passive transport
7
Q
Where are GLUTs located
A
in all cells of the body, on the side of the cell bordering the capillaries
8
Q
Which GLUT is regulated by insulin
A
GLUT 4
9
Q
Where is GLUT 4 located
A
- skeletal muscle cells (myocytes)
- Cardiac muscle cells (cardiomyocytes)
- Fat cells (adipocytes)
10
Q
Which GLUTs aren’t regulated by insulin
A
1-3 and 5-13
11
Q
Where is insulin synthesized
A
pancreatic beta cells
12
Q
what is insulin
A
a small peptide hormone
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
14
Q
why is glucose immediately phosphorylated upon entrance into a cell
A
- so that it is “trapped” in that cell and won’t leave
- so that it won’t affect the concentration gradient of glucose and glucose will still be able to passively enter the cell
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
16
Q
What are the normal levels of blood glucose
A
75-100 mg/dL
17
Q
What are the three ways to increase blood glucose
A
- glucose absorption in the gut
- Glucose recovery from the kidneys
- glucose release from the liver
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
19
Q
What is glucose clearance
A
glucose being taken out of the blood and transported into the tissues
20
Q
What is the primary action of insulin
A
to cause glucose clearance (uptake of glucose from the blood and into the cells)
21
Q
What does the enzyme phosphatase do
A
it dephosphorylates Glucose-6-Phosphate to glucose in the liver
22
Q
where is phosphatase found
A
in the liver only
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
24
Q
Through what transporter does glucose leave the liver and enter the bood
A
GLUT-2
25
Can muscle cells uptake glucose even when insulin is not present
yes
26
what stimulates glucose uptake in muscles when insulin is not present
muscle contaction
27
what is the process by which muscle contraction in skeletal muscle causes the uptake of glucose.
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
28
When is insulin high, acutely
1. after a meal
2. in anticipation of a meal
3. in the morning
29
When is insulin high chronically
insulin resistance (pre-diabetes) or diabetes
30
What is the effect of the sympathetic nervous system on insulin and glucagon
decreases insulin and increases glucagon
31
what is the effect of the parasympathetic nervous system on insulin and glucagon
increases insulin and decreases glucagon
32
What does insulin do in muscle tissue
1. increases glucose uptake
| 2. helps in anabolism (building up of muscle)
33
What does insulin do in the liver
1. inhibits ketogenesis
2. activates lipogenesis
3. activates glycogenesis
34
What does insulin do in adipose tissue
1. causes glucose uptake
2. activates lipogenesis
3. activates adipogenesis
35
What levels in the blood are decreased with the release of insulin
1. glucose
2. fats
3. Ketones
36
Along with insulin, what are the other major hormones that promote fat storage and inhibits fat usage
None, insulin is the only major hormone that promotes fat storage and inhibits the use of fats
37
how easy is it to gain fat without insulin
nearly impossible
38
What hormones counter the affect of insulin on fats (Which ones cause the breakdown and usage of fats?)
1. glucagon
2. catecholectamines
3. cortisol
4. Growth Hormone (GH)
39
What is the affect of glucagon, cortisol, catecholectamines, and growth hormone on blood glucose levels
they increase blood glucose levels
40
Are glucagon, cortisol, catecholectamines, and GH catabolic or anabolic
catabolic
41
what is the effect of insulin on blood glucose levels
it decreases blood glucose levels
42
is insulin catabolic or anabolic
anabolic
43
What is the primary regulator of insulin and glucagon
plasma glucose concentration
44
plasma glucose concentration is the primary regulator of insulin and glucagon. what happens when it's high, what happens when it's low
When it is high, insulin is secreted and glucagon isn't
| When it is low glucagon is secreted and insulin isn't
45
What is the effect of glucagon on muscle tissue
there is no effect
46
why doesn't glucagon have an effect on muscle tissue
because there are no glucagon receptors in muscle tissue
47
What is the effect of glucagon on the liver
1. glycogenolysis
2. gluconeogenesis
3. ketogenesis
48
What is the effect of glucagon on adipose tissue
Lipolysis
49
Which types of cells don't have glucagon receptors?
- adipocytes
- myocytes
- hepatocytes
myocytes - muscle cells
50
Which types of cells don't have insulin receptors
- adipocytes
- myocytes
- hepatocytes
All cells have insulin receptors
51
What are the molecules and enzymes (E:) of glycolysis
```
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)
```
52
What portion of glycolysis is referred to as the preparatory phase
From the start, up until the 6 carbon molecule splits into two 3 carbon molecules
53
Why are the first few steps (up until the splitting point) called the preparatory phase
because up until this point, energy has only been used, no energy has been given off
54
What is the payoff phase of glycolysis
the second half of glycolysis, after the 6 carbon molecule splits, up to the creation of pyruvate
55
why is the second half of glycolysis referred to as the payoff phase
because it is in the second half of glycolysis that NADH and ATP are created
56
how many ATP are created for each glucose molecule that goes through glycolysis, how do you get this number?
