Biochemistry: Glycolysis

Front 1

What are the irreversible steps of glycolysis?

Back 1

1. Hexokinase/Glucokinase
2. PFK I
3. Pyruvate Kinase

Front 2

What enzymes do you go use to take pyruvate to phoshpoenolpyruvate (PEP)?

Back 2

1. Pyruvate carboxylase
2. PEP Carboxy Kinase (PEPCK)

Front 3

What is the gluconeogenesis intermediate when going from pyruvate to PEP?

Back 3

Oxaloacetate (OAA)

Front 4

What regulatory mechanisms effect Glyceraldehyde-3-phosphate (G3P) dehydrogenase?

Back 4

1. Inhibited by low pH
2. Presence of arsenic forms 1-arseno-3-PG (BAD)--locks up glycolysis

Front 5

What is the reactant for aldolase? What are the products? Which is favored?

Back 5

1. Fructose-1,6-Bisphosphate (F1,6BP)
2. G3P and DHAP
3. DHAP 20:1

Front 6

If DHAP is the favored product, what allows glycolysis to continue?

Back 6

Law of Mass Action. As G3P is pulled out, DHAP is isomerized to maintain equilibrium.

Front 7

How many ATP are used to activate glucose for glycolysis? By what enzymes?

Back 7

1. 2 ATP
2. hexokinase/glucokinase and PFK I

Front 8

There are two phases to glycolysis, what are they?

Back 8

1. Endergonic phase
2. Exergonic phase

Front 9

What does the endergonic phase of glycolysis cost?

Back 9

2 ATP per glucose

Front 10

How much energy is gained in the exergonic phase? What forms?

Back 10

4 ATP per glucose
2 NADH per glucose
Total of 10 ATP equivalents

Front 11

Where is NADH made in glycolysis?

Back 11

1. G3P Dehydrogenase

Front 12

How is pyruvate kinase regulated?

Back 12

1. Activated by ADP and F1,6BP
2. Inhibited by ATP and Alanine

Front 13

How is PFK I regulated?

Back 13

1. Activated by F2,6BP and AMP
2. Inhibited by Citrate and ATP

Front 14

What metabolic pathway will yield ATP the fastest?

Back 14

Glycolysis.
100 times faster than oxidative phosphorylation

Front 15

What source of energy will active muscles use?

Back 15

Glycogen

Front 16

Describe what happens when active muscles go anarobic. Describe the pathways used.

Back 16

1. Cori cycle.
2. Gluconeogenesis

Pyruvate to lactate via LDH. Lactate is transported in the blood to the liver. Lactate to pyruvate to glucose via gluconeogenesis. Glucose back to the muscles for glycolysis

Front 17

Where does the energy come from to make glyceraldehyde-3-phosphate to 1,3-bisphosphoglycerate?

Back 17

Oxidation of aldehyde to acid

Front 18

Describe the difference between Hexokinase and glucokinase.

Back 18

1. GK has higher KM
2. HK is inhibited by high G6P and ATP, GK is not

Front 19

Where is Glucokinase and Hexokinase found?

Back 19

Glucokinase is found in the liver, pancreas, intestines, and brain.
Hexokinase is found everywhere else.

Front 20

Which will trap glucose at lower concentrations, GK or HK?

Back 20

HK, glucokinase will only trap glucose at high concentrations.

Front 21

How is the rate of PFK I effected by [ATP]?

Back 21

Minimum rates at high and low ATP concentrations.

1. Decreased rate at low [ATP] because ATP is a reactant.
2. Decreased rate at high [ATP] because of allosteric inhibition site to prevent unnecessary ATP production.

Front 22

Describe the functions of PFK II.

Back 22

Works when [F6P] is high = higher Km than PFK I
Creates F2,6BP, which is an allosteric activator of PFK I
Essentially, tells PFK I to hurry up.

Front 23

How does alanine contribute to the glycolytic pathway? Why?

Back 23

Can be converted into pyruvate.
Body will use alanine, because amino acids cannot be stored, and must be used up or excreted.

Front 24

Where does alanine effect regulation of glycolysis?

Back 24

Alanine will inhibit pyruvate kinase.

Front 25

How does mannose feed into glycolysis?

Back 25

1. Hexokinase will turn mannose into M6P
2. M6P isomerase turns M6P to F6P

Front 26

How does fructose feed into glycolysis?

Back 26

1. Can be trapped as F6P (minor path)
2. Made into F1P, broken into Glyceraldehye and DHAP. Then glyceraldehyde kinase will yield G3P.

Front 27

What causes fructosemia and fructosuria?

Back 27

A defect in fructokinase, which traps fructose in the cell.

Front 28

A defect in F1P Aldolase will lead to what defect? Why?

Back 28

1. Hypophosphatemia
2. Phosphate trapped in F1P--build up of F1P. Decreased availability of phosphate for glycogen degradation

Front 29

How does galactose feed into glycolysis?

Back 29

1. Galactose is trapped by galactokinase to give Gal-1-P
2. Activated to UDP-Galactose
3. Epimerase makes UDP-Glucose
4. UDP-Glucose becomes G1P
5. Phosphoglucomutase makes G6P

ALSO, Uridyl transferase can make Gal-1P into UDP-Glucose

Front 30

What defect most commonly causes galactosemia?

Back 30

Uridyl Transferase

Front 31

How is UTP made?

Back 31

ATP to ADP will turn UDP into UTP for activation of sugars.

Front 32

Describe glycogen synthesis.

Back 32

UTP reacts with glucose to make UDP-glucose, which will elongate glycogen from the non-reducing end.

Front 33

Describe the action of the branching enzyme.

Back 33

Will break an alpha 1,4 bond and create an alpha 1,6 bond

Also known as 4:6 transferase

Minimum of 11 units necessary, will move 8 units to new position, at least 8 units from a branch point.

Front 34

Describe glycogen phosphorylase activity.

Back 34

Inorganic phosphate will be used to break alpha 1,4 bond on non-reducing end to give glycogen minus 1 unit, and a G1P

Front 35

Describe the actions of the debranching enzyme.

Back 35

When only 4 glucose units are left on a branch, it breaks and adds 3 units to main chain, and releases branch point.

Front 36

Describe the effects of insulin, under well fed conditions.

Back 36

Liver and Muscle:
Uptake of glucose.
Promotes synthesis of glycogen

Front 37

Describe the effects of glucagon and epinephrine.

Back 37

Muscle:
Uptake of glucose
Breakdown of glycogen

Liver:
Release of glucose into bloodstream
Breakdown of glycogen

Pancreas:
Epinephrine shuts down insulin production by Beta-cells

Front 38

What enzyme allows the liver to release glucose into the bloodstream? Can muscles do this?

Back 38

1. Glucose-6-Phosphatase
2. No

Front 39

Describe how glucagon and epinephrine signal across the cell membrane.

Back 39

1. glucagon/epinephrine will bind receptor
2. Receptor will communicate with G-protein complex (Alpha/Beta/Gamma)
3. Alpha unit will bind GTP, and release from Beta/Gamma units
4. Alpha-GTP will bind adenyl-cyclase
5. Adenyl Cyclase will hydrolyze ATP to cAMP (3',5'-cAMP)
6. cAMP is the intracell messenger (second messenger)

Front 40

How is glycogen phosphorylase activated?

Back 40

It is phosphorylated by glycogen phosphorylase kinase

Front 41

How is glycogen phosphorylase kinase activated?

Back 41

It is phosphorylated by protein kinase

Front 42

How is protein kinase activated?

Back 42

Its inhibitor is bound by cAMP, making it active.

Front 43

What does protein kinase do once active?

Back 43

1. It will phosphorylate glycogen synthase--inactivation
2. It will phosphorylate glycogen phosphorylase kinase--activation

Front 44

What enzymes are involved in the cascade triggered by epinephrine?

Back 44

1. G-protein
2. Adenyl Cyclase
3. Protein kinase
4. Glycogen phosphorylase kinase
5. Glycogen phosphorylase
6. Glycogen synthase

Front 45

What breaks down cAMP into AMP?

Back 45

Phosphodiesterase (PDE)

Front 46

How is phosphodiesterase inhibited? Why would you want to inhibit it?

Back 46

1. Methyl xanthines (caffeine, theophylline)
2. leads to a high [cAMP], more breakdown of glycogen, more energy

Front 47

How are the effects of glucagon and epinephrine reversed?

Back 47

Phospho-protein-phosphatase (PPP) inhibitor will be phosphorylated in the activation cascade making it inactive. PPP will then dephosphorylate activated enzymes.

Front 48

What are the subunits of the insulin receptor?

Back 48

2 alpha units
2 beta units

Front 49

What residues on the insulin receptor are responsible to intracell signaling?

Back 49

phosphorylation of tyrosine residues