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
57
How many NADH are created for each glucose molecule that goes through glycolysis. How do you get this number
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)
58
What is the Actual net ATP gain from glycolysis
2 ATP, the 4 created in the second half of glycolysis minus the two reactions that use ATP in the first half of glycolysis
59
What are the reactions in glycolysis that use ATP
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
Which two steps in the preparatory phase of glycolysis add a phosphate to the molecule
1. the hexokinase/glucokinase reaction
| 2. the PFK-1 reaction
61
what is significant about the location of the phosphate that is added in the PFK-1 reaction
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
Which steps in glycolysis are irreversable
Step 1. Glucokinase/hexokinase
Step 3. phosphofructokinase-1 (PFK-1)
Step 9. Pyruvate kinase
63
How many pyruvate are formed in glycolysis from each molecule of glucose
2
64
Where does pyruvate go after it is formed in glycolysis
to the mitochondra
65
How does pyruvate enter the inner membrane of the mitochondria
through a pyruvate carrier
66
Pyruvate gets converted to what molecule in the mitochondria
Acetyl-CoA
67
What is the enzyme that converts pyruvate into Acetyl-CoA
the pyruvate dehydrogenase complex
68
What are all of the products created in the pyruvate dehydrogenase complex reaction
1. Acetyl-CoA
2. NADH
3. CO2
69
High Levels of what lead to deactivation of the pyruvate dehydrogenase complex
1. ATP
2. NADH
3. Acetyl-CoA
70
What are the 5 cofactors that are needed for the pyruvate dehydrogenase complex to work
1. Coenzyme A
2. NAD+
3, TPP
4. Lipoic Acid
5. FAD
71
Besides the high levels of ATP, NADH, and Acetyl-CoA what inhibits the pyruvate dehydrogenase complex
Phosphorylation by pyruvate dehydrogenase kinase
72
What dephosphorylates the Pyruvate dehydrogenase complex, and does that activate it, or inactivate it
pyruvate dehydrogenase phosphatase, and this activates it
73
What is the primary reason that the liver runs glycolysis
to convert glucose into glycogen and fat
74
What are the regulators of glycolysis
1. Glucose
2. ATP
3. AMP
4. Fructose, 2-6-bisphosphate
5. PK phosphorylation
6. Fructose-1,6-bisphosphate
75
How does ATP regulate glycolysis
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
What are the two places that ATP acts on in inhibiting glycolysis
1. PFK-1
| 2. PK
77
How does glucose regulate glycolysis
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
How does AMP regulate glycolysis
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
At which places does a low level of AMP regulate glycolysis
PFK-1
80
How does Fructose-2,6-bisphosphate regulate glycolysis
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
What enzyme leads to creation of fructose-2,6-bisphosphate. and what is the initial substrate this enzyme uses
PFK-2 is the enzyme that converts fructose-6-phosphate into fructose-2,6-phosphate.
82
We know that the product of PFK-2 (fructose-2,6-bisphosphate) activates PFK-1. but what are the regulators of PFK-2
insulin
| glucagon
83
What are the three locations of glycolysis that are regualted by insulin and glucagon
Glucokinase
PFK-1
Pyruvate Kinase
84
What is the effect of insulin on glucokinase, PFK-1 and pyruvate kinase
insulin activate glucokinase, PFK-1, and Pyruvate kinase
85
When is insulin present, and able to activate glycolysis
in a fed state
86
what is the effect of glucagon on glucokinase, PFK-1, and pyruvate kinase
glucagon represses activity of glucokinase, PFK-1, and pyruvate kinase
87
When is glucagon present, and able to repress glycolysis
in a fasting state
88
How does insulin affect Glucokinase
it helps to stimulate its creation, and release from the nucleus
89
how does glucagon affect glucokinase
it represses its activity
90
how does insulin affect PFK-1
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
how does glucagon affect PFK-1
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
How does insulin affect Pyruvate kinase
insulin dephosphorylates pyruvate kinase (PK), which activates it
93
How does glucagon affect pyruvate kinase (PK)
1. glucagon binding activates adenylate cyclase
2. adenylate cyclase turns ATP into cAMP
3. cAMP activates PKA
4. PKA phosphorylates and inactivates PK
94
What are the non-hormonal regulators of glucokinase
high Km
95
What are the non hormonal regulators of PFK-1
activators
AMP
fructose-2,6-bisphosphate
Deactivators
ATP
96
What are the non hormonal regulators of PK
activators
fructose-1,6-bisphosphate
dephosphorylation
inactivators
phosphorylation
ATP
Alanine
97
What are the three enzymes of glycolysis that need to be bypassed in gluconeogenesis (only in liver)
1. Glucokinase
2. PFK-1
3. PK
98
How is the bypass of glucokinase in the liver done
by glucose-6-phosphatase
99
how is the bypass of PFK-1 in gluconeogenesis done
by Fructose-1,6-bisphosphatase. But this enzyme is regulated too.
100
What is the process by which fructose-1,6-bisphosphatase is regulated so that it can bypass the PFK-1 reaction
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
How is the bypass of the pyruvate kinase reaction done
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
Where does the bypass reaction of PK happen
first portion is in the mitochondria, then the second portion is in the cytosol
103
What are the enzymes that play in the PK bypass reaction
1. Pyruvate carboxylase
2. MDH
3. MDH
4. PEPCK (phosphoenolpyruvate carboxykinase)
104
What is the effect of insulin on gluconeogenesis, and how does it do that
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
What is the effect of glucagon on gluconeogenesis, and how does it do that
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
What is the effect on pyruvate carboxylase by insulin and glucagon (pyruvate carboxylase is used in the pyruvate kinase bypass reaction)
insulin and glucagon have no effect on pyruvate carboxylase
107
What is the effect on PEPCK (PEPcarboxykinase) by insulin and glucagon (PEPCK is used in the pyruvate kinase bypass reaction)
Insulin inhibits PEPCK
| glucagon activates PEPCK
108
What is the affect of high levels of alanine on glycolysis/gluconeogenesis
high levels of alanine inhibit pyruvate kinase (increasing gluconeogenesis)
109
If no hormones regulate pyruvate carboxylase, then what does
Acetyl-CoA
110
how does Acetyl-CoA regulate pyruvate carboxylase
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
Why is it significant that the pathways of glycolysis and gluconeogenesis are reciprocally regulated (What activates one pathway deactivates the other)
to avoid a futile cycle
112
We know how to do gluconeogenesis from pyruvate right, what different things can be converted into pyruvate
1. Lactate
2. alanine
3. cysteine
4. glycine
5. serine
6. tryptophan
113
What happens once Lactate, alanine, cystein, glycine, serine, and tryptophan have been converted into pyruvate (in gluconeogenesis)
the pyruvate is converted into Oxaloacetate, then into malate, then shipped out of the _____, converted back into Oxaloacetate, then back into PEP
114
Some Amino acids aren't converted into pyruvate, but into Oxaloacetate, which ones are they
Aspargine
| Aspartate
115
Is glycerol a gluconeogenic substrate
yes
116
how does glycerol enter the gluconeogenic pathway
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
Can we get glucose from fatty acids
nope
118
Why can't we get glucose from fatty acids
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
Why can lipolysis increase glucose production if beta-oxidation doesn't
becuase lipolysis is the breakdown of a triglyceride. triglycerides have glucogenic parts
120
what are the parts of a triglyceride
glyceride
| fatty acids
121
which pars of a triglyceride are glucogenic
glyceride
122
If fatty acids can't be turned into glucose, what do they become in lipolysis
Acetyl-CoA
123
What is the NET gain of ATP in glycolysis
2 ATP (2 Used, 4 made)
124
What is the NET gain of NADH in glycolysis
2 NADH
125
When using glycerol to make glucose, how many glycerol molecules are needed to make one glucose molecules
2
126
when using glycerol to make glucose, how many ATP are required to make a molecule of Glucose
2 (1 per glycerol molecule)
127
When using glycerol to make glucose, how many NADH are required to make a molecule of glucose
2 (1 per glycerol molecule)
128
Where does gluconeogenesis from glycerol occur
only in the liver
129
In starvation what is the first source of glucose
Amino Acids from the muscle
130
If Fatty acids can't produce glucose, what good are they in starvation when we need energy
They can be a source of ketone bodies,
131
What is the initial substrate in the formation of ketone bodies
Acetyl-CoA
132
What is the good that comes from ketone bodies
they can be used like glucose (for energy)
133
When do we get anaerobic glycolysis
Anaerobic glycolysis occurs in the absence of oxygen, or when energy demand is high and immediate
134
What is the difference between aerobic and anaerobic glycolysis
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
How many ATPs are made from aerobic glycolysis (not including the Aceyl-CoA going through the crebs cycle)
7
2 from glycoglysis
5 from the two NADHs made (2.5 ATP per NADH that goes through the ETC-Ox-phos system)
136
how many ATP are made from anaerobic glycolysis
2
137
if the NADH made in glycolysis can't go to the ETS-Ox Phos system becuase of anaerobic conditions what happens to it
The NADH is used by lactate dehydrogenase to create lactate from pyruvate. and NAD+ results
138
What is the enzyme that makes lactate,
lactate dehydrogenase
139
When do we make lactate
in anaerobic conditions
140
What is the significance of Lactate dehydrogenase using NADH and leaving NAD+
the NAD+ can be used to continue glycolysis, so more ATP can be made
141
When do we have anaerobic glycolysis
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
What happens to the lactate that is created by lactate dehydrogenase in anaerobic conditions (usually from RBC's and working muscle)
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
What happens to the lactate that has been taken to resting skeletal muscle or heart
it is converted into pyruvate, then it goes through the krebs cycle and ETS-Ox phos
144
what happens to the lactate that has been taken to the liver
it is converted into pyruvate, then it goes through gluconeogenesis to produce glucose
145
what is the Cori cycle
the catabolism of glucose carbons to lactate in the peripheral tissue, then the anabolism of lactate back into glucose in the liver